biology of tooth movement

Biology Of Biology Of Orthodontic Tooth Orthodontic Tooth

MovementMovement

Presented by: Dr. Khushbu Agrawal

Post GraduateMIDSR Dental College

Latur

CONTENTCONTENT

Historical perspective Tooth-supporting structuresResponse to normal functionTheories of orthodontic mechanismsPhases of tooth movement Pathways of tooth movement

2

Signaling molecules and metabolites in orthodontic tooth movementBehavior of oral soft and hard tissues in response to orthodontic force Tissue reactions with varied force application Deleterious effects of orthodontic force Conclusion References

3

History

1728-1746- Pierre Fauchard 1880- Kingsley1891- Walkhoff - equilibrium1904- Sandstedt - examination of paradental tissues during orthodontic tooth movement 1911- Oppenhiem 1932- Schwarz - capillary blood pressure

HISTORYHISTORY

4*Biologic mechanism of tooth movement by Krishnan 2nd edition

Edgewise appliance- heavy forces1956-Begg-light force system

Shock Reaction

1951-Reiten -complexity of tissue reaction.Type of force and tooth movement & individual variation.30 g – hyalinization232- stretched gingival fibres.

1952-Storey & Smith-Differential force concept


1960s-Baumrind & Buck -no significant difference in pressure and tension sites

1969-Bone bending theory

1972-Kvam & Rygh- ultrastructural changes in the blood vessels and hyalinized tissue.

- Root resorption- TRAP positive macrophages.


TOOTH-SUPPORTING TOOTH-SUPPORTING STRUCTURESSTRUCTURES

Orthodontic tooth movement

Changes in tooth supporting structures

Periodontium is a connective tissue organ covered by epithelium, that attaches the teeth to the bones of the jaws and provides a continually adapting apparatus for support of teeth during function

7

4 connective tissues of periodontium are

Two fibrous - Lamina propria of the gingiva. - Periodontal ligament

Two mineralized - Cementum - Alveolar bone

8

1. Gingiva 1. Gingiva

Parts of gingiva:Free or marginal gingiva Attached gingiva

Components:Collagen fibresFibroblastsNerves Matrix

9

*Orthodontics, current principles and techniques by Graber & Vanarsdall -5th edition

Fibres of gingiva:CircularDentogingivalDentoperiostealTransseptal fibres (Accesory fibres)

10


Connective tissue interface separating the tooth from the supporting bone

Heavy collagenous supporting structure- 0.15 to 0.38 mm in width

Apart from collagen fibres:Cellular elements-mesenchymal, vascular & neural Tissue fluids

2.Periodontal 2.Periodontal ligamentligament

11


Constant remodeling- fibres, bone & cementumPrincipal fibres:

1. Alveolar crest group2. Horizontal group3. Oblique group4. Apical group5. Inter-radicular6. Transseptal group

12


Cells:Proginator cellsSynthetic cells- Osteoblasts, Fibroblasts, CementoblastsResorptive cells- Osteoclasts, Fibroblasts, Cementoclasts

Tissue fluid:Derived from the vascular systemShock absorber-retentive chamber with porous walls.

13


Attaches the PDL fibres to the root

Avascular, no innervation, no remodeling

Continuous deposition through out life

Contributes to the process of repair – after orthodontic tooth movement

3. Cementum 3. Cementum

14


Surrounds the tooth –CEJ-Lamina duraBundle bone- alveolar bone properVolkmann’s canals – vascular communication with marrow spacesRenewed constantly – functional demandsMesial & distal movement – spongiosa: extraction space- RapidLabially- lingually- caution

4. Alveolar 4. Alveolar bone bone

15


Masticatory function – intermittent heavy force 1-2 kg for soft substances -50kg for hard substances

Heavy forces- > 1 sec-force transmitted to boneBone bending

Upon wide opening – distance between mandibular molars decreases by 2-3 mm

Normal function Normal function RESPONSE TO NORMAL RESPONSE TO NORMAL FUNCTIONFUNCTION

16

*Contemporary orthodontics by William Proffit- 5th edition

Physiologic Response To Heavy Pressure Against A Tooth

17


FORCE (PRESSURE)FORCE (PRESSURE)

PDL- Adaptive

Prolonged force

Remodeling of adjacent bone

Short duration

18


Resting pressure from lips, check and tongue against the teeth

19*Contemporary orthodontics by William Proffit- 5th edition

Continued eruption – after tooth emerges into oral cavity, further eruption depends on metabolic events within PDL

Active stabilization – threshold for orthodontic force (5-10gm/cm2 )

Role of Pdl in eruption Role of Pdl in eruption and stabilizationand stabilization

20


Tooth and their supporting tissues have a lifelong ability to adapt to functional demands and hence drift throughout the alveolar process – “Physiologic tooth migration”

Remodeling of PDL and alveolar bone

Physiologic tooth Physiologic tooth migrationmigration

21


Resorptive surface & depository surface

Unmineralised precementum – resorption-resistant coating layer

22


23*Vinod Krishnan and Davidovitch. Cellular, molecular & tissue level reactions to othodontic force. AJODO 2006

Orthodontic force:“force applied to teeth for the purpose of effecting tooth movement, generally having a magnitude lower than an orthopedic force,”

Orthopedic force:“force of higher magnitude in relation to an orthodontic force, when delivered via teeth for 12 to 16 hours a day, is supposed to produce a skeletal effect on the maxillofacial complex.”

Optimal Orthodontic Optimal Orthodontic Force Force


Orthdontic mechanotherapy:Remodeling and adaptive changes in paradental tissues20-150 g per tooth

Craniofacial orthopedic:Higher magnitudes of force to modify bone form >300g of mechanical forceDeliver macro-scale mechanical forces, which produce micro-structural sutural bone strain and induce cellular growth response in sutures

25

Optimal orthodontic force: based on proper mechanical principles

Move teeth without traumatizing dental or paradental tissues, and without moving dental roots redundantly (round-tripping), or into danger zones (compact plates of alveolar bone)

light Orthodontic force

heavy

Light forces – gentler – more physiologic 26

27

According to Schwarz (1932):According to Schwarz (1932):“the optimal orthodontic force approximated the capillary vessels’ blood pressure”

Current concept:Current concept:Force of certain magnitude and characterstics Maximal tooth movementWithout tissue damage Maximal patient cooperationDiffer for each tooth and each patient

*Vinod Krishnan and Davidovitch. Cellular, molecular & tissue level reactions to othodontic force. AJODO 2006

Pressure- Tension theory by Schwarz in 1932

Fluid –Dynamic theory by Bien in 1966

Bone bending theory by Baumrind in 1969

Neither incompatible nor mutually exclusive

Theories Of Orthodontic Theories Of Orthodontic Tooth MovementTooth Movement

28

Sandstedt (1904), Oppenheim (1911), and Schwarz (1932)

Pressure-tension Pressure-tension Theory Theory

29

The hypothesis explains thatPressure side- the PDL disorganization and diminution of fiber production, cell replication decreases due to vascular constriction.

Tension side- stimulation produced by stretching of PDL fiber bundles results in an increase in cell replication

Compressed Pdl Streched Pdl30

SOME IMPORTANT TERMINOLOGIES:

1. Frontal bone resorption Survival of cells within the PDL and a remodeling of tooth socket by a relatively painless bone resorptionOccurs with application of lighter forces

2. Undermining bone resorptionResoption of bone from underside immediately adjacent to the necrotic PDL area and its removal together with the necrotic tissueOccurs with application of heavy forces

31

3. Hyalinization ( According to Reitan in 1960)

Cell-free areas in the PDL, in which the normal tissue architecture and staining characteristics of collagen in the processed histologic material have been lostFirst sign is presence of pyknotic nuclei in cells, followed by areas of acellularity, or cell-free zones

32

Hyalinization could be observed 1. In Pdl after application of even minimal force,

like for tipping movement2. More hyalinization in tooth with short roots3. Very little hyalinization in case of translation

33

Succesion of events making central theme of pressure-tension theory:

1. Inflammation causing cellur recruitment and tissue remodeling

2. Frontal resortion and undermining resorption

3. Loss of bone mass at PDL pressure areas and apposition at tension areas


Fluid Dynamic theory

Force of longer duration- interstitial fluid squeezed out

Vascular stenosis – decreased oxygen level- compression

Alteration in the chemical environment

Fluid Dynamic Theory Fluid Dynamic Theory

35

Farrar (1888) – bone bending

Baumring and Grimm (1969) – confirmed this hypothesis

Orthodontic appliance is activated- forces delivered to the tooth are transmitted to all tissues near force application- bend bone

Bone Bending Theory Bone Bending Theory


This hypothesis explains :

the relative slowness of en-masse tooth movement, when much bone flexion is needed for the rapidity of alignment of crowded teeth, and when thinness makes bone flexion easier

the rapidity of tooth movement toward an extraction site

the relative rapidity of tooth movement in children, who have less heavily calcified and more flexible bones than adults


Confusion regarding this concept:

“Orthodontic tension refers to PDL whereas a orthopedist will say area is under compression, because near the stretched PDL appears concave”


What is piezoelectricity ??A phenomenon observed in many crystalline materials in which a deformation of the crystal structure produces a flow of electric current as electrons are displaced from one part of the crystal lattice to another

39

Bioelectric signals in Bioelectric signals in orthodontic tooth orthodontic tooth

movementmovement


2 characteristics of piezoelectricity:

A quick decay rate the production of an equivalent signal, opposite in direction, when the force is released

40

Streaming potential: ions in the fluids + electric field (bone bends) = Electric signals in the form of small voltagesRapid onset and alteration with changing stresses


Applications of piezoelectricity:

Important for maintenance of bone around tooth

Sustained force- not significant

Vibrating application

41


In 1962, Bassett and Becker proposed that, In response to applied mechanical forces, there is generation of electric potentials in the stressed tissues. These potentials might charge macromolecules that interact with specific sites in cell membranes or mobilize ions across cell membranes.


In 1973, Zengo et al


In 1980, Davidovitch et al proposed thatA physical relationship exists between mechanical and electrical perturbation of boneBending of bone causes 2 classes of stress-generated electrical effects

Also they suggested that, Piezoelectric potentials result from distortion of fixed structures of the periodontium—collagen, hydroxyapatite, or bone cell surface. But in hydrated tissues, streaming potentials predominate as the interstitial fluid moves


According to Burstone (1962), 3 phases of tooth movement:1. An initial phase2. A lag phase3. A postlag phase

PHASES OF TOOTH PHASES OF TOOTH MOVEMENTMOVEMENT

45

According to Pilon(1996) and Leuwen(1999), 4 phases in the curve of tooth movement can be demonstrated:

1. First phase- 24 hours to 2 days - Movement inside bony socket- Cellular and tissue reaction- Compression and stretching of PDL fibres

and cells - Recruitment of osteoblasts and osteoclasts


2. Second phase- Can last fron 4 to 20 days - Development of hyalinized areas- Undermining and indirect bone resortion- Recruitment of new osteoblasts progenitors- Pdl fibroblasts multiplication

47

3. Third phase and 4. Fourth phase- Starts about 40 days after initial force

application- Direct or frontal bone resorption on pressure

side- Bone deposition on tension side- Most of the tooth movement- Hyalinized areas in case of heavy force

application

48

Bohl (2004) suggests –development of hyalinization zones has a definite relationship to the force magnitude, but it was found to have no relationship to the rate of tooth movement

Owmann-Moll (1996) and Leeuwen (1996) –Location of hyalinization is mostly buccal or lingual to mesiodistal plane


Mostafa et al (1983) described integrated model showing 2 pathways of tooth movement:

1.1. Pathway I Pathway I - More physiologic response- Associated with normal bone growth and remodeling

2.2. Pathway II Pathway II - Alternative pathway- Classic inflammatory response after force

application

PATHWAYS OF TOOTH PATHWAYS OF TOOTH MOVEMENTMOVEMENT


Recent model based on:Stress in any form- compressive, tensile, shear, will evoke many reactions in the cell, leading to development of strain

Orthodontic force, light or heavy – inflammation of paradental tissues


SEQUENCE OF EVENTS AFTER FORCE APPLICATION:

Movement of PDL fluid

Development of strain in cells and ECM

Direct transduction of mechanical forces to nucleus of cells leading to activation of specific genes

Release of nociceptive and vasoactive neuropeptides

Interaction with endothelial cells 52

*Vinod Krishnan and Davidovitch. Cellular, molecular & tissue level reactions to othodontic force. AJODO 2006

Adhesion of circulating leucocytes to endothelial cells

Plasma extravasation from dilated blood vessels

Diapedesis of leucocytes into extravascular spaces

Synthesis and release of signal molecules(cytokines, GF, CSFs) from leucocytes

Interaction with various paradental cells

Activation of cells to participate in modeling and remodeling of paradental tissues


54

Signaling molecules and Signaling molecules and metabolites in orthodontic metabolites in orthodontic

tooth movement tooth movement

Von Euler in 1934 – term “prostaglandin”

Harren et al in 1977 – PGs important mediators of stress

Yamasaki et al in 1984 – increase osteoclasts after local injection of PGs in paradental tissues

Chumbley and Tuncay in 1986 – reduced rate of tooth movement after administration of indomethacin, an anti-inflammatory agent and specific inhibitor of PG

58

Prostaglandins Prostaglandins

Forces on paradental tissues

Cells subjected to first messengers

Binding to signal molecules to cell membrane receptors

Enzymatic conversion of cytoplasmic ATP and GTP to cyclic AMP and cyclic GMP

(intracellular second messengers)59

Sutherland and Rall in 1958 – second-messenger basis for hormone actions

First messenger

Binds to cell membrane

Second messenger

Interacts with cellular enzyme60

Intracellular second-Intracellular second-messenger system messenger system

Two main second-messenger systems are:1. The cyclic nucleotide pathway and2. The Phosphatidyl Inositol (PI) dual signaling system

The second messenger systems

Mobilize internal calcium and activate protein kinase C

Lead to cellular events like mobility, contraction, proliferation, synthesis and secretion

61

C-AMPC-AMPInternal signaling pathway – many external stimuli – narrow range of second messengers

cAMP & cGMP- 2nd messengers of bone remodeling

Bone cells- response to Hormones/Mechanical stimuli

Rodan et al (1975) – 1st evidence of cAMP – mechanical force

Davidovitch et al (1976) – cat model - increase in number of c-AMP positive cells in area of bone resorption/deposition

62

The PI dual signaling The PI dual signaling systemsystem

The phosphoinositide (PI) pathway – another 2nd messenger system

Cell surface receptor activation

Hydrolysis PI 4,5 biphosphonates

inositol triphosphate formation

ins (1345) P4 Inc. Ca 2+ entry

Protein phosphorylation

64

65

Vitamin D and Vitamin D and diacylgylcerol diacylgylcerol

Serum Ca 2+

PTH (kidneys) Ca 2+ hydroxylation 25 HCC

1, 25 DHCC

Osteoclastic differentiation & stimulates bone resorption

Dose dependent – Osteoblast stimulation & bone mineralization

Kale et al (2004) reported that 1, 25, DHCC is more effective than PGE2 in modulating bone turnover during tooth movement, because of its well-balanced effects on bone formation and resorption

Kawakami et al (2004) on basis of their study concluded that local applications of 1,25(OH)2D3 could enhance the reestablishment of dental supporting tissues, especially alveolar bone, after orthodontic treatment

66

Neurotransmitters The relationship of nerves to tooth movementMechanoreceptors in the apical half of root – Ruffini-like & Nociceptive endings

Force sensing fibres (unmyelinated C fibres/ myelinated Aδ)

Nerve terminal strainedStored neuropeptides released

(Substance P, VIP, CGRP)

PG E2 & cAMP67

NeurotransmitterNeurotransmitters s

Substance P-Increased vascular permeabilityDavidovitch(1988) – increased PGE2 & cAMP in 1 min

CGRP (Kvinnsland in 1990) & VIP in compressed PDL and pulp (Saito et al in 1990) was found within an hour of force application

68

Vasoactive neurotransmitters from from PDL nerve terminals

Leucocyte migrate out of the capillaries

Participate in immune reactions (phagocytosis) and also produce numerous signal molecules

Other PDL cells like osteoblasts, fibroblasts, epithelial cells, endothelial cells, and platelets, can also

synthesize and secrete these molecules

Cytokines Growth factors Colony-stimulating factors

69

Cytokines Cytokines

70

Systemic hormones & mechanical stimuli-influence-cytokines

Osteoblast derived cytokines-ideally located to regulate the action of other cell types

IL-1, 2, 3, 6 and 8, TNFα, IFNɤ.

In-vitro cell cultures-1983-Gowen et al – IL-1 potent bone resorptive agent1986- Bertolini- TNFs stimulate bone resorption & inhibit bone formation

Davidovitch(1988) - first experimental evidence -immunolocalization of IL-1ß & Grieve et al (1994)

Secretion of IL-1 is stimulated by mechanical force, Neurotransmitters and other cytokines (inflammatory process)

Actions - attracts leukocytes, stimulates fibroblasts. Osteoblasts - target cells-conveys message to osteoclast to resorb bone.

TNFα - Proinflammatory cytokine - directly stimulates differentiation of osteoclast progenitor with – M-CSF to osteoclasts

71

Alhashimi et al in 2000 studied role of IFNɤ -

Evokes the synthesis of IL-1ß & TNF-α.

Cytokines induce – Nitric oxide production – potent Osteoclast-Osteoblast coupling agent

IFNɤ – causes resorption by apoptosis of effector T-cells

72

Cytokines- RANKL/RANK/OPG Cytokines- RANKL/RANK/OPG systemsystem

Drugrain et al (2003)-RANKL/RANK/OPG – TNF related ligand- downstream regulator of osteoclast formation & activationRANKL – osteoblast lineage & RANK binding on osteoclast OPG – decoy receptor competing with RANK

73

Binding of RANK-RANKL-rapid differentiation of osteoclast -precursors to osteoclasts

OPG - prevents final stages of differentiation & activation of mature osteoclasts

74

TGFß-Transforming growth factor ß, FGF, IGF, PDGF, CTGF Effect osteoblastic/osteoclastic actions in various ways –

they are regulated/activated by other signaling molecules and effect their action either directly on DNA or again down signaling.

TGFß –TGFß1,activins,inhibins,BMPs

Enhances osteoclast differentiation – stimulated by RANKL & M-CSF

75

Growth factors Growth factors

FGF & IGF- similar function- stimulate osteoblast synthesis

PDGF acts by binding to the extracellular portion and activation of Tyrosine kinases.

CTGF- localized in oseoblasts & stimulates osteoblast precursors & mineralization of new bone

76

M-CSF , G-CSF & GM-CSF –regulate granulocyte & monocyte macrophages

Osteoclast synthesis occurs-Bone marrow cells cultured with M-CSF

Fibroblasts synthesize –M-CSF in presence of GFs

77

Colony stimulating Colony stimulating factors factors

In physiologic tooth movement – expression of mRNA for oteonectin, osteocalcin and osteopontin

Osteoblast and osteoclasts – positive for oteonectin and osteocalcin

Osteopontin expressed in osteoblasts around bone-resorbing surfaceselevated after 12 hours of force application

78

Genetic Genetic mechanismsmechanisms

Pavlin and Gluhak-Heinrich (2001) stated that The primary responses to osteogenic loading are induction of differentiation and increased cell function, rather than an increase in cell numbers. They detected alkaline phosphatase and bone sialoprotein genes after 24 hours of treatment, followed by a concomitant stimulation of osteocalcin and collagen I between 24 and 48 hours, and deposition of osteoid after 72 hours

79

80

Behavior of oral soft and Behavior of oral soft and hard tissues in response hard tissues in response

to orthodontic forceto orthodontic force

Osteoclasts – prerequisite for bone resorption

Arise from1. Activation of osteoclasts already present in

PDL 2. Proliferation of stem cells in remote 3. Local hemopoetic tissues

81

Bone remodelingBone remodeling

Robert and Fergusan (1995) through animal study showed that –

Mature PDL is virtually devoid of mature osteoclasts in physiologic conditions Osteoclasts appear within few days of orthodontic force application

According to Mundy and Roodman hypothesis (1987)

Osteoclasts are derived from stem cells in haemopoietic organs, and granulocyte-macrophage colony-forming units are the earliest identifiable precursors of osteoclasts

82

Proposed pathway:

Granulocyte-macrophage Colony-forming Units

Promonocyte

Early Preosteoclast

Late Preosteoclast

Osteoclast83

Robert and Fergusan (1995) also showed that – Osteoclast numbers per unit bone surface area show a peak level about 50 hours after orthodontic force applicationNew osteoclasts reach the PDL from haemopoietic organs via the blood circulation, and from alveolar bone marrow cavities, during the orthodontic treatment period, which can last 2 to 3 years.

84

Bone Resoption CascadeBone Resoption CascadeAfter osteoblast differentiation the unmineralized

osteoid layer in the bone surface is removed by the lining osteoblasts

Osteoclast polarization by attaching itself to specific extracellular bone matrix proteins

Osteoclast activation by local and systemic factors

Production of hydrogen ions and proteolytic enzymes in the hemivacuole under the ruffled border of the cell

85

Another concept proposed by Fuller et al (1991) states that

Osteoblasts can activate osteoclasts through cell-to-cell contacts.The osteoclasts thus activated produce hydrogen ions and proteolytic enzymes in the ruffled border of the cell

86

Roodman (1996) stated that –TGFß, blocks bone resorption, can induce apoptosis of osteoclasts, Osteoclast-stimulating factors, such as PTH and vitamin D3, inhibit osteoclast apoptosis.

The progression of bone remodeling requires continual addition of osteoclasts, because they have only a limited life span— less than 12.5 days

88

Mononuclear cells – macrophage lineage – on bone surface Further collagen degradation Deposition of proteoglycan – “cement line”Release of growth factorsCoupling mechanism

89

Reversal phaseReversal phase

Differentiation of osteoblast precursor cells from primitive mesenchymal cells

Maturation of osteoblasts

Matrix formation

Mineralization 90

Bone formation phaseBone formation phase

EVENTS IN BONE FORMATIONS:EVENTS IN BONE FORMATIONS:

Appositional phase – chemoattraction of osteoblasts of their precursors

Formation of osteoid matrix Mineralization after 13 days at initial rate of less

than 1 um per dayOsteoblasts at bottom of cavity – plump, tall nuclei,

thick osteoid – flatten gradually – quiescent linig cells Osteocytes – surrounded by calcified matrix and

remain in bone lacunae

91

A] Tension sideA] Tension sidePDL widening Increase in vascularity, number of connective tissue cells Deposition of osteoid at edge of the socket wall Blood vessels distended, fibroblasts rearranged Secretion of new Sharpey’s fibresDeposition of new matrix along socket wall Overstreched PDL – pain, reduced function, cell death

94

PDL remodelingPDL remodeling

95

B] Pressure sideB] Pressure sidePDL narrowing, alveolar bone crest deformationEdema, gradual obliteration of blood vessels Degenerative process, necrotic tissue,

hyalinization3 to 5 weeks later, wider posthyalinized PDL Withstand greater mechanical influences

Significance of PDL:Significance of PDL:Maintaince of width around tooth Medium for force transferMeans by which alveolar bone remodels

PDL – Ruffini-like endings and free nerve endings – Key role in maintaining PDL structure and function

96

Shirazi M (2002) and D’Atillio (2004) demonstrated enhancement of nitric oxide synthase production after mechanical force application in animals and humans, suggesting that nitric oxide might be a key regulator of orthodontic tooth movement by regulating the functions of osteoblasts and osteoclasts, and thereby modulating bone metabolism.

Takahashi et al (2003) demonstrated differential regulation of the expression of MMP-8 and MMP-13 genes, and concluded that this dichotomy could play an important role in defining the specific characteristics of PDL remodeling.

97

Redlich et al (1999) demonstrated that 2 disparate processes occur in the gingiva after transduction of orthodontic force –

First – injury of the gingival connective tissue, manifested by torn and ripped collagen fibersSecond – the genes for both collagen and elastin are activated, whereas those for tissue collagenases are inhibited.

According to Danciu et al (2004) mechanical strain can deliver anti-apoptopic and proliferative stimuli to human gingival fibroblasts

98

Gingival effectsGingival effects

Changes in gingiva after Changes in gingiva after orthodontic force application:orthodontic force application:

Tissue accumulation Enlargement of gingival papillae when extraction

spaces are being closedVertical clefts of epithetlium and CT Discontinuation of transeptal fibres and

reestablishment during healing phase Increase amount of oxytalin fibres and GAGsIncrease rate of synthesis of fibroblastsIncrease in size of elastin fibres on pressure side

99

In a study by Bolcato-Bellemin et al (2000) suggests that –

Orthodontic force effects on the gingiva are similar in cases of extraction space closure and rotation correctionsThe cause of relapse after treatment is most likely the increased elasticity of the compressed gingiva, brought about by biosynthesis of new elastic fibers and GAGs.

100

GCF – transudte or exudateTotal fluid flow – 0.5 to 2.4 mL/dayApparent minimal inflammation – 0.05 to 0.20 ul/minGCF testing – noninvasive and repetitive sample with minimal help Analyze biomarkers like prostaglandin, IL-1, IL-6, TNF-, epidermal growth factors, 2 microglobulin, cathepsin, aspartate aminotransferease, alkaline phosphatase, and lactate dehydrogenase

101

Biomarkers of Biomarkers of gingival crevicular gingival crevicular

fluidfluid

Last et al (1985) and Embery and Waddington (2001) described many GAGs, and proteoglycan and tissue proteins in GCF, providing evidence for the presence of underlying state of biochemical reflections in paradental tissues.

Last et al (1985) first time demonstrated chondroitin-4-sulphate in GCF from the pressure side of tooth movement, indicating biologic alteration in the deep seated tissue

102

103

Tissue reactions with Tissue reactions with varied force varied force applicationsapplications

Most fixed appliances – light continuous forces

After a limited period of time – continuous force subsides – becomes interrupted

Biologically favorable

Rest periods – time used by tissues for reorganization

104

Continuous, interrupted, Continuous, interrupted, and intermittent forcesand intermittent forces

The characteristic feature of continuous/interrupted tooth movement – formation of new bone layers in the richly cellular tissue at the entrance of open marrow spaces as soon as the tooth movement stops

Bonafe-Oliveira (2003) demonstrated that continuous orthodontic forces can resorb the alveolar bone concomitantly with the formation of new bony tissue at PDL tension sites

105

Intermittent forces – impulse or shock of short duration – removable appliances

Small compressions zones in PDL, short hyalinization periods, and lengthy rest periods

Improved the paradental circulation and promote an increase in the number of PDL cells, because its fibers usually retain a functional arrangement

Reitan (2000) – semi-hyalinization

106

Sustained force- cyclic nucleotides appear- only after 4 hoursLonger & constant the force- faster the tooth movement

Effects of force duration Effects of force duration and force decayand force decay

107

Teeth move in response to force- force changes

May drop to zero

108

Continuous force-Light- frontal resorptionHeavy- undermining resorption- constant-further Undermining.Resorption

Destructive to the PDL & tooth

Force decay- Light force – Frontal Resorption- no movement till activationHeavy – Undermining Resorption- force drops-repair & regeneration occurs

109

Clinically- Underming resorption seen- forces must decline to allow for repair

Avoid heavy continuous force

Underming Resorption - requires 7-14 days- repair phase

Do not activate more frequently- 2nd & 3rd Undermining resorption cycles-irreparable damage

110

Light forces – favorable tooth displacement, minimal discomfort and pain to the patient

Heavy forces – classic 3 phase reaction:

111

Light vs heavy forces and Light vs heavy forces and rate of tooth movementrate of tooth movement

Konho et al (2002) light forces can tip teeth without friction, with a constant rate of tooth movement, and without the 3 phases

However, in most cases, this kind of tipping is uncontrolled and can cause root resorption, despite the small magnitude of the applied force.

112

Quinn and Yoshikawa (1985) – dose-response relationship between magnitude of force applied and extent of tissue reaction

113

Conclusion – force magnitude plays only a subordinate role in orthodontic tooth movement

Pilon et al (1996) – application of 2 forces (50 and 100 CN) to second premolars in dogs resulted in the same rate of tooth movement.

Owman-Moll et al (1996) – clinical study in humans produced similar results.

114

Optimal force – The amount of force & the area of distribution The force distribution varies with the type of tooth movementTipping -

Force distribution and Force distribution and type of tooth movementtype of tooth movement

115

Forces should be kept low- high concentration of forces

Destruction of the alveolar crest

116

Bodily tooth movement-uniform loading of the teeth is seen.

To produce the same pressure - same biologic response - force required is twiceIntermediate forces - part tipping/translating

117

Torque - Initially - Pressure close to middle region - PDL wider at the apex

Later part - apical region begins to compress

Rotation - 2 pressure & tension sides

Tipping - some hyalinization does occur

118

Intrusion - very light forces - concentrated in a small area Stretch- principal fibres

Extrusion - Only areas of tensionLight forces - could loosen teeth considerably

119

Values depend in part on size of tooth, smaller values appropriate for incisors, higher for multirooted posterior teeth

120

Tissue reaction – pattern of stress-strain distribution in paradental tissues

Iatrogenic sequelae to orthodontic force:Caries, gingivitis, marginal bone loss, pulpal reactions, root resorption, and allergic reactions to appliance material

121

Deleterious effects of Deleterious effects of orthodontic force orthodontic force

Cementation of orthodontic bands or resin-bonded attachments – local soft tissue local soft tissue responseresponse

Proximity to gingival sulcus – plaque accumulation

122

Gingival Gingival problemsproblems

Gingival recessionGingival recession – 1.3 to 10%

Gieger M (1980) – at least 2 mm of keratinized gingiva should be present to withstand orthodontic force and prevent recession.

Dirfman (1978)mandibular incisors are most likely to express gingival recession Due to thin or nonexistent labial plate of bone and inadequate or absent keratinized gingiva that covers labially prominent teeth

123

Plaque accumulation and gingival Plaque accumulation and gingival inflammation inflammation – altered oral hygiene habits

Specific bacterial type mainly of spirochetes and motile rodsbacteroids and streptococcus species

Orthodontic mechanotherapy Local change in oral ecosystem

Plaque accumulation Inflammatory process

124

Permanent damage or no significant long-lasting effects ???

Labart et al (1980) demonstrated increased pulpal respiration rate in rat incisor pulp (1-2 times more than controls), when subjected to orthodontic stress for 72 hours.

Harmersky et al (1980) showed a depression in pulpal respiratory rate after orthodontic force application in humans

125

Pulpal reactionsPulpal reactions

Initial decrease in blood flow, lasting approximately 32 minutes followed by an increase in blood flow, lasting 48 hours.

Nixon et al (1993) reported an increase in the number of functional pulpal vessels after orthodontic force application.

Derringer and Linden (1996) increase in specific angiogenic growth factors in dental pulp vascular endothelial growth factor, FGF-2, PDGF, and TGF-beta

126

Yamaguchi M (2004) described apoptosis in dental pulp tissues of rats undergoing orthodontic treatment.

Perinetti et al (2004) demonstrated that an enzyme, aspartate aminotransferase (which is released extracellularly upon cell death), is significantly elevated after orthodontic force application.

127

128

Root resorptionRoot resorption

Function-Attachment of the tooth to boneUnlike bone- not resorbed- continuous depositionMajor repair tissue

OTM possible – More resistant to resorption than bone

Difference – avascularity

C

D

Cementum

129

Repair:Acellular/cellular/both

Anatomic repair - former outline of root

Functional repair - full outline not reconstructed-bony projection- normal width of PDL

130

HistoryBates (1856) 1st to discuss Root resorption

Ottolengui (1914) – orthodontic tooth movement causes root resorption

Ketcham (1927) radiographic evidence- also suggested that the appliance may be responsible

131

IntroductionEARR – External apical root resorption (or) OIIRR -Orthodontically induced inflammatory root resorption

Most common iatrogenic consequence of orthodontics

Several investigators elucidated factors-Magnitude of forceDuration of forceType of applianceIndividual variations- Genetic tendencies 132

Resorption ProcessResorption continues – all hyaline tissue is removed- Pressure dropsAny cemental damage – repaired

Appearance of osteoclasts/ odontoclasts-

In addition to M-like cells, TRAP –positive cells are seen

Eliminate tissue-till there is new mechanical stimulus- differentiate into-osteoclasts (or) odontoclasts 133

Force

Hyalinization

Removal of hyaline tissue

Damage to the protective surface-resorption

Release of force-repair More force

Odontoblastic differentiation

Lacune extending to dentine

Permanent loss of root structure

134

PrevalenceMore root resorption in

Tooth moved the farthest Extraction treatmentIntrusion and torquing movementsTapered or conical roots

“shed roof” effect – resorption typically attacks the root tip and travels coronally

Frequency Maxillary – centrals, molars, caninesMandibular – laterals and centrals

135

ClassificationA] Three external root resorption types:

1. Surface resorption - Self-limiting process- small outlining areas followed by spontaneous repair.

Undetected radiographically and is repaired by a cementum-like tissue.

Commonly seen after orthodontic treatment is surface resorption.

136

2. Inflammatory resorption -Where initial root resorption has reached dentinal tubules of an infected necrotic pulpal tissue or an infected leukocyte zone. a. Transient inflammatory resorption - common

after treatmentb. Progressive inflammatory resorption - when

stimulation is for a long period

3. Replacement resorption - Bone replaces the resorbed tooth material that leads to ankylosis -rarely seen after orthodontic treatment.

137

B] Breznaik & Wasserstein - 3 levels of severity

1. Cemental or Surface resorption - outer layers are resorbed

2. Dentinal resorption with repair - outer layers of dentin are resorbed – normal morphologic alterations

3. Circumferential root resorption - full resorption of all the hard tissues components of root apex - root shortening

138

C] PROFITT - external root resorption types:-

1) Moderate Generalized – long treatment duration

2) Severe Generalized – evidence of resorption before treatment

3) Severe Localized – may be caused due to orthodontic treatment - cortical plates

139

D] Levander et al (1998)

140

Diagnosis EARR – degree a root has shortened from its original length by clastic activity.

Progress periapical radiographs and panoramic radiographs

IOPAs best-especially high risk patients Visual assessed-CalipersComputer-aided measurementDigital imagesCT

141

Factors effecting root resorption

BIOLOGIC FACTORS-BIOLOGIC FACTORS-

Individual susceptibility - major factor- variation in the pattern of metabolic signals

Age - Poor correlationHigher susceptibility in adults- PDL changes

Gender - Lack correlation- conflicting resultsSameshima & Sinclair - males- more prone - not significant

142

Ethnicity - less severe in Asians compared to Caucasians & Hispanics

Systemic factors - endocrine problems including hypothyroidism, hypopituitarism, hyperpituitarism, hypophosphatasia – increased root resorption

Nutrition - Becks - root resorption in animals deprived of dietary calcium and vitamin D.

Later suggested -not a major factor -Controversial results.- Ca 2+ dietDrugs-corticosteroids & alcohol- increases root resorption

143

UNTREATED POPULATION - 0%- 90%- resorptionHigh correlation- initial presence of resorption- increased from 4% to 77% after treatment

HABITS - Nail-biting, tongue thrust associated with open bite, and increased tongue pressure

TOOTH STRUCTURE - Deviating root form is more susceptible to post-orthodontic root resorption.

Root form - normal (N), blunt (A), eroded (B),pointed (C), bent (D), bottle shaped (E)

144

PREVIOUSLY TRAUMATIZED TEETH – Traumatized teeth can exhibit external root resorption without orthodontic treatment.

Orthodontically moved traumatized teeth with previous root resorption are more sensitive to further loss of root material.

ENDODONTICALLY TREATED TEETH – higher frequency and severity of root resorption of endodontically treated teeth

Wickwire et al & Mattison – no significant differenceRemington et al – endodontically treated teeth are more resistant to root resorption because of an increased dentin hardness

145

ALVEOLAR BONE – More dense the alveolar bone, the more root resorption occurred during orthodontic treatment.Contact of roots with cortical plates- inc. resorption-Horiuchi et al.

MALOCCLUSION -Taner et al- Class II > Cass IJanson et al-Class II div2> div 1 > class III- more intrusion & torquing requirement

146

GENETIC - nearly 50% of the variation is due to genetic factors

Harris- landmark study-heritable component of RR

Gene mutation expressed- stress is appliedAl-Qawasmi et al-

linkage disequilibrium of IL-1ß polymorphism in allele 1 & EARRAlso analyzed the candidate gene loci-found microsatellite marker - D18S64 tightly linked to TNFRSF11A - influenced EARR

Low et al-Osteoprotegrin & RANKL involved

147

MECHANICAL FACTORS -

1. Fixed versus removable: Ketcham - normal function is disturbed by the splinting - root resorption. Stuteville- jiggling forces caused by removable appliances are more harmful to the roots.

148

2. Begg vs Edgewise -Beck, Harris & Malmegren - no difference Begg light wire & Tweed techniqueMcNab et al (2000)- higher incidence with Begg-3.72 times when extractions were also done

149

Ahu Acar (1999)

Continuous vs discontinuous force application

Length of treatment time & root resorption - less time & discontinuous forces

150

COMBINED BIOLOGIC AND MECHANICAL FACTORS

Treatment duration - Most studies report that the severity of root resorption is directly related to treatment duration.

Relapse - Ten Hoeve & Mulie- Teeth are prone to additional root loss during relapse as a result of light muscles forces

After appliance removal - Progressive root resorption-lasts for 5-6 weeks

151

Slow down the root resorption rate – drugs, hormones, and growth factors

Baily (2004) demonstrated a reduction of root resorption and acceleration in healing of already resorbed sites with reparative cementum over 4 weeks of low-intensity pulsed ultrasound application.

152

Clinical considerationsBEFORE TREATMENT

General considerationsInform patient & parents- unpredictability of root resorption

IOPAs- -must- Pre & post treatmentPeriodic control radiographs- at least once/year

Familial considerationsObtain radiographs- if anyone else (sibling) treated in the Family

General Health- Systemic disordersAsthma and allergies 153

DURING TREATMENTAppliance choice

No particular appliance- light & intermittent forces Jiggling forces & intermaxillary elastics-avoid

Habits- stopped

Traumatized teeth- constant monitoring

Treatment time Longer intervals during activation Short overall treatment duration

154

Root resorption detected during treatment-If severe-terminate treatment-reassessBite plane – disocclude

AFTER TREATMENTRadiographs-

Mandatory - if detectedFollow - up radiographsAdvisable - full mouth

155

Contemporary orthodontics by William Proffit- 5th editionOrthodontics, current principles and techniques by Graber & Vanarsdall -5th editionBiologic mechanism of tooth movement by Krishnan 2nd edi.Caranza’s clinical periodontology by Michael Neuman and Caranza – 10th editionVinod Krishnan and Davidovitch. Cellular, molecular & tissue level reactions to othodontic force. AJODO 2006:129;469e.1-469e32

156

REFERENCESREFERENCES

biology of tooth movement

Health & Medicine

Transcript of biology of tooth movement