1

DEVELOPMENTAL DISTURBANCES OF TEETH

2

CONTENTSbull INTRODUCTIONbull CLASSIFICATIONbull DEVELOPMENTAL DISTURBANCES IN

SIZEbull DEVELOPMENTAL DISTURBANCES IN

NUMBERbull DEVELOPMENTAL DISTURBANCES IN

SHAPEbull DEVELOPMENTAL DISTURBANCES IN

STRUCTUREbull DEVELOPMENTAL DISTURBANCES IN

ERUPTIONbull REVIEW LITERATURE 3

bull CONCLUSION bull REFERENCES

4

INTRODUCTION

bull DEVELOPMENTbull The orderly and sequential changes that occur

with the passage of time as an organism moves from conception to death

bull Also referred to as gradual growth which indicates changes in character

5

INTRODUCTIONbull Development of teeth and face is regulated

by genesbull Dental developmental anomalies appear as

a result of disruption in the odontogenesis process by the action of certain disruptive factors

bull The disruptive factors can be genetic factors or environmental factors or even combinations of these factors

6

INTRODUCTION

bull But the genetic programme is very sensitive to disturbances in the environment such as exposure to infection or toxic chemicals including drugs

7

DISTURBANCES OF TEETH

1048708 Environmental

1048708 Developmental

8

INTRODUCTION

bull Developmental disturbances means an abnormality where the pathology starts in the embryonic stage of human life before the formation of the dentition

9

bull SIZE OF TEETH bull SHAPE OF TEETH bull NUMBER OF TEETHbull STRUCTURE OF TEETH bull GROWTH (ERUPTION) OF TEETH

10

CLASSIFICATION

Developmental disturbances in the size of the teeth

MicrodontiaMacrodontia

Developmental disturbances in the shape of the teeth

GeminationFusionConcresenceDilacerationTalonrsquos cuspDens-in-denteDens evaginatusTaurodontismSupernumerary root

11

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

DEVELOPMENTAL DISTURBANCES OF TEETH

2

CONTENTSbull INTRODUCTIONbull CLASSIFICATIONbull DEVELOPMENTAL DISTURBANCES IN

SIZEbull DEVELOPMENTAL DISTURBANCES IN

NUMBERbull DEVELOPMENTAL DISTURBANCES IN

SHAPEbull DEVELOPMENTAL DISTURBANCES IN

STRUCTUREbull DEVELOPMENTAL DISTURBANCES IN

ERUPTIONbull REVIEW LITERATURE 3

bull CONCLUSION bull REFERENCES

4

INTRODUCTION

bull DEVELOPMENTbull The orderly and sequential changes that occur

with the passage of time as an organism moves from conception to death

bull Also referred to as gradual growth which indicates changes in character

5

INTRODUCTIONbull Development of teeth and face is regulated

by genesbull Dental developmental anomalies appear as

a result of disruption in the odontogenesis process by the action of certain disruptive factors

bull The disruptive factors can be genetic factors or environmental factors or even combinations of these factors

6

INTRODUCTION

bull But the genetic programme is very sensitive to disturbances in the environment such as exposure to infection or toxic chemicals including drugs

7

DISTURBANCES OF TEETH

1048708 Environmental

1048708 Developmental

8

INTRODUCTION

bull Developmental disturbances means an abnormality where the pathology starts in the embryonic stage of human life before the formation of the dentition

9

bull SIZE OF TEETH bull SHAPE OF TEETH bull NUMBER OF TEETHbull STRUCTURE OF TEETH bull GROWTH (ERUPTION) OF TEETH

10

CLASSIFICATION

Developmental disturbances in the size of the teeth

MicrodontiaMacrodontia

Developmental disturbances in the shape of the teeth

GeminationFusionConcresenceDilacerationTalonrsquos cuspDens-in-denteDens evaginatusTaurodontismSupernumerary root

11

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

CONTENTSbull INTRODUCTIONbull CLASSIFICATIONbull DEVELOPMENTAL DISTURBANCES IN

SIZEbull DEVELOPMENTAL DISTURBANCES IN

NUMBERbull DEVELOPMENTAL DISTURBANCES IN

SHAPEbull DEVELOPMENTAL DISTURBANCES IN

STRUCTUREbull DEVELOPMENTAL DISTURBANCES IN

ERUPTIONbull REVIEW LITERATURE 3

bull CONCLUSION bull REFERENCES

4

INTRODUCTION

bull DEVELOPMENTbull The orderly and sequential changes that occur

with the passage of time as an organism moves from conception to death

bull Also referred to as gradual growth which indicates changes in character

5

INTRODUCTIONbull Development of teeth and face is regulated

by genesbull Dental developmental anomalies appear as

a result of disruption in the odontogenesis process by the action of certain disruptive factors

bull The disruptive factors can be genetic factors or environmental factors or even combinations of these factors

6

INTRODUCTION

bull But the genetic programme is very sensitive to disturbances in the environment such as exposure to infection or toxic chemicals including drugs

7

DISTURBANCES OF TEETH

1048708 Environmental

1048708 Developmental

8

INTRODUCTION

bull Developmental disturbances means an abnormality where the pathology starts in the embryonic stage of human life before the formation of the dentition

9

bull SIZE OF TEETH bull SHAPE OF TEETH bull NUMBER OF TEETHbull STRUCTURE OF TEETH bull GROWTH (ERUPTION) OF TEETH

10

CLASSIFICATION

Developmental disturbances in the size of the teeth

MicrodontiaMacrodontia

Developmental disturbances in the shape of the teeth

GeminationFusionConcresenceDilacerationTalonrsquos cuspDens-in-denteDens evaginatusTaurodontismSupernumerary root

11

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

bull CONCLUSION bull REFERENCES

4

INTRODUCTION

bull DEVELOPMENTbull The orderly and sequential changes that occur

with the passage of time as an organism moves from conception to death

bull Also referred to as gradual growth which indicates changes in character

5

INTRODUCTIONbull Development of teeth and face is regulated

by genesbull Dental developmental anomalies appear as

a result of disruption in the odontogenesis process by the action of certain disruptive factors

bull The disruptive factors can be genetic factors or environmental factors or even combinations of these factors

6

INTRODUCTION

bull But the genetic programme is very sensitive to disturbances in the environment such as exposure to infection or toxic chemicals including drugs

7

DISTURBANCES OF TEETH

1048708 Environmental

1048708 Developmental

8

INTRODUCTION

bull Developmental disturbances means an abnormality where the pathology starts in the embryonic stage of human life before the formation of the dentition

9

bull SIZE OF TEETH bull SHAPE OF TEETH bull NUMBER OF TEETHbull STRUCTURE OF TEETH bull GROWTH (ERUPTION) OF TEETH

10

CLASSIFICATION

Developmental disturbances in the size of the teeth

MicrodontiaMacrodontia

Developmental disturbances in the shape of the teeth

GeminationFusionConcresenceDilacerationTalonrsquos cuspDens-in-denteDens evaginatusTaurodontismSupernumerary root

11

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

INTRODUCTION

bull DEVELOPMENTbull The orderly and sequential changes that occur

with the passage of time as an organism moves from conception to death

bull Also referred to as gradual growth which indicates changes in character

5

INTRODUCTIONbull Development of teeth and face is regulated

by genesbull Dental developmental anomalies appear as

a result of disruption in the odontogenesis process by the action of certain disruptive factors

bull The disruptive factors can be genetic factors or environmental factors or even combinations of these factors

6

INTRODUCTION

bull But the genetic programme is very sensitive to disturbances in the environment such as exposure to infection or toxic chemicals including drugs

7

DISTURBANCES OF TEETH

1048708 Environmental

1048708 Developmental

8

INTRODUCTION

bull Developmental disturbances means an abnormality where the pathology starts in the embryonic stage of human life before the formation of the dentition

9

bull SIZE OF TEETH bull SHAPE OF TEETH bull NUMBER OF TEETHbull STRUCTURE OF TEETH bull GROWTH (ERUPTION) OF TEETH

10

CLASSIFICATION

Developmental disturbances in the size of the teeth

MicrodontiaMacrodontia

Developmental disturbances in the shape of the teeth

GeminationFusionConcresenceDilacerationTalonrsquos cuspDens-in-denteDens evaginatusTaurodontismSupernumerary root

11

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

INTRODUCTIONbull Development of teeth and face is regulated

by genesbull Dental developmental anomalies appear as

a result of disruption in the odontogenesis process by the action of certain disruptive factors

bull The disruptive factors can be genetic factors or environmental factors or even combinations of these factors

6

INTRODUCTION

bull But the genetic programme is very sensitive to disturbances in the environment such as exposure to infection or toxic chemicals including drugs

7

DISTURBANCES OF TEETH

1048708 Environmental

1048708 Developmental

8

INTRODUCTION

bull Developmental disturbances means an abnormality where the pathology starts in the embryonic stage of human life before the formation of the dentition

9

bull SIZE OF TEETH bull SHAPE OF TEETH bull NUMBER OF TEETHbull STRUCTURE OF TEETH bull GROWTH (ERUPTION) OF TEETH

10

CLASSIFICATION

Developmental disturbances in the size of the teeth

MicrodontiaMacrodontia

Developmental disturbances in the shape of the teeth

GeminationFusionConcresenceDilacerationTalonrsquos cuspDens-in-denteDens evaginatusTaurodontismSupernumerary root

11

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

INTRODUCTION

bull But the genetic programme is very sensitive to disturbances in the environment such as exposure to infection or toxic chemicals including drugs

7

DISTURBANCES OF TEETH

1048708 Environmental

1048708 Developmental

8

INTRODUCTION

bull Developmental disturbances means an abnormality where the pathology starts in the embryonic stage of human life before the formation of the dentition

9

bull SIZE OF TEETH bull SHAPE OF TEETH bull NUMBER OF TEETHbull STRUCTURE OF TEETH bull GROWTH (ERUPTION) OF TEETH

10

CLASSIFICATION

Developmental disturbances in the size of the teeth

MicrodontiaMacrodontia

Developmental disturbances in the shape of the teeth

GeminationFusionConcresenceDilacerationTalonrsquos cuspDens-in-denteDens evaginatusTaurodontismSupernumerary root

11

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

8

INTRODUCTION

bull Developmental disturbances means an abnormality where the pathology starts in the embryonic stage of human life before the formation of the dentition

9

bull SIZE OF TEETH bull SHAPE OF TEETH bull NUMBER OF TEETHbull STRUCTURE OF TEETH bull GROWTH (ERUPTION) OF TEETH

10

CLASSIFICATION

Developmental disturbances in the size of the teeth

MicrodontiaMacrodontia

Developmental disturbances in the shape of the teeth

GeminationFusionConcresenceDilacerationTalonrsquos cuspDens-in-denteDens evaginatusTaurodontismSupernumerary root

11

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

INTRODUCTION

bull Developmental disturbances means an abnormality where the pathology starts in the embryonic stage of human life before the formation of the dentition

9

bull SIZE OF TEETH bull SHAPE OF TEETH bull NUMBER OF TEETHbull STRUCTURE OF TEETH bull GROWTH (ERUPTION) OF TEETH

10

CLASSIFICATION

Developmental disturbances in the size of the teeth

MicrodontiaMacrodontia

Developmental disturbances in the shape of the teeth

GeminationFusionConcresenceDilacerationTalonrsquos cuspDens-in-denteDens evaginatusTaurodontismSupernumerary root

11

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

bull SIZE OF TEETH bull SHAPE OF TEETH bull NUMBER OF TEETHbull STRUCTURE OF TEETH bull GROWTH (ERUPTION) OF TEETH

10

CLASSIFICATION

Developmental disturbances in the size of the teeth

MicrodontiaMacrodontia

Developmental disturbances in the shape of the teeth

GeminationFusionConcresenceDilacerationTalonrsquos cuspDens-in-denteDens evaginatusTaurodontismSupernumerary root

11

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

CLASSIFICATION

Developmental disturbances in the size of the teeth

MicrodontiaMacrodontia

Developmental disturbances in the shape of the teeth

GeminationFusionConcresenceDilacerationTalonrsquos cuspDens-in-denteDens evaginatusTaurodontismSupernumerary root

11

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Developmental disturbances in the number of the teethAnodontiaHypodontia Supernumerary teethPredeciduous dentitionPost permanent dentition

Developmental disturbances in the structure of the teethAmelogenesis imperfectaDentinogenesis imperfectaRegional odontodysplasiaDentin dysplasia

Developmental disturbances in the growtheruption of the teeth

Premature eruptionDelayed eruptionAnkylosed teethSubmerged teeth impacted teeth

12

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Anomalies at different stages of tooth development

13

Dental lamina formation stage Anodontia

Initiation and proliferation Oligodontia Supernumerary teeth Geminated fused teeth

Histodifferentiation -defects in multiple dental tissues

Regional odontodysplasia

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

14

Morphodifferentiation ( defects in size amp shape Macrodontia Microdontia Dens invaginatus Dens evaginatus Hutchinson s incisors mulberry molars ‟Talon cusp Taurodontism

Apposition ( defects in structure of enamel amp dentin ) Amelogenesis imperfecta Enamel Hypoplasia Dentinogenesis imperfecta Dentin dysplasia

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Microdontia it is described as teeth are smaller than usual

1 True Generalized Microdontia

2 Relative Generalized Microdontia

3 Focal or Localized Microdontia

DEVELOPMENTAL DISTURBANCES OF SIE OF TEETH

15

MICRODONTA MACRODONTIA

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

all teeth are smaller than

normal

teeth are well formed

occur in some cases of down syndrome

pituitary dwarfism

exceedingly rare

(1) True Generalized Microdontia

16

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

normal or slightly smaller than

normal teeth

are present in jaws that are

somewhat larger than normal Inheritance of jaw size from one parent and tooth size from other parent can lead to this variations

(2) Relative Generalized Microdontia

17

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

common condition

affects most often maxillary lateral incisior + 3rd molar

these 2 teeth are most often congenitally missing

(3) FocalLocalized Microdontia

18

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

common forms of localized microdontia is that which affects maxillary lateral incisior

peg lateral

instead of parallel diverging mesial + distal surfaces

19

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

sides converge or taper

together incisally

forms cone-shaped crown

root is frequently shorter

than usual

TREATMENT

bull Composite Porcelain Veneers

20

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

MACRODONTIAAlso called as megalodontia or megadontiaIt refers to teeth that are larger than usual

21

(1) True Generalized Macrodontia

(2) Relative Generalize Macrodontia

(3) Focal or Localized Macrodontia

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

all teeth are larger than

normal

associated with

pituitary gigantismpineal hyperplasia with hyperinsulinism

exceedingly rare

(1) True Generalized Macrodontia

MACRODONTIA

22

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

normal or slightly larger than normal teeth in small jaws

results in crowding of teeth

insufficient arch space

(2) Relative Generalized Macrodontia

23

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

uncommon condition

unknown etiologyTrue marodontia often confused with fused teeth

usually seen with mandibular 3rd molars

(3) FocalLocalized Macrodontia

24

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TREATMENT

25

1048708 Stripping to reduce tooth size 1048708 Can be combined with build ndash up of antimere if only one tooth is affected 1048708 Extraction amp replacement by prosthesis

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

DEVELOPMENTAL DISTURBANCES IN SHAPE AND FORM

26

Crown Fusion Gemination Taurodontism Talonrsquos Cusp Leongrsquos Cusp Dens Invaginatus Peg-shaped Lateral Hutchinson Incisor Mulberry Molar

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Root

Concresence

Enamel Pearl

Dilaceration

Ankylosis

Shape and Form

27

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

DOUBLE TEETH

28

1048708joined by crownroot or both Gemination and fusion1048708 May have very similar clinical appearance1048708 Higher frequency in anterior and maxillaryregions1048708 Rate is about 01 in permanent dentitionand 05 in deciduous1048708 Bilateral cases more infrequent1048708 Etiology unknown but trauma has beenSuggestedClinical importance 1048708 Crowding spacing 1048708 Periodontal problem 1048708 Caries 1048708 Eruption disturbance 1048708 Aesthetics

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

GEMINATION

29

an attempt of single tooth bud to divide with resultant formation of tooth with bifid crown

partial cleavage

appearance of 2 crowns

that share same root canal

trauma has been suggested

as possible cause

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

30

TWINNING

bull Designate the production of equivalent structures by division resulting in one normal

and one supernumerary tooth

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

FUSION

31

Fusion of adjacent tooth buds with resultant formation of joined tooth with confluence of dentin Fusion may be complete or incomplete based on the stage of tooth development at the time of fusion

Union of two separate tooth buds

When counted tooth count reveals missing tooth when anamalous tooth is counted as one

Fusion of (a) molar tooth with supernumerary (b) maxillarypremolar with fused roots (c) premolars

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

32

FUSION

Contact occurs before calcification ndash two teeth may be completely united to form a single large tooth

Contact after calcification of the crowns the roots may be unitedTooth may have fused or seperated root cnals

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Differentiating factors

Check for number of teeth

Check for root canal

33

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Treatment of Gemination and fusion

34

Deciduous dentition can results in Crowding abnormal spacing delayed eruption of permanent teeth Extraction Otherwise Surgical division amp endodontic treatment is done

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TAURODONTISM-(tauro bull donrsquot_ teeth)

35

Taurodontismrsquo was originated by Sir Arthur Keith in 1913It is an enlargement of the body and pulp chamber of a tooth with apical displacement of the pulpal floor

Shawrsquo classified taurodont teeth according to degree of apical displacement of pulpal floor

Hypotaurodontmild

Mesotaurodontmoderate

Hypertaurodont severe

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

36

HereditaryMutation resulting from odontoblastic deficiency during dentinogensis of rootsA primitive patternFailure of Hertwigs epithelial root sheath to invaginate at proper horizontal level

Clinical Features The deciduous or permanent dentition (more common)Molars(3rd2nd1st)May be unilateral or bilateralIncreased frequency in patients with cleft lippalatealso associated with syndromes like downs syndromeklinefelter syndrometrichodento-oseous syndrome Oculo‐dental‐digital dysplasiaOrofacial digital syndectodermal displasiabullSex chromosomal aberrationsAmelogenesis imperfecta IEIV

CAUSES

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Radiographic features

37

Rectangular in shape

Pulp chamber is large

Bifurcation or trifircation few millimeter

Lack of constriction

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TREATMENT

38

Requires no specific therapy

Pulp therapy in taurodonts Challenging task bleeding during access Canal locating instrumenting obturating difficult

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

39

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

ACCESSORY CUSPS

40

Cuspal morphology of the teeth exhibit minor variations

CUSP OF CARABELLI

TALONS CUSP

DENS EVAGINATUS

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

An accessory cusp located on An accessory cusp located on the palatal surface of thethe palatal surface of the mesiolingual cusp of a maxillary molar mesiolingual cusp of a maxillary molar

May be seen in deciduous or permanent teethMay be seen in deciduous or permanent teeth amp varies from cusp to small indented pit or fissure amp varies from cusp to small indented pit or fissure

41

CUSP OF CARABELLI

90 in whites and rare in Asians90 in whites and rare in AsiansRequires no therapy unless deep groove is presentRequires no therapy unless deep groove is present

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

PROTOSTYLID

bullOccasionally on the mesiobuccal cusp of mandibular permanent or deciduous molar

42

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TALON CUSP

43

Eaglersquos talonbullA well delineated additional cusp that is located on the surface of an anterior tooth amp extends at least half the distance from the CEJ to the incisal edge(lingual side) bullComposed of normal enamel and dentin and contains a horn of pulp tissue

bullPrevalence ranges from 1-8

bull Chawla et al-77 prevalence- north Indian children

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

bullIn primary dentition maxillary central incisor most

common site

PATTERNS OF TALON CUSPS three types based on morphologybull Trace talon bullSemi-talon bullTalon Forms T ndashform Y -shaped

bullSeen in patients with rubinstein teybi syndromestruge weber syndromemohr syndrome

bullRadiographicallythe cusp is seen overlying the central portion of crown amp includes enamel and dentin

bullClinical problems include esthetics caries control and occlusal accombidation

44

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TREATMENT

45

bullOcclusal interferencebull Prophylactically restoring the groove to prevent caries Or bullFissure sealants to prevent caries around the margins

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

DENS EVAGINATUSAlso called Leongrsquos premolar Evaginated odontome

46

bullIt is a developmental condition that appears clinically as an accessory cusp or a globule of enamel on the occlusal surface between the buccal and lingual cusps of premolars bullunilaterally or bilaterallybullRare in whites 15 in asians

bullOccurs in persons of mongoloid ancestryndashchinese japanese filipinos eskimos and american indians‐

bullEvolves by proliferation and evaginationof an area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the dental organ during early tooth development

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Extra cusp can lead tobullIncomplete eruptionbullDisplacement of teethbullPulp exposure following occlusal wear or fracture

Radiographic features

bullOcclusal surface exhibits a tuberculated apearance and often pulpal extension is seen in the cusp

Treatment

Extraction is indicated if tooth is nonvital

Grinding of the tubercle amp indirect pulp

capping with calcium hydroxide47

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

SHOVEL SHAPED INCISOR

48

bullAssociated with dens evaginatusbullAffected incisors demonstrate prominent lateral margins creating a hallowed lingual surface that resembles the scoop of shovelbullMaxillary central incisors most affectedbullPredominantly in asians native americans and alaskans

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

DENS INVAGINATUS

49

bull Also called as Dens In Dente Dilated composite odontome

bull It is a deep surface invagination of the crown or root by enamel before calcification occurs

bull Causes

ndash Increased localized external pressure

ndash Focal growth retardation

ndash Focal growth stimulationbull Maxi Permanent Lateral incisor most

commonly involved while central rare

bull Condition is frequently bilateral

bull Prevalence 004-10

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Oehlers (1957) divided this condition into 2 forms

Coronal Type 123 Radicuar

Coronal dens invaginatus has been classified into three major types

50

Type IAn invagination that is confined to the crown

Clinical significance Predisposition to caries Pulpal pathology Periapical pathology (Type III) Early diagnosis ndash mandatory

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Type II

Extends below the CEJ amp ends in the blind sac that may or may not communicate with adjacent dental pulp

51

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Type III

Extends through the root amp perforates in the apical or lateral radicular area without any immediate communication with pulp

Enamel line often replaced by cementum close to the radicular perforation

Perforation provides communication from oral cavity to the intraosseous periradicular tissue ampoften produce inflammatory lesions

52

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

RADICULAR TYPE

53

bullRadicular invagination results from infolding of hertwigrsquos sheath and origin is within the root after development is complete

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

RadiographbullAffected tooth demonstrate an enlargement of the rootbullDilated invagination lined by enamel

bull Radiographs reveal a pear shaped invagination of enamel and dentin with a narrow constriction at the opening on the surface of the tooth and closely approximating the pulp in its depth

bull Severe form ndash an invagination that extends nearly to the apex of the root

TYPE II CORONAL DENS INVAGINATUS

TYPE III CORONAL DENS INVAGINATUS

54

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TreatmentSmall type I opening of the invagination is restored to prevent carious involvement

Large typeContents of the lumen amp any carious dentin must be removed amp calcium hydroxide base is placedPulpal pathosis or pulpal communication then endodontic therapy is recommended

55

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

MULBERRY MOLARS (MOONS MOLAR)

56

bullMolars have multiple poorly developed cuspsbullSeen in congenital syphilisbullMulerry molar shows numerous disorganized globular projection that resembles like mulberrybullCondition occurs due to spirochete infection of enamel organ of teeth during amelogenesis

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

HUTCHINSON INCISOR

57

characteristic of congenital

syphilislateral incisors are peg-shaped

or screwdriver-shaped widely spaced notched on their biting end with a crescent-shaped defect

named after Sir Jonathan

Hutchinson English surgeon +

pathologist who 1st

described it

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

SHAPE AND FORM

58

ROOT

Concrescence Union of two adjacent teeth bycementum alone May occur before or after eruption Seen most commonly posterior andmaxillary regions Etiology believed to be trauma orOvercrowding

Usually involves two teeth But involving three teeth has also been reported

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

FACTORS ASSOCIATED

59

LOCAL FACTORSbullAbnormal occlusal traumabullAdjacent inflammationbullUnopposd toothimpacted without antagonist

SYSTEMIC FACTORS

Acromegaly and pituitary gigantismndashArthritisndashCalcinosisndashPagetrsquos disease of bonendashRheumatic feverndashThyroid goiterndashVitamin A deficiency

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

60

bullDiagnosed by radiographic examination

Histopathology bullDeposition of excessive cementum over the original layer of primary cementum

bullMay be hypocellularor exhibit areas of cellular cementum resembling bone called osteocementum

bullPolarized light to differentiate dentin and cementum

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TREATMENT

61

often requires no therapy

unless union interferes with

eruption then surgical

removal may be warranted

since with fused teeth

extraction of one may result in

extraction of the other

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

DILACERATION

62

Abnormal angulation or bend in root or less frequently crown of tooth

Majority due to trauma to tooth germ calcified portion

Permanent maxillary incisors are frequently involved followed by mandibular incisors

Dilaceration in a permanent tooth often follows traumatic injury (avulsion or intrusion) to the deciduous predecessor in which the tooth is driven apically into the jaw Can also develop secondary to adjacent cyst tumor or odontogenic hamartoma

kinked tooth rdquo or ldquo sickle ndash tooth

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TREATMENT

63

Vary according to severity

Extraction if it is non vital then surgical removal is suggested

Can be problematic during extraction sometimes

Deciduous teeth ndash Extraction

Permanent teeth

Minor ndash no treatment

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

ECTOPIC ENAMEL

64

Thought to arise from localized bulging in the odontoblastic layer with prolonged contact between HERS and dentin leading to enamel formation

Enamel in unusual location

Enamel pearlEnamel pearl

Common-roots of max molars followed by mand Molar

Deciduous molar is not rare

11-97 - highest in Asians

Majority occurs on the roots at furcation area

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

ENAMEL PEARLS

65

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

CERVICAL ENAMEL PROJECTION

66

Represent dipping of enamel from the CEJ toward the bifurcation of molar teeth

Mandibular molars affected more frequent

prevalence is greater in Asians (86-324) Extensions is correlated with localized loss of periodontal attachment with furcation involvement

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TREATMENT

67

Oral hygiene should be maintained

Flattening or removal of enamel pearl or furcation plasty can be done

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

SUPERNUMERARY ROOTS

68

Refers to the development of an increased number of roots on a tooth compared with that described in dental anatomy

bullMay involve any tooth

bullMandibular cuspids and bicuspidsmay have two roots

bullMaxillary and mandibular molars may exhibit additional roots

bullSignificant during extraction

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH

69

AnodontiaHypodontiaHyperdontiaOligodontiaSupernumerary teeth

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

ANODONTIA

70

bullCongenital absence of teeth

EtiologyHereditaryAutosomal dominentHereditary ectodermal dysplasiaCleidocranial dysplasiaX-ray radiations

TypesTrue

TotalPartial (hypodontia)

FalsePseudo

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

71

Clinical featuresWomenMongoloidWhites

True total anodontiaAll teeth missingCan be either deciduous or permanent

True partial anodontiaAbsence of one or more teethCommonly missing teeth ndash 3rd molars max lateral incisors max mand 2nd premolars

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

72

False anodontiaDue to extraction of teeth

PseudoanodontiaDue to multiple unerupted teeth

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

HYPODONTIA

73

lack of development of one or more teeth

Common dental anomalyEtiology bull Familial tendency ndash point mutations transmitted in autosomal dominant pattern

bull Missing third molars could be an evolutionary trend towards fewer teeth

bullIt is associated with hereditary ectodermal dysplasia

bull Xray radiation of face during early age ndash affecting the sensitive tooth buds

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

74

35-8 (excluding third molars) Female predominance about 151 Uncommon in primary dentition (lt1) About 20-23 of population missing third molars After third molars second premolars and laterals most frequent

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

75

Syndromes associated withhypodontia Ectodermal dysplasia Chondroectodermal dysplasia (Ellis-vanCreveld) Progeria Down Hallermann-Streiff Rieger Crouzons Albright hereditary osteodystrophy

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

76

Prevalence of supernumerary teeth is about 1-3 (higher rate in Asians) Single tooth hyperdontia represent 75-85 of cases

More common in permanent dentition

Almost 90 in maxilla

Maxillary incisor region most common site then 4th molarspremolars and canines

If multiples usually in mandibular premolar region

HYPERDONTIA

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

77

Syndromes associated withhyperdontia Cleidocranial dysplasia Oral-Facial-Digital Apert syndrome

cleidocranial dysostosis

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

78

Classification of supernumerary teeth

Modified Howard s classification‟

Supplemental supernumerary teeth

Accessory supernumerary teeth

bull Classified according to morphology and location four different types

bull Conical

bull Tuberculate

bull Supplemental

bull Odontome

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

79

Supplemental supernumerary teethThese teeth duplicate the typical anatomy of anterior and posterior teeth

Mesiodens bullMost common Supplemental supernumerary teethbullSmall tooth with cone shaped crown and short rootbullLocated near the midline in the incisor region of maxilla between the central incisorsbullOccurs single multiple erupted impacted bullCauses retarded eruption displacement of adjacent tooth or resorption of adjacent root and thus improper alignment of teeth

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

80

DISTOMOLARSFound in molar regionLocated distal to 3rd molarsGenerally these teeth are smaller than normal 2nd amp 3rd molarsBut crown morphology is abnormal

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

81

PARAMOLARS

It is an supernumerary molar

Usually small and rudimentarySituated buccally or lingually to one of the maxillary molars

Interndashproximally between 1st 2nd 3rd maxillary molars

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TRANSPOSITION

82

Normal teeth erupting into an inappropriate position

bullUsually involves the canine and first premolarsbullCanine erupting between two premolarsbullCould be confused with supernumerary teeth

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

83

Developmental disturbances in the growtheruption of the teeth

Premature eruption

Delayed eruption

Ankylosed teeth

Submerged teeth impacted teeth

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

84

NATAL TEETHPremature eruption of teeth like structuresPresent at birthThey are hyper mobile because of their limited root developmentConical or normal in size and shapeSome teeth are so mobile that there is danger of displacement and possible aspiration ndash removal is indicated other wise not

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

85

Sharp incisal edges may cause laceration of lingual surface of tongue rarr RIGAndashFEDE DISEASEAssociated with Ellis-van creveld syndrome

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

86

Neonatal teeth

These are the teeth or teeth like structures that erupt prematurely during neonatal period

From birth to 30 days

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

87

TREATMENT

Extraction of teeth (if causing inconvenience)

Or Rounding of the sharp angles of the teeth

Extraction should be done after 10 days of life

If not necessary tooth should not be removed

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

88

ERUPTION SEQUESTRUM

Anomaly associated with tooth eruption in children

Described by Starkey and Shafer It is a tiny irregular spicule of bone overlying the crown of an erupting permanent molar found just prior to or immediately following the emergence of the tip of the cusps through the oral mucosa

Etiology As the molar teeth erupt through the bone they can separate a small osseous fragment from the surrounding bone similar to a cork screw In most cases the fragment undergoes complete resorption before eruption If the bony spicule is large or the eruption is rapid complete resorption cannot occur and hence it is observed

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

89

CLINICAL FEATURES The child may complain of slight soreness in the area during function

The spicule directly overlies the central occlusal fossa but is within the soft tissue

It may be seen lying in a tiny depression over the crest of the ridge

As the tooth erupts the fragment of bone completely sequesters through the mucosa and is lostrsquo Radiographic features It can be recognized even before the tooth eruption Seen as a tiny irregular opacity overlying the central occlusal fossa but separated from the tooth itself

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

DELAYED ERUPTION

90

In deciduous and permanent teeth it is difficult to assess unless a gross variation is presentbullCaused by Systemicconditions like rickets cretinism cleidocranial dysplasia

bullLocalfactors like fibromatosis gingivae

bullTreatment of the primary condition may lead to eruption of teeth

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

91

IMPACTED TEETH

occurs due to obstruction

from crowding

from some other physical

barrier

occasionally may be due

to an abnormal eruption

path presumably because

of unusual orientation of

tooth germ

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

92

Any tooth may be impacted ndashusually mandibular third molars(22) maxillary third molars(18) and maxillary cuspids(09) premolars and supernumerary teeth

Mandibular teeth are more severly

impacted

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

ANKYLOSIS

93

fusion of a tooth to surrounding

bone

with focal loss of periodontal

ligament bone + cementum

become inextricably mixed

cause fusion of tooth to

alveolar bone

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

94

Reported prevalence of clinicallydetectable ankylosis- 15 to 9

Primary molars are most commonly involved teeth with most cases in mandible

Even with extreme root resorption teeth lack mobility

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

95

bullDiagnosis is suspected clinically and confirmed with radiographsbullThere is partial absence of the periodontal ligament with areas of apparent blending between the root of the tooth and alveolar bonecomplicationsDevelopment of malocclusionbullLocal periodontal disturbancebullDental caries of both the ankylosed tooth and adjacent teeth

TREATMENTDepends on whether tooth are ankylosed or not permanent successor present or not

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

96

DEVELOPMENTAL DISTURBANCES IN THE STRUCTURE OF THE TEETH

Amelogenesis imperfecta

Dentinogenesis imperfecta

Regional odontodysplasia

Dentin dysplasia

Enamel hypoplasia

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

AMELOGENESIS IMPERFECTA

97

also known as

Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

98

Group of conditions caused by

defects in the genes encoding

enamel matrix proteins genes that encode for enamel

proteins amelogenin mutated in enamelin in patients others with this

condition

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

99

A heterogeneous group of hereditarydisorders that demonstrate developmentalalterations in the structure of enamel in theabsence of a systemic disorder

Many subtypes Numerous patterns of inheritance Wide variety of clinical manifestations Frequency varies between 1718 and114000 Both dentitions involved

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

100

Formation of enamel a multistep process Formation of enamel matrix Mineralization of matrix Maturation of matrix Hereditary defects of enamel formation usually classified as

Hypoplastic Hypocalcified Hypomaturative

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

101

Amelogenesis imperfectaWitkop classification

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

102

Hypoplastic Amelogenesis Imperfecta

Inadequate formation of matrixFEATURESTeeth erupt with insufficient amounts of enamel

Enamel present is mineralizedappropriately and contrasts well with dentin on radiograph

Teeth may have abnormal shape and open contacts Open bite may be present

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

103

bullHypoplastic generalized pitted pattern

bullHypoplastic localized patern

bullHypoplastic autosomal dominant smooth pattern

bullHypoplastic rough pattern

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

104

HYPOPLASTIC GENERALIZED PITTED PATTERN

Pin point to pin head sized

pits scattered

Buccal surfaces affected mure severly

Pits may arranged in rows and columns

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

105

HYPOPLASTIC LOCALIZED PATTERN

Horizontal rows of pitsa linear

depression

Middle third of buccal surfaces of teeth is aeffected

Both dentition orprimary only may be aeffected

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

106

HYPOPLASTIC AUTOSOMAL DOMINANT SMOOTH PATTERN

Enamel of all teeth exhibit smooth surfacethin hard glossy surface

Absence of appropriate enamel thickness

Colour varies from opaque white to translucent brown

Radiographically thin peripheral radiopaque enamel

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

SMOOTH PATTERN

107

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

HYPOPLASTIC ROUGH PATTERN

108

Enamel is thin with hard rough surface

Teeth taper towards incisal-occlusal surfaces

open contact points

significant attrition and anterior open bite

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

109

bullENAMEL AGENESIS

bullDemonstrate total lack of enamelbullTeeth are shape and colour of dentin with yellow brown huebullOpen contactsbullCrowns taper towards incisallybullDentin is roughbullRadiograph demonstrates no peripheral enamel overlying dentinbullA lack of eruption of many teeth occurs frequently

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

HYPOMATURATION TYPE

110

Enamel matrix is laid down properly andbegins to mineralize but there is a defect inmaturation of enamelrsquos crystal structure Affected teeth normal in shape Mottled appearance-white brown or

yellow Enamel soft and chips away from dentin Enamel has similar radiodensity to dentin

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

111

AUTOSOMAL DOMINANT

HYPOMATURATION TYPE

AUTOSOMAL RECESSIVE

X LINKED RECESSIVE

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

HYPOMATURATVE-AUTOSOMAL DOMINANT

112

Commonly in malesBoth permanent and primaryprimary teeth-ground glass opaque white

Permanent teeth ndashmottled yellow whitedarkened on absorption of stains

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

HYPOMATURATIVE-AUTOSOMAL RECESSIVE

113

Both primary and permanent dentitionEnamel shows milky to shiny agar brown deeply stained on contact with exogenous agentsChips away around teeth restorationTeeth may resorbs within alveolus

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

HYPOPLASTIC X-LINKED RECESSIVE

114

Aeffects both dentitions

White opaque areas on enamel of incisal and occlusal third of crown ndashSNOW CAPPED PATTERN

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

HYPOCALCIFIED ndashAMELOGENESIS IMPERFECTA

115

Proper amount of enamel matrix is formed but butit doesnrsquot mineralize properly

Teeth shaped normally upon eruption but enamelis soft and easily lost

Enamel yellow-brown upon eruption but quicklybecomes brown to black Accumulate calculus

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

HYPOMATURATION HYPOPLASTIC TYPE

116

bullEnamel hypomaturation is the dominant feature

bullEnamel is yellowish white to ‐yellowish brown‐bullPits are seen on buccal surfacebullEnamel is similar to dentin in densitybullLarge pulp chambers with varying degrees of taurodontism

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

HYPOPLASTIC-HYPOMATURATIVE AD

117

bullEnamel hypoplasia is the dominant feature

bullEnamel is thin

BOTH PATTERNS SEEN IN TRICHODENTO OSSEOUS SYNDROME

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TRICHO-DENTO-OSSEOUS SYNDROME

118

bullAutosomal dominant disorder

bullShows hypoplastic hypomaturation ‐with severe taurodontism

bullKinky hairat birth which may straighten with age

bullOsteosclerosisof the base of skull and mastoid process

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TREATMENT

119

Vary accoring to sub type and severity

Main problems associated are estheticssensitivityand loss of vertical dimension

Full coverage restoration recommended in attrition cases

Less severe cases can be improved by placements of full crowns and facial veneers

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

DENTINOGENESIS IMPERFECTA

120

bullCalled Hereditary opalescent dentin Capdepontrsquos teeth

bullOnly the mesodermal portion of the odontogenic apparatus is affected

bullDentin is defective

bullCould be due to hereditary factors

bullCan be seen in association with osteogenesis imperfecta

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

CLINICAL FEATURES

121

Deciduous teeth are more severely affected

bullGray to brownish violet or yellowish brown with a characteristic translucent or opalescent hue

bullBroad crown with constriction of cervical area constriction ndash TULIP SHAPE

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

122

Enamel may be lost earlyon incisal and occlusal surfaces due to the abnormal DEJbullDEJ lacks the usual scalloping

bullDentin is attrited rapidly

bullOcclusal surfaces of affected teeth are severely flattened

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

123

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

CLASSIFICATION BY SHIELDS

124

Type I ndashDI that always occur with OIndashautosomal dominant

bullType II ndashDI that never occurs with OIndashhereditary opalescent dentin ndashautosomal dominant

bullType III ndashDI ndashBrandy wine typendashsimilar autosomal dominant

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

1 in 8000

occurs in families with

Osteogenesis Imperfecta

primary teeth are more severely

affected than permanent teeth

125

TYPE I DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Radiographically

partial or total obliteration

of pulp chambers + root canals by continued formation

of dentin roots may be short + blunted cementum periodontal

membrane + bone appear

normal

126

Type I DENTINOGENESIS IMPERFECTA

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

never occurs in association with osteogenesis imperfecta unless by chance

most frequently referred to as hereditary opalascent dentin

only have dentin abnormalities and no bone disease

127

Type II DENTINOGENESIS IMPERFECTA

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Radiographically

partial or total obliteration of pulp chambers + root canals by continued formation of dentin roots may be short + blunted cementum periodontal membrane + bone appear normal

Type II Dentinogenesis Imperfecta

128

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

ldquoBradwine typerdquo

racial isolate in Maryland

multiple pulp exposures in deciduous not seen in type I or II

periapical radiolucencies

Type III Dentinogenesis Imperfecta

129

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

enamel appears normal

large size of pulp chamber

is due not to resorption but

rather to insufficient + defective

dentin formation

Type III Dentinogenesis Imperfecta

130

Witkop describes it as Shell teeth

Radiographic features

Roots are extremely short

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

HISTOLOGIC FEATURES

131

bullDentin has irregular tubules with large areas of uncalcified matrix

bullTubules are larger in diameter and lesser in number

Cellular inclusions probably odontoblasts can be seen in dentin

bull

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

132

bullThe odontoblasts with limited ability to form well organized dentinal matrix ‐appear to degenerate readily and get entrapped within the matrix

bullPulp chamber is obliterated by continuous dentin deposition

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Treatment

DENTINOGENESIS IMPERFECTA

133

oPreservation of vertical dimension of occlusion

o Continued commitment amp support to both child amp family

o Stainless steel crowns to protect against attritiono o Initial composite build ndash up for anteriors to be replaced by veneers later Overdentures implants later

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

also known as ldquoRootless Teethrdquo

rare disturbance of dentin

formation atypical dentin formation

DENTIN DYSPLASIA

134

First described by Ballschmiede(1920) ndashspontaneous exfoliation of multiple teeth

bullRushton(1939) designated it as dentin dysplasia

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

135

Rare autosomal-dominant condition that affects dentin

Prevalence about 1100000

abnormal pulpal morphology

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

CLASSIFICATION

136

ShieldsType I ndashdentin dysplasiaType II ndashanomalous dysplasia of dentin

bullWitkopsType I ndashRadicular dentin dysplasia ndashMore commonType II ndashCoronal dentin dysplasia

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Classification

Type I (Radicular Type)

Type II (Coronal Type)

DENTIN DYSPLASIA

137

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

both dentitions are of

normal color

Most common type

prevalence 1100000

Type I (Radicular Type)

138

(Rootless teeth)

Wide variation in root formation because dentinal

disorganization may occur at different stages of tooth

development

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Radiographically

roots are extremely short pulps almost completely

obliterated periapical radiolucencies

bull granulomas

bull cysts

bull chronic abscesses

Type I (Radicular Type)

139

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

autosomal dominant

Root length is normal

Colour blue -amber to brown translucency

coronal pulps are usually large

(thistle tube appearance)

filled with globules of abnormal

dentin

Type II (Coronal Type)

140

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Radiographically

(Deciduous) roots are extremely short pulps almost completely

obliterated

(Permanent) abnormally large pulp

chambers in coronal portion of

tooth

Type II (Coronal Type)

141

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

also known as

Odontogenic Dysplasia Odontogenesis Imperfecta Ghost Teeth

142

REGIONAL ODONTODYSPLASIA

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

one or several teeth in a

localized area are affected

maxillary teeth are involved

more frequently than

mandibular area

etiology is unknown

143

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

teeth affected may exhibit

a delay or total failure in

eruption

shape is altered irregular in appearance

144

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Radiographically

marked reduction in

radiodensity teeth assume a ldquoghostrdquo

appearance both enamel + dentin appear

very thin pulp chamber is exceedingly

large

145

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Treatment

poor cosmetic appearance

of teeth extraction with restoration

by prosthetic appliance

146

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

ENAMEL HYPOPLASIA

147

An incomplete or defective formation of the organic enamel matrix of teeth

bullIt occurs only when the injury occurs during the development or more specifically formative stage of enamel

TYPES

IHereditary type enamel hypoplasia

IIEnvironmental type hypoplasia

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Hereditary type enamel hypoplasia

148

bullThis is an ectodermal disturbance that occurs during the embryonic development of the enamel

bull The mesodermal components are normal Both the deciduous and permanent teeth are involved and only the enamel is affected

The three types of hereditary type of enamel hypoplasia are thebullHypoplastic type where there is a defective formation of organic matrix

bullHypocalcification type in which there is a defective mineralization of the matrix

bullHypomaturation type where there is a defective maturation of the matrix

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Environmental type enamel hypoplasia-

149

This is caused by the environmental factors that causes damage to the enamel cells

Either deciduous or permanent teeth are involved and sometimes a single tooth is involved

Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically during the formative stage of enamel development

The environmental factors which produce enamel hypoplasia can include

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

150

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

CLINICAL FEATURES

151

Mild

Few small grooves pits or fissures on enamel surface

ModerateEnamel may exhibit rows of deep pits arranged horizontally across tooth surface

Severepitting and brownish staining of the surface Tendency of enamel to wear or fracture

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

TREATMENT

152

Treatment of enamel hypoplasia is always individualized and depends on the location and severity of then condition The location of enamel hypoplasia also affects treatment options

gt Anterior teeth - For sensitive teeth with no wear desensitizing agent (such as potassium nitrate) as needed can be used

If there are esthetic concerns composite or porcelain veneers may be bonded to afected tooth

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

153

Posterior teeth ndash 1 For sensitive teeth with minimal wear desensitizing agent

(such as potassium nitrate) can be used

2 For mildly hypoplastic molars place pit and fissure sealant on the occlusal surface - at 6 month re-evaluation

3 Remove demineralized enamel and restore with composite - at 6 month re-evaluation if composite is lost either replace using good isolation techniques or go to step 4

4 Perform minimal reduction of tooth and cement a stainless steel crown - evaluate clinically and radiographically as indicated

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

CASE REPORTS

154

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

155

A CASE REPORT OF A PATIENT AFFECTED BY AMELOGENESISIMPERFECTASHOWING A POSSIBLE MINIMALAND CONSERVATIVE ADHESIVE TREATMENT APPROACH

A 14 years old boy with amelogenesis imperfecta consulted a dentist for full mouth rehabilitation

After examination step by step minimum conservative approach planned

S Ardu O Duc I KrejciR Perroud

Clinical views at the patientrsquos first appointment

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

156

In the posterior area conservative resin composite onlays were realized whereas in the anterior areafreehand bonded composite restorations wereperformed according to the natural layering technique proposed

Intraoral view of the conservative preparations for resin composite onlays and clinical view after posterior onlays placement

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

157

Intraoral view of the preparations for freehand bonded composite restorations and clinical view after teeth rehydration Last imageshows the clinical view after the placement of a cantilever bonded bridge 23

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

158

Clinical views at the end of the treatment together with the final treatment status at the 3-month recall Except for the lithium disilicatebridge from 21ndash23 all other teeth are single-unit lithium disilicate bonded crowns

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

159

bullcase report describes a possible application of aminimally invasive approach for treating amelogenesisimperfecta in a young adolescent

bullThis conservativeadhesive treatment allows a two-stageintervention that accompanies the patient duringhis adolescence until the complete formation of hardand soft tissues

bullThis will allow acceptable estheticsand lack of pain during eating and will allow thepatient to have a more normal social life

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

160

Dan Emil GEORGESCU Rodica LUCA and Elisa Mădălina CHIRCA

Conducted study to assess the frequency of development anomalies of teeth and soft tissue in the anterior region of a school children from Bucharestcross sectional study is conductedMaterial and methods 226 children from two secondary schools aged between 5-8years

bullChildren were examined in the school dental office

bull The presence of dental development anomalies or of other types was recorded

bull The frequency of developmental anomalies was determined

bull487 of the examined school children had oral developmental anomalies

Fused teeth

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

161

Dental size anomalies (044) - one fusion and one gemination and 9 abnormal maxillary frenum attachment (398)

Dental anomalies were found in front teeth in both dentition

Diastema was found in permanent dentition between the two upper central incisors The evaluated age group had a low frequency for front teeth dental development anomalies

Follow up of all children is necessary until the eruption of all permanent teeth

Gemination

Diastema between the two upper permanent central incisors

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

162

Endodontic treatment of developmentalanomalies in posterior teeth Treatment ofgeminatedfused teeth Nelly Steinbock

Two cases of complex endodontic treatment of fusedgeminated teeth are presented

The first is an 11-year-old girl with an anomalous lsquodoublersquo first mandibular molar and premolar diagnosed as having necrotic pulp with chronic apical abscess of endodontic origin

Fused crowns of the mandibular right first molar and second premolar

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

163

Two separate endodontic access cavities were prepared in the fused crown in the molarand the premolar area

bullFive canal orifices were found ndash two leading to the distal root canals(emerging from the molar pulp chamber) and the other three leading to the mesial roots andemerging from the floor of the premolar pulp chamber

bullThe canals were instrumented manually using K-files and irrigated with 3 sodiumhypochlorite solution

bull Working length was determined with an electronic apex locator

Working length radiograph of the fused mandibular right first molar and second premolar

bullFollow-up 6 months later showed that the tooth was restored with composite filling

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

164

The second is a 16-year-old boy with lsquodoublersquo second and supernumerary mandibular molars who was diagnosed with irreversible pulpitis

Preoperative radiograph of the geminated second molar tooth (fusion of molar with supernumerary)

Clinical examination revealed an anomalous second molar that could have been a fusion of the mandibular right second molar with a supernumerary tooth in its mesiobuccal aspect

bullRadiographic examination

bullTwo separate access cavities were prepared

bullFive canal orifices were found on the mesial side of the pulpchamber floor ndash two leading to the supernumerary tooth and three leading to the mesial rootof the molar

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

165

Working length determination radiograph demonstrating five of the six canals

bullIrrigated with 3 sodium hypochlorite solution

bullThe tooth was obturated usingthe lateral condensation technique with AH-26 as a sealer

DISCUSSION

bullFusion and gemination are developmental

anomalies with inherently unusual and bizarre

anatomy

bullA prerequisite for endodontic treatment of

anomalous teeth is a careful examination

of radiographs from various angles

In both the cases there was a communication between two parts of the pulp chambers and root canal systems Thus endodontic treatment was performed on bothparts of these teeth

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

166

Dental Anomalies in Chinese Children with Cleft Lip and Palate

Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

bull The prevalence of anomalies in children with CLP and to ascertain if there were any differences between the prevalence figures for CLP and non-CLP children

bull The sample consisted of 231 pairs of age and gender matched CLP and non-CLP southern Chinese aged between 12 and 16 years

bull The dental records of the subjects were examined to gather data on anomalies of tooth number size and shape

Missing permanent maxillary lateral incisor and canines

Number of types of dental anomalies per individual

Hypodontia (576) Microdontia (424)

The cleft type associated with the highest percentage of supernumerary teeth was CL (250)

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

167

bullApproximately 10 of BCLP UCLP and CP children were found to have taurodontism

Taurodontism of permanent maxillary first

molars bullThis group of Chinese CLP children exhibited the

various types of dental anomalies

bull Statistically higher prevalences of hypodontia

supernumerary teeth and microdontia were

demonstrated in the CLP children than in the non-

CLP children

A conical shaped supernumerary tooth in relation to permanent maxillary right canine

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

CONCLUSION

168

Anomalies on tooth have aesthticfunctionalpsychological impact on the individualso any abnormalities or pathologies on hard or soft tissues in oral cavity must prompt clinician to think beyond the local factors for proper diagnosis and treatment

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

ReferencesReferences

BooksBooks

Neville et al Oral and Maxillofacial PathologyNeville et al Oral and Maxillofacial Pathology 33rdrd Edition Edition

Shafer et al A textbook of Oral PathologyShafer et al A textbook of Oral Pathology 33rdrd Edition Edition

Anil govindrao ghomtextbook of oral medicineAnil govindrao ghomtextbook of oral medicine 44thth edition edition

Cawson RA Cawsonrsquos Essentials of OralCawson RA Cawsonrsquos Essentials of Oral Oral Pathology and Oral MedicineOral Pathology and Oral Medicine 88thth Edition Edition

169

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

Burkits textbook of oral medicine11th edition

Dental Anomalies in Chinese Children with Cleft Lip and Palate Hai Ming Wong1 Moon Cheung Lai2 and Nigel Martyn King3

Endontic treatment of developmental anomalies in posterior teethtreatment of fusion and gemination teeth(endodontic journal 2003)

170

Amelogenesis ImperfectaA Conservative and Progressive Adhesive Treatment ConceptS Ardu O Duc I KrejciR Perroud (operative dentistry 2013)

171

171