biology of tooth movement

Biology Of OrthodonticBiology Of Orthodontic
Tooth MovementTooth Movement
Presented by:
Dr. Khushbu Agrawal
Post Graduate
MIDSR Dental College
Latur

CONTENTCONTENT
Historical perspective
Tooth-supporting structures
Response to normal function
Theories of orthodontic mechanisms
Phases of tooth movement
Pathways of tooth movement
2

Signaling molecules and metabolites in orthodontic
tooth movement
Behavior 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- Kingsley
1891- Walkhoff - equilibrium
1904- 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 forces
1956-Begg-light force system
Shock Reaction
1951-Reiten -complexity of tissue reaction.
Type of force and tooth movement & individual variation.
30 g – hyalinization
232- stretched gingival fibres.
1952-Storey & Smith-Differential force concept
5
edition

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.
6
edition

TOOTH-SUPPORTINGTOOTH-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. Gingiva1. Gingiva
Parts of gingiva:
Free or marginal gingiva
Attached gingiva
Components:
Collagen fibres
Fibroblasts
Nerves
Matrix
9
*Orthodontics, current principles and techniques by Graber & Vanarsdall -5th
edition

Fibres of gingiva:
Circular
Dentogingival
Dentoperiosteal
Transseptal fibres
(Accesory fibres)
10
edition

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.Periodontal2.Periodontal
ligamentligament
11
edition

Constant remodeling- fibres, bone & cementum
Principal fibres:
1. Alveolar crest group
2. Horizontal group
3. Oblique group
4. Apical group
5. Inter-radicular
6. Transseptal group
12
edition

Cells:
Proginator cells
Synthetic cells- Osteoblasts, Fibroblasts, Cementoblasts
Resorptive cells- Osteoclasts, Fibroblasts, Cementoclasts
Tissue fluid:
Derived from the vascular system
Shock absorber-retentive chamber with porous walls.
13
edition

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. Cementum3. Cementum
14
edition

Surrounds the tooth –CEJ-Lamina dura
Bundle bone- alveolar bone proper
Volkmann’s canals – vascular
communication with marrow spaces
Renewed constantly – functional
demands
Mesial & distal movement – spongiosa:
extraction space- Rapid
Labially- lingually- caution
4. Alveolar4. Alveolar
bonebone
15
edition

Masticatory function – intermittent heavy force
1-2 kg for soft substances
-50kg for hard substances
Heavy forces- > 1 sec-force transmitted to bone
Bone bending
Upon wide opening – distance between mandibular molars
decreases by 2-3 mm
Normal functionNormal functionRESPONSE TO NORMALRESPONSE TO NORMAL
FUNCTIONFUNCTION
16
*Contemporary orthodontics by William Proffit- 5th
edition

Physiologic Response To Heavy Pressure Against A
Tooth
17
edition

FORCE (PRESSURE)FORCE (PRESSURE)
PDL- Adaptive
Prolonged force
Remodeling of
adjacent bone
Short duration
18
edition

Resting pressure from lips, check and tongue
against the teeth
19
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 eruptionRole of Pdl in eruption
and stabilizationand stabilization
20
edition

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 toothPhysiologic tooth
migrationmigration
21
edition

Resorptive surface & depository surface
Unmineralised precementum – resorption-resistant coating
layer
22
edition

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 ForceOptimal Orthodontic Force
24

Orthdontic mechanotherapy:
Remodeling and adaptive changes in
paradental tissues
20-150 g per tooth
Craniofacial orthopedic:
Higher magnitudes of force to modify
bone form
>300g of mechanical force
Deliver 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 movement
Without tissue damage
Maximal patient cooperation
Differ for each tooth and each patient

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 ToothTheories Of Orthodontic Tooth
MovementMovement
28

Sandstedt (1904), Oppenheim (1911), and Schwarz (1932)
Pressure-tension TheoryPressure-tension Theory
29

The hypothesis explains that
Pressure 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 Pdl
30

SOME IMPORTANT TERMINOLOGIES:
1. Frontal bone resorption
Survival of cells within the PDL and a remodeling of tooth
socket by a relatively painless bone resorption
Occurs with application of lighter forces
2. Undermining bone resorption
Resoption of bone from underside immediately adjacent to
the necrotic PDL area and its removal together with the
necrotic tissue
Occurs 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 lost
First 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 movement
2. More hyalinization in tooth with short roots
3. 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
34

Fluid Dynamic theory
Force of longer duration- interstitial fluid squeezed out
Vascular stenosis – decreased oxygen level- compression
Alteration in the chemical environment
Fluid Dynamic TheoryFluid 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 TheoryBone Bending Theory
36

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
37

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”
38

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 inBioelectric signals in
orthodontic toothorthodontic tooth
movementmovement
edition

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 voltages
Rapid onset and alteration with changing stresses
edition

Applications of piezoelectricity:
Important for maintenance of bone around tooth
Sustained force- not significant
Vibrating application
41
edition

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.
42

In 1973, Zengo et al
43

In 1980, Davidovitch et al proposed that
A physical relationship exists between mechanical and
electrical perturbation of bone
Bending 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
44

According to Burstone (1962), 3 phases of tooth movement:
1. An initial phase
2. A lag phase
3. A postlag phase
PHASES OF TOOTHPHASES 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
46

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
49

Mostafa et al (1983) described integrated model showing
2 pathways of tooth movement:
1.1. Pathway IPathway I
- More physiologic response
- Associated with normal bone growth and remodeling
1.1. Pathway IIPathway II
- Alternative pathway
- Classic inflammatory response after force application
PATHWAYS OF TOOTHPATHWAYS OF TOOTH
MOVEMENTMOVEMENT
50

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
51

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

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
53

54
Signaling molecules andSignaling molecules and
metabolites in orthodontic toothmetabolites in orthodontic tooth
movementmovement

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
ProstaglandinsProstaglandins

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 enzyme
60
Intracellular second-Intracellular second-
messenger systemmessenger system

Two main second-messenger systems are:
1. The cyclic nucleotide pathway and
2. 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-AMP
Internal 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 systemThe PI dual signaling system
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 andVitamin D and
diacylgylceroldiacylgylcerol
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 movement
Mechanoreceptors in the apical half of root – Ruffini-like &
Nociceptive endings
Force sensing fibres
(unmyelinated C fibres/ myelinated Aδ)
Nerve terminal strained
Stored neuropeptides released
(Substance P, VIP, CGRP)
PG E2 & cAMP
67
NeurotransmittersNeurotransmitters

Substance P-Increased vascular permeability
Davidovitch(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

CytokinesCytokines
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, IFN .ɤ
In-vitro cell cultures-
1983-Gowen et al – IL-1 potent bone resorptive agent
1986- 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
IFN – causes resorption by apoptosis of effector T-cellsɤ
72

Cytokines- RANKL/RANK/OPGCytokines- RANKL/RANK/OPG
systemsystem
Drugrain et al (2003)-
RANKL/RANK/OPG – TNF related ligand- downstream
regulator of osteoclast formation & activation
RANKL – 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 factorsGrowth 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 stimulatingColony stimulating
factorsfactors

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 surfaces
elevated after 12 hours of force application
78
GeneticGenetic
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 andBehavior of oral soft and
hard tissues in response tohard tissues in response to
orthodontic forceorthodontic force

Osteoclasts – prerequisite for bone resorption
Arise from
1. 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
Osteoclast
83

Robert and Fergusan (1995) also showed that –
Osteoclast numbers per unit bone surface area show a
peak level about 50 hours after orthodontic force
application
New 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 Cascade
After 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 factors
Coupling 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 day
Osteoblasts 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 side
PDL 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 fibres
Deposition of new matrix along socket wall
Overstreched PDL – pain, reduced function, cell death
94
PDL remodelingPDL remodeling

95
B] Pressure sideB] Pressure side
PDL narrowing, alveolar bone crest deformation
Edema, gradual obliteration of blood vessels
Degenerative process, necrotic tissue, hyalinization
3 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 transfer
Means 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 fibers
Second – 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 orthodonticChanges in gingiva after orthodontic
force application:force application:
Tissue accumulation
Enlargement of gingival papillae when extraction spaces are
being closed
Vertical clefts of epithetlium and CT
Discontinuation of transeptal fibres and reestablishment
during healing phase
Increase amount of oxytalin fibres and GAGs
Increase rate of synthesis of fibroblasts
Increase 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 corrections
The 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 exudate
Total fluid flow – 0.5 to 2.4 mL/day
Apparent minimal inflammation – 0.05 to 0.20 ul/min
GCF 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 ofBiomarkers of
gingival creviculargingival 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 withTissue reactions with
varied forcevaried 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, andContinuous, interrupted, and
intermittent forcesintermittent 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 hours
Longer & constant the force- faster the tooth movement
Effects of force duration andEffects of force duration and
force decayforce decay
107

Teeth move in response to
forceforce changes
May drop to zero
108

Continuous force-
Light- frontal resorption
Heavy- undermining resorption- constant-further
Undermining.Resorption
Destructive to the PDL & tooth
Force decay-
Light force – Frontal Resorption- no movement till activation
Heavy – 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 andLight 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 movement
Tipping -
Force distribution and typeForce distribution and type
of tooth movementof 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 twice
Intermediate 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 tension
Light 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 orthodonticDeleterious effects of orthodontic
forceforce

Cementation of orthodontic bands or resin-bonded
attachments – local soft tissue responselocal soft tissue response
Proximity to gingival sulcus – plaque accumulation
122
Gingival problemsGingival problems

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 gingivalPlaque accumulation and gingival
inflammationinflammation – altered oral hygiene habits
Specific bacterial type
mainly of spirochetes and motile rods
bacteroids 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 bone
Unlike bone- not resorbed- continuous deposition
Major 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

History
Bates (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

Introduction
EARR – External apical root resorption (or) OIIRR
-Orthodontically induced inflammatory root resorption
Most common iatrogenic consequence of orthodontics
Several investigators elucidated factors-
Magnitude of force
Duration of force
Type of appliance
Individual variations- Genetic tendencies
132

Resorption Process
Resorption continues – all hyaline tissue is
removed- Pressure drops
Any 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 structure134

Prevalence
More root resorption in
Tooth moved the farthest
Extraction treatment
Intrusion and torquing movements
Tapered or conical roots
“shed roof” effect – resorption typically attacks the root
tip and travels coronally
Frequency
Maxillary – centrals, molars, canines
Mandibular – laterals and centrals 135

Classification
A] 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 treatment
b. 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

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-Calipers
Computer-aided measurement
Digital images
CT
141

Factors effecting root
resorption
BIOLOGIC FACTORS-BIOLOGIC FACTORS-
Individual susceptibility - major factor- variation in
the pattern of metabolic signals
Age - Poor correlation
Higher susceptibility in adults- PDL changes
Gender - Lack correlation- conflicting results
Sameshima & 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+
diet
Drugs-corticosteroids & alcohol- increases root
resorption
143

UNTREATED POPULATION - 0%- 90%- resorption
High 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 difference
Remington 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 I
Janson 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 applied
Al-Qawasmi et al-
linkage disequilibrium of IL-1ß polymorphism in allele 1
& EARR
Also 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 technique
McNab 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 considerations
BEFORE TREATMENT
General considerations
Inform patient & parents- unpredictability of root
resorption
IOPAs- -must- Pre & post treatment
Periodic control radiographs- at least once/year
Familial considerations
Obtain radiographs- if anyone else (sibling) treated in
the Family
General Health-
Systemic disorders
Asthma and allergies
153

DURING TREATMENT
Appliance 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-reassess
Bite plane – disocclude
AFTER TREATMENT
Radiographs-
Mandatory - if detected
Follow - up radiographs
Advisable - full mouth
155

Contemporary orthodontics by William Proffit- 5th
edition
Orthodontics, current principles and techniques by Graber &
Vanarsdall -5th
edition
Biologic mechanism of tooth movement by Krishnan 2nd
edi.
Caranza’s clinical periodontology by Michael Neuman and
Caranza – 10th
edition
Vinod Krishnan and Davidovitch. Cellular, molecular & tissue level
reactions to othodontic force. AJODO 2006:129;469e.1-469e32
156
REFERENCESREFERENCES

biology of tooth movement

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