Therapeutic dentistry department Un-carious defects of teeth.
Classification. Pathomorphology, clinic and diagnostics of defects
that are developed before and after eruption of teeth.
Treatment.
Slide 2
Uncarious lesions of teeth Developmental Alterations of Teeth
Post-eruptive Alterations of Teeth
Slide 3
Developmental Alterations of Teeth I. Lesions that occur in the
stage of dental follicle development, before eruption: 1.
hypoplasia; 2. hyperplasia of enamel (enamel pearls); 3. endemic
fluorosis; 4. developmental disturbances and disorders of eruption;
5. genetic disturbances of tooth development.
Slide 4
Posteruptive Alterations of Teeth II. Lesions that occur after
teeth have been erupted: 1. tooth wear: attrition, abrasion,
wedge-shaped defect; 2. erosion; 3. necrosis of hard tooth tissues;
4. hyperesthesia; 5. trauma of teeth; 6. fluorosis; 7.
discolorations of teeth: intrinsic stains extrinsic stains
Slide 5
LOCALIZED DISTURBANCES IN ERUPTION PRIMARY IMPACTION- Teeth
cease to eruption before emergence ANKYLOSIS -Cease of eruption
after emergence and anatomic fusion of tooth cementum or dentin
with alveolar bone DEVELOPMENTAL DISTURBANCES AND DISORDERS OF
ERUPTION
Slide 6
Impaction 3rd molars, maxillary canines, mandibular premolars,
mandibular canines, maxillary premolars, maxillary central
incisors, maxillary lateral incisors, and mandibular second molars;
usually angulated or diverted Factors associated with impaction:
Crowding and deficient maxillofacial development Overlying cysts or
tumors Trauma Reconstructive surgery Thickened overlying bone or
soft tissue A host of systemic disorders, diseases or
syndromes
Slide 7
Classification : Partially erupted or full bony impaction
according to angulation: Mesioangular, distoangular, vertical,
horizontal or inverted
ANKYLOSIS Clinical And Radiographic Features Pathogenesis is
unknown, may be secondary to many factors and result in PDL barrier
deficiency. May occur at any age, any tooth Most affect 8~9yr-old
children and D, E, D, E PDL absent Occlusal, periodontal problems,
impaction of the underlying teeth Treatment and Prognosis Variable
: extraction, orthodontics, segmental osteotomy
Slide 10
Premature eruption Neonatal teeth: within 30 days Natal teeth:
newborns Most are prematurely erupted deciduous teeth Removal only
if mobile and at risk of aspiration
Slide 11
Disturbances in tooth form may present as dilacerated teeth,
double teeth, dens invaginatus and enamel pearls Anhidrotic
ectodermal dysplasia showing conical teeth, giving an undesirable,
Dracula-like appearance.
Slide 12
Gemination, Fusion, Concrescence
Slide 13
Gemination single tooth germ division single root & root
canal + 2 complete or incomplete separated crowns tooth no.: normal
twinning
Slide 14
Fusion Union of 2 separate tooth germs Contact of tooth germ
before calcified Confluent of the dentin Complete- form a single
tooth Incomplete- after calcified begins Tooth no. : less one
Slide 15
Concrescence Fusion after root formation Cementum united
Traumatic injury or crowding Pre-extraction x- ray check
Slide 16
Talon cusp Eagles talon Lingual projection from the cingulum
area of ant. teeth Most contain a pulp horn Both in deciduous &
permanent dentition
Slide 17
Dens invaginatus ( central tubercle, occlusal tuberculated
premolar; Leongs premolar; evaginated odontome; occlusal enamel
pearl ) An accessory cusp or a globule of enamel on central groove
or buccal cusp of premolars or molars; unilateral or bilateral. 15%
in Asians, rare in whites
Slide 18
Dens invaginatus Kaohsiung Medical University, Oral Pathology
and image Diagnosis Dept.
Slide 19
Shovel-shaped incisors
Slide 20
Dens in dente (Dens invaginatus; Dilated composite odontome)
Tooth within a tooth, incidence 5% Invagination of the enamel organ
into dental papilla before calcification Coronal type: 3 types
maxillary lateral incisors are common
Slide 21
Dens invaginatus, coronal type II
Slide 22
Dens invaginatus Radicular type Hertwigs sheath invagination
Food deposition caries pulp infection Restorated as soon as
possible
Slide 23
Taurodontism Bull-like teeth Bi- or trifurcation near the apex
Pulp chamber : greater apico- occlusal height and no constriction
at the cervical of the tooth
Slide 24
Enamel pearls Enamel pearl. There is a small mass of enamel at
the root bifurcation
Slide 25
Supernumerary roots Any tooth may develop accessory roots No
rtg required, but critical important in endodontic procedure
Slide 26
Dilaceration Angulation, sharp bend of root or crown Trauma
during tooth is forming Pre-extraction x- ray check
Slide 27
Missing teeth 1.6-9.6%, excluding 3 rd molars, female
predominance Hypodontia: missing one or more teeth Oligodontia:
missing 6 or more teeth Anodontia: total missing DISTURBANCES IN
THE NUMBER OF TEETH
Slide 28
Hypodontia
Slide 29
Congenital absence of lateral incisors with spacing of the
anterior teeth.
Mesiodens The most common in supernumerary. Premaxillary area,
usually between upper central incisors Cone-shaped crown &
short root One or two in number
Slide 32
Kaohsiung Medical University, Oral Pathology and image
Diagnosis Dept.
Slide 33
Microdontia True: 1.General -pituitary dwarfism 2. Single -peg
lat., 3rd molar Relative microdontia DISTURBANCES OF TOOTH
SIZE
Slide 34
Macrodontia True macrodontia : 1. Generalized-pituitary
gigantism 2. Localized- single, hemifacial hypertrophy Relative
macrodontia: small jaw, child
Slide 35
Disturbances in the structure of teeth Disturbances of enamel
Genetic disturbances - Amelogenesis imperfecta. Local disturbances:
- Infection. - Trauma. - Idiopathic. Generalised disturbances: -
Infections. - Fluorosis. - Neonatal events, e.g. premature birth,
rhesus incompatibility.
Slide 36
Amelogenesis imperfecta (Hereditary enamel dysplasia;
Hereditary brown enamel; Hereditary brown opalescent teeth) Defects
in-- Formative stagehypoplastic type defective formation of matrix
Calcification stage hypocalified defective mineralization of formed
matrix Maturation stage hypomaturation enamel crystallites remain
immature Genes mutation : AMELX, ENAM, MMP-20, KLK4, DLX3
Slide 37
Thin enamel with pitted, rough or smooth & glossy surface;
yellowish to brown undersized, squared crown, lack of contact flat
occlusal surface & low cusps, attrition 1. Hypoplastic
type
Slide 38
Hypoplastic type Kaohsiung Medical University, Oral Pathology
and image Diagnosis Dept.
Slide 39
Hypoplastic type
Slide 40
2.Hypomaturation normal thickness of enamel, but mottled
surface; cloudy white, yellow or brown, opaque in color softer than
normal same density as dentin
Slide 41
Kaohsiung Medical University, Oral Pathology and image
Diagnosis Dept. Hypomaturation type
Slide 42
normal thickness of enamel, density less than dentin normal
size & shape when erupt, abrade or fracture away rapidly
permeability increase, darkened & stained 3.Hypocalcified type
4.Hypomaturation-hypocalcified with taurodontism
Slide 43
Hypocalcified type
Slide 44
Tricho-dento-osseous syndrome Hypoplastic-Hypomaturation
type
Slide 45
Factors associated with enamel defects Local- 1.Local acute
mechanical trauma 2. Electric burn 3. Irradiation 4. Local
infection: periapical inflammatory disease ACQUIRED DISTURBANCES OF
ENAMEL FORMATION
Slide 46
Environmental enamel defects: 1.Hypoplasia: pits, grooves or
large area of missing enamel 2. Diffuse opacities: variation in
translucency, normal thickness, white opacity without clear
boundary 3. Demarcated opacities: increased opacity, a sharp
boundary with adjacent normal enamel, normal thickness Acquired
disturbances of enamel formation
Slide 47
Most acquired enamel defects result in areas of HYPOPLASIA,
which may be due to either a defect in matrix production or a
defect in mineralisation. Acquired disturbances of enamel formation
Localized - only a single tooth is affected Generalized - several
teeth are affected
Slide 48
Turners hypoplasia, Turners tooth Permanent teeth Periapical
inflammatory disease of the overlying deciduous tooth, less
frequently in anterior teeth Traumatic injury- not rare -45%
children sustain injury to their deciduous teeth, 23% permanent
teeth development disturbed Turners hypoplasia secondary to
previous trauma
Slide 49
Turners teeth
Slide 50
Generalized defects are sometimes referred to as chronological
hypoplasia The overwhelming majority of chronological hypoplasia
are the result of disturbances in the rst 10 months of life and the
teeth usually affected are: The rst permanent molars. Upper central
incisors. Lower lateral incisors and canines.
Slide 51
Chronological hypoplasia due to metabolic upset. Unlike the
hereditary types of amelogenesis imperfecta, defects are linear and
thought to correspond to a short period of amelogenesis disturbed
by a concurrent severe illness
Congenital syphilis; Hutchinson's teeth. The characteristics
are the notched incisal edge and the peg shape tapering from neck
to tip.
Slide 54
Disturbances of dentine Disturbances in the structure of teeth
This genetic disorder is characterised by defective dentine matrix
production and two types have been described. Dentinogenesis
imperfecta type 1 occurs in association with osteogenesis
imperfecta, in which there is defective bone formation. It is very
uncommon. Dentinogenesis imperfecta type 2 is the commonest form.
It has the following features: Both the permanent and primary
dentition are affected. The teeth have a normal shape on eruption
but appear amberbrown or purpleblue in colour. The enamel shears
away from the poorly formed dentine which quickly wears away. The
pulps become obliterated with abnormal dentine.
Slide 55
Clinical features type I : deciduous severe than permanent
teeth; type II: equally affected; type III: both dentitions
affected. Gray to brownish violet or yellowish brown color, with
translucent or opalescent hue. Enamel lost early through fracture,
esp. on the incisal & occlusal surface, and dentin attrition
rapidly. Caries rate is not increased.
Slide 56
Dentinogenesis imperfecta
Slide 57
Regional odontodysplasia (odontodysplasia; odontogenic
dysplasia; odontogenesis imperfecta; ghost teeth) One or several
teeth in a localized area Maxi. > Mand.; both dentitions most in
ant. area Delayed or total failure eruption Irregular appearance
Defective mineralization Developmental Structural Abnormalities
Involving Both Enamel and Dentin
Slide 58
Radiographic features 1. Radiodensity , ghost appearance 2.
Large pulp, thin enamel & dentin On one side of the midline the
deciduous incisors have poor root formation with thin radicular
dentine and enamel. A poorly organised spotty calcification is
present at the site of the permanent successors.
Slide 59
Shell teeth Initial reported in the Brandywine population
Normal thickness of enamel associated with extremely thin dentin
and dramatically enlarged pulps (due to insufficient and defective
dentin formation) Short roots. Odontogenesis Imperfecta
Slide 60
Kaohsiung Medical University, Oral Pathology and image
Diagnosis Dept.
Slide 61
ENDEMIC DENTAL FLUOROSIS Acceptable measures of fluorine in
water according to hygienic standards is 0,8-1,2 (1,5) mg/l.
Fluorosis is the term given to changes in the enamel which are
associated with excess ingestion of uoride Fluorosis. Moderate
effects from an area of endemic fluorosis. Irregular patchy
discolouration.
Slide 62
Dental fluorosis Retention of the amelogenin protein in enamel
structure hypomineralized enamel permanent hypomaturation increased
surface and subsurface porosity alters light reflection and create
white, chalky area
Slide 63
Dental fluorosis Critical period for clinical dental fluorosis
is the 2 nd and 3 rd year of life, dose dependent Caries
resistant
Slide 64
II. Lesions that occur after teeth have been erupted: 1. tooth
wear: attrition, abrasion, wedge- shaped defect; 2. erosion; 3.
necrosis of hard tooth tissues; 4. hyperesthesia; 5. trauma of
teeth; 6. fluorosis; POSTERUPTIVE DEFECTS
Slide 65
Attrition Tooth to tooth contact during occlusion and
mastication, some are physiologic Accelerated by: poor quality or
absent enamel, premature contact, intraoral abrasives, erosion,
grinding habits Incisal, occlusal and interproximal surfaces
Slide 66
Abrasion Pathologic loss of tooth structure or restoration
secondary to the action of an external agent (ex. Toothbrush, hair
grips, toothpicks, chewing tobacco, biting thread, dental flossing)
Toothbrush abrasion: horizontal buccal cervical notches of exposed
radicular cementum and dentin with smooth surface. Greater on
prominent teeth ( canines, premolars, and teeth adjacent to
edentulous area) and side of the arch opposite to the dominant hand
Demastication- when tooth wear is accelerated by chewing an
abrasive substance between opposing teeth (both attrition and
abrasion)
Slide 67
Abrasion
Slide 68
Long-term use of tobacco pipe Improper use of hair grips
Slide 69
Abfraction Repeated tooth flexure caused by occlusal stresses
(tensile stress) concentrate at the cervical fulcrum may produce
disruption in the chemical bonds of enamel crystal cracked enamel
can be lost or removed by erosion or abrasion Wedge-shaped cervical
defects, deep, narrow V-shaped, not allow toothbrush to contact
base; if the defect, often affect a single tooth Almost exclusively
on facial surface and more often in bruxism, higher in mandibular
dentition
Slide 70
Abfraction
Slide 71
Erosion Chemical process, exposure to acidic foods or drinks,
medications (chewable Vit. C, aspirin), involuntary regurgitation
(ex. esophagitis, pregnancy), voluntary regurgitation (ex.
psychologic problems, bulimia) Perimolysis- dental erosion from
gastric secretion Facial surface of maxillary anteriors affected-
dietary source Posterior teeth extensive loss of occlusal surface,
and palatal surface concave dentin surrounded by an elevated enamel
rim- regurgitation of gastric secretion
Slide 72
Erosion concave dentin surrounded by an elevated enamel
rim
Slide 73
A bulimia patient Erosion
Slide 74
Treatment and prognosis of tooth wear Resolve pain and
sensitivity Identify the cause of tooth structure loss
Protection
Slide 75
ENVIRONMENTAL DISCOLORATION OF TEETH Extrinsic- surface
accumulation of exogenous pigment Intrinsic-secondary to endogenous
factors that result in discoloration of underlying dentin
Slide 76
Extrinsic stains Bacterial- Chromogenic bacteria, green, black-
brown, orange coloration Frequently in children, labial surface of
maxillary ant. in gingival third Iron- formation of ferric sulfide
Tobacco Food and beverage- chlorophyll Gingival hemorrhage- Hb.
breakdown to biliverdin Restorative material ex. Amalgam
Medications- iron, iodine, silver nitrate, chlorhexidine, stannous
fluoride
Slide 77
Intrinsic stains Amelogenesis imperfecta Dentinogenesis
imperfecta Dental fluorosis Erythropoietic porphyria autosomatic
recessive disorder of porphyrin metabolism, increased synthesis and
excretion of porphyrins and their related precursors Porphyrin
deposition in teeth, reddish- brown coloration, red fluorescence
when exposed to a Woods UV light Present both in dentin and enamel
in deciduous teeth, but only dentin affected in permanent
teeth
Intrinsic stains Medications- Tetracycline (bright yellow to
dark brown), chlortetracycline (gray-brown), oxytetracycline
(yellow), minocycline hydrochloride Time of administration dose,
duration Avoid from pregnancy up to 8 yrs of age
Slide 81
Minocycline hydrochloride Tx for Acne Blue-gray from incisal
3/4, to dark green or black in roots, also affect developed teeth
Skin, nail, sclera, conjunctiva, thyroid, bone discoloration in
susceptible individuals Stained alveolar bone