biologic basis of orthodontic therapy

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Biology of Tooth Movement

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Contents

Tooth supporting tissuesPDL-structure and function

Role of PDL – eruption & stabilization

Response to orthodontic forceBiologic basis of tooth movement

Biologic electricity Pressure-tension

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Contents

How teeth move clinically-Concepts of optimal force

Effects of force distribution and types of tooth movement

Force duration and decay

Effects of drugs

Root resorption in orthodontic tooth movement

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The PeriodontiumPeriodontium 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.4 connective tissues

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

Two mineralized -Cementum -Alveolar bone

GingivaFree gingiva is in close contact with the enamel surface

Its margin is located 0.5 to 2mm coronal to the CEJ after completed tooth eruption.

Attached gingiva is firmly attached to the underlying alveolar bone and cementum by connective tissue fibres.

The predominant tissue component is Connective Tissue, which consists of Collagen Fibres (66%), Fibroblasts (5%) and Vessels, Nerves & Matrix (35%)

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Gingiva

CircularDentogingivalDentoperiostealTransseptal fibres (Accesory

fibres)

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PDLConnective tissue interface separating the tooth from the supporting bone.Heavy collagenous supporting structure- 0.5mm aroundApart from fibres-

Cellular elements-mesenchymal, vascular & neural Tissue fluids

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PDL

Progenitor cells

Synthetic cells a) Osteoblasts b) Fibroblasts c) Cementoblasts

Resorptive cells A) Osteoclasts B) Fibroblasts C) Cementoclasts

Fibres -Collagen -Oxytalan

Ground Substance -Proteoglycans -Glycoproteins

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PDL

Principal fibres -1. Alveolar crest group2. Horizontal group3. Oblique group4. Apical group5. Transseptal group

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PDLTissue fluid-

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

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Cementum

Attaches the PDL fibres to the root

Avasular, no innervation, no remodeling

Continuous deposition through out life.

Contributes to the process of repair – after orthodontic tooth movement.

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Alveolar Bone

Surrounds the tooth to a level approx. 1mm apical to the CEJ. The bone is covered with the Periosteum, which functions as an osteogenic zone throughout life. The alveolar bone further consists of two components, the alveolar bone proper and the alveolar process.

Classification of Bone

Based on Structure.Compact Bone or

cortical bone - the dense outer shell of the skeleton.

Cancellous Bone or trabecular bone - comprises of a system of plates, rods, arches and struts traversing the medullary cavity encased within the shell of compact bone.

Based on the Arrangement of Collagenous Matrix.

1)Immature Bone: This is further subdivided into:

Woven Bone : Relatively weak, disorganized and poorly mineralized. The first bone formed in response to orthodontic loading usually is the woven type.

Bundle Bone: is a functional adaptation of lamellar structure to allow attachment of PDL fibers.

2)Mature Bone :

Lamellar Bone: highly organized, well-mineralized tissue. Full strength of lamellar bone that supports an orthodontically moved tooth is not achieved until approx. 1 year after completion of active treatment.

Composite Bone: formed by deposition of lamellar bone within a woven bone lattice. It is an intermediary type of bone in the physiologic response to orthodontic loading.

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Role of PDL

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Physiologic Tooth MigrationTeeth and supporting tissues have a life long ability to adapt to functional demands and hence drift through alveolar process – Physiologic tooth migrationIn human beings and primates, teeth in post. segments migrate mesially, in rodents-distally

Teeth also exhibit continued eruption, even after full emergence, accompanying the growth in height of alveolar process.Teeth migrate bringing supraalveolar fiber system with them. Such movement implies remodeling of PDL and alveolar bone.

Turnover rate of PDL is not uniform throughout ligament.Cells are more active on bone side than near root cementum.Therefore major remodelling takes place near alveolar bone.

Remodeling process1. Alveolar bone

Osteoclasts seen in scattered lacunae in resorptive surface along alveolar bone wallOsteoblasts deposit non-mineralized osteoid along alveolar bone wall from which tooth is moving away (depository side)

2. Periodontal ligamentOlder fibres of PDL are surrounded by osteoid and become embedded in boneNew collagen fibrils produced by cells on bone surfaceSites of active rebuilding of fibrous apparatus lie in the middle of the ligament and alveolar bone side.

3. CementumSlow apposition occurs throughout life Unmineralized precementum layer has resorption resistant coating layer thus protecting root surface during physiological migration.

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Force (pressure)

Short duration

PDL- Adaptive

Prolonged force

Remodeling of adjacent bone

Orthodontic Tooth Movement

No great difference from physiologic tooth movementTissue changes are more marked and extensiveTo move a tooth , minimal of 5-10g/cm2 force is requiredBelow this threshold level, forces on tooth are actively stabilized by PDL and are ineffective

Tissue Response in Periodontium

Dental movements 1. with the bone 2. through the bone

1. With the bone movement- frontal (direct) resorption of bone in direction of movement should occur with balance between resorption and apposition

2. Through the bone movement- due to excessive force application

Indirect resorption in areas surrounding compressed , necrotic PDLSmall amounts of bone apposition initially Once bony barrier is dissolved tooth moves rapidly in direction of force PDL in tension sites is stretched .Bone apposition proceeds vigorously

Duration of Movement

1. Initial period – period of hyalinization and indirect bone resorption

2. Secondary period- period of direct bone resorption and rapid tooth movement

Initial Period

Compression in limited areas of membraneVascular circulation and cell differentiation impededDegradation of cells and vascular structuresGlass like appearance under light microscope - hyalinization

Hyalinization

Almost unavoidable in clinical orthodonticsSterile necrotic area limited to 1 or 2 mm in diameter3 stages –

1. Degeneration2. Elimination of destroyed tissue3. Establishment of new tooth

attachment

Degeneration

Starts where pressure is highest (bony spicules)May be limited to parts of PDL membrane or from root surface to alveolar bone

Vascular changesRetardation of blood flowDisintegration of vessel walls

Cellular changesSwelling of mitochondria and endoplasmic reticulumRupture and dissolution of cytoplasmic membranePyknotic nucleiNo bone resorption from PDL membraneCells can’t differentiate into osteoclasts

Elimination of Destroyed Tissue

Perepheral areas of hyalinized tissue eliminated by invasion of cells and blood vessels from adjacent undamaged PDLHyalinized material ingested by macrophages Adjacent alveolar bone removed by indirect resorption by cells differentiated into osteoclasts on surfaces of adjacent marrow spaces

When orthodontic forces applied to human teeth are kept within the normal range, osteocytes of the alveolar bone adjacent to the hyalinized PDL reveal no signs of degeneration or cell death with necrosis of the bone.

2. Secondary Period of Tooth Movement

As long as force is kept within limits , further bone resorption is directFibrous attachment apparatus is reorganizedLarge number of osteoclast seen along bone surface Rapid tooth movement

Osteoid tissue deposited on tension sideNew bone deposited until width of membrane returns to normal and fibrous system remodeled

Tension sideApposition on PDL surfaceResorption on spongiosa surface of

alveolar bone

Pressure sideResorption on PDL surfaceApposition on spongiosa surface

Theories of Tooth Movement

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1. The pressure-tension theory relates tooth movement to biochemical-responses by the cells and extracellular components of the PDL, and alveolar bone.

2. The bio-electric theory deals with tooth movement as a bioelectric phenomenon that may occur as a result of mechanical distortion of collagenous matrices, mineralized or nonmineralized, in the alveolar bone, the PDL, and the teeth.

Pressure Tension theory

Classic hypotheses on the mechanism of tooth movement, based on the work of Oppenheim(1911), and Schwarz(1932)Relies on chemical rather than electrical signals as stimulus for cell differentiation

Postulate the movement of the tooth within the periodontal space, generating a "pressure" side and a "tension" side.

On the "pressure" side, cell replication is said to decrease as a result of vascular constriction, causing bone resorption.

On the "tension" side, cell replication is said to increase because of the stimulation afforded by the stretching of the fibre bundles of the periodontal ligament (PDL), thus causing bone deposition.

In terms of fibre content, the PDL on the "pressure" side is said to display disorganization and diminution of fibre production, while on the "tension" side, fibre production is said to be stimulated.

The Bio-electric Theory: (Farrar 1876)

Distortion of cells and extracellular matrix is associated with alteration in tissue and cellular electric potentials. Bones generally have a remarkable ability to remodel their structure in such a way that the stress is optimally resisted.

Mechanical deformation of the crystalline structure of the hydroxyapetite and the crystalline structure of collagen induce migration of electrons that generate local electric fields- piezoelectricity.

Such signals die away quickly even though the force is maintained.

When the force is released & the crystal lattice returns to the original shape, a reverse flow of electrons occurs.

Rhythmic activity would cause a rhythmic flow of electrons in both directions

Ions in the fluids surrounding the living bone interact with these electrical fields. These currents of small voltages are called streaming potentials Bending of bone may create negative fields occurring in the concave aspect of the bone surface leading to deposition. Areas of convexity are associated with positive charges and evoke bone resorption.

Both animal and human experiments indicate that when low voltage direct current is applied to the alveolar bone, modifying the bioelectric potential, a tooth moves faster than its control in response to an identical spring.

BIOCHEMICAL REACTIONS TO ORTHODONTIC TOOTHMOVEMENT

ORTHODONTIC FORCE

BIO-PHYSICAL REACTIONSBone deformation

Compression of PDLTissue Injury

PRODUCTION OF FIRST MESSENGERSHormones (e.g.. PTH)

ProstaglandinsNeurotransmitters

PRODUCTION OF SECOND MESSENGERSC amp, C gmp, Ca++

Increase in cells of Resorption (osteoclasts)Increase in cells of Deposition (osteoblasts)

Bone Remodelling

ORTHODONTIC TOOTH MOVEMENT

Inflammation due to tissue injury

Activation of Collagenase

TYPES OF TOOTH MOVEMENT and TISSUE REACTIONS

Tipping

Simplest form of orthodontic tooth movement produced when a single force is applied against the crown of a tooth. When this is done, the tooth rotates around its Centre of Resistance, a point located about halfway down the root.

The PDL is compressed near the root apex on one side and at the crest of the alveolar bone on the opposite side. Maximum pressure at alveolar crest and root apex and minimum at CR

In tipping only half of PDL area that could be loaded actually is.So forces kept quite low – around 50 gms.

Bodily movement

Total PDL area is loaded uniformlyTwice as much force as for tipping is required for bodily movement- around 100gms

RotationPure Rotation of a tooth requires a couple. No net force acts at the CResTheoretically, force can be distributed over the entire PDL ,so larger forces can be applied than in other tooth movementsHowever it is impossible to apply rotational force without tippingSo force needed for rotation similar to tipping

Extrusion Extrusive movements ideally does not produce any areas of compression within the PDL, but only tension.However like rotation if tooth is tipped at all during extrusion , areas of compression are created So force required should be of same magnitude as tipping

Intrusion Light force is required because the force is concentrated in a small area at the tooth apex. Primarily the anterior teeth are intruded.

Stretch is exerted primarily on the principal fibres.

Rearrangement of the principal fibres occurs after a retention period of 2 to 3 months.

Unlike extruded teeth, intruded teeth in young patients undergo only minor positional changes after treatment.

Relapse usually does not occur, partly because the free gingival fibre bundles become slightly relaxed.

Force Types

Light, continuous forces

Never declines to zero.

Interrupted forcesDeclines to zero

Intermittent forcesDeclines to zero

Continuous force – force maintained at some appreciable fraction of the original from one patient visit to the next.Interrupted- force levels decline to zero between activations

Both of these can be produced by fixed

appliances that are constantly present

Intermittent- force levels decline abruptly to zero intermittently, when the orthodontic appliance is removed by the patient or perhaps when a fixed appliance is temporarily deactivated, and then return to original level some time later

Effects of force duration and decay

Light continuous force- relatively smooth progression of tooth movement from frontal resorption.

Heavy continuous force- tooth movement delayed till undermining resorption occurs. Then tooth will change its position rapidly , and constant heavy force will again compress tissues preventing PDL repair. Such a heavy continuous force can be quite destructive.

Light interrupted forces- tooth moves a small amount by frontal resorption and remains in that position till appliance is activated again.Heavy interrupted forces- tooth moves when undermining resorption is complete. Since force has dropped to 0 at that point, it will remain in that position till next activation. So there are periods of regeneration and repair before reapplication of force.

Heavy continuous forces are to be avoided; heavy intermittent forces though less efficient , can be clinically acceptable.Orthodontic appliances should not be reactivated more frequently than at 3 week interval.

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Effects of Force Magnitude

Deleterious Effects of Orthodontic Tooth

Movement

Mobility and PainMobility-moderate mobility can occur.

Severe mobility- indication of excessive use of forcesPain-Excessive pain immediately after applying force is undesirableReason- development of ischeamic areasPain can be due to allery-

latex nickel

Effect on Pulp

Pulpal Reactions

Profitt and Fields stated ‘although pulpal reactions to orthodontic treatment are minimal, there is probably a modest and transient inflammatory response within the pulp, atleast at the beginning of treatment’

Occasional reports of loss of tooth vitality during orthodontic treatment.

Heavy continuous forces can lead to a sequence of abrupt movements capable of severing blood vessels at their point of entry.

Studies suggest that pulp reactions to orthodontic movement may range from circulatory vascular stasis to necrosis.Intrusive and extrusive forces can cause odontoblastic degeneration due to circulatory disturbances in pulp.

Vasodilation and Angiogenic Response to Orthodontic Forces

Dental pulp is encased within a rigid non-compliant shell.

Survival of pulp depends on blood vessels.

Changes in pulpal blood flow or vascular tissue pressure might be detrimental to pulpal health.

Studies suggest that orthodontic forces might produce congestion as well as dilation of blood vessels along with edema of pulpal tissue.

ROOT RESORPTION

Internal resorption (OIIRR)Unavoidable pathologic consequence of orthodontic tooth movement.Defined as iatrogenic damage that occurs ,unpredictably, after orthodontic treatment, whereby resorbed apical portion is replaced with normal bone.

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PROFITT- external root resorption types:-

1) Moderate Generalized- -long Rx duration

2) Severe Generalized – -evidence of resorption before Rx -etiology???

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

Etiology not fully understood.

Studies suggest endodontically treated tooth roots resorb significantly less than their contralateral controls. So dental pulp might be involved in OIIRR.

A study was done to correlate internal resorption and inflammation in dental pulp.

Results suggested that stimulation with increased levels of IL-1β, IL-6, TNF-α, PGE 2, and RANK-L in a time and conc. dependent manner.

Drug effects on response to orthodontic force

Agents that stimulate OTMVitamin D administration can enhance response to orthodontic forceDirect injection of prostaglandin into PDL increases rate of tooth movement but is quite painful.

Agents that depress response to OTM

Bisphosphonates used in treatment of osteoporosis [eg alendronate(Fosamax) or risedronate (Actonel)]Prostaglandin inhibitors

1. Corticosteroids and NSAID’s 2. agents with mixed agonistic and

antagonistic effects on various PG’s(trycyclic antidepressants, antiarrhythmic agents, antimalarial drugs)

Various Studies

PGE and IL-1β levels in GCF were tested in 10 patients , each having one treatment tooth undergoing orthodontic movement and one control tooth. GCF was sampled at these sites before activation and at 1, 24 , 48, and 168 hours. Results demonstrated that bone resorbing PGE and IL-1β, are detectable in GCF during early phases of tooth movement and return to baseline within 7 days (AJO-DO 1994; 105:369-74)

Involvement of nitric oxide in orthodontic tooth movement was studied in rats using specific inhibitors of NOS. Results suggested that NO is an important biochemical mediator in the response of periodontal tissue to orthodontic force and produced primarily through the activity of constitutive NOS (AJO-DO 2002;122: 306-9)

PGE2, with or without simultaneous administration of Calcium Gluconate (Ca), was tested over a 21-day period of experimental tooth movement in rats. An acceleration in tooth movement was noted after PGE2 injection. The addition of Ca moderated the increase in the rate of tooth movement due to PGE2, but most importantly, the increase in root resorption, observed in the PGE2 only group, was negated by simultaneously administering Ca.

It was concluded that Ca ions stabilize teeth against root resorption when the rate of tooth movement is enhanced by PGE2.(EJO-2003 )

Levels of IL-8 were tested during mechanical forces on PDL tissues at different stages of orthodontic therapy. Local host response toward orthodontic forces might increase IL-8 and neutrophil accumulation , and this may be one of the triggers for remodeling process. (AO-2005)

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Cellular & Molecular Mechanism

Mechanical force to Molecular

events

‘Highly sophisticated process’

The DNA in PDL and alveolar bone cell chromosomes holds the key to OTM.

Normal OTM- osteoblastic and osteoclastic genes – correct expression of proteins at right time & places

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Genomic Regulation

96 genes-osteogenesisFunctionally 44-GFS,30 –ECM proteins 8 -cell adhesion molecules

Osteoblasts and fibroblasts are almost geneticaly identical.all genes expressed in osteoblasts are also expressed in fibroblasts.

Only 2 osteoblast specific transcription factors are known that are not present in the fibroblasts

TF Cbfa1TF osteocalcin

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Osteoblastic Regulation

Earliest expressed- TF Cbfa1-most specific for bone formation

Other genes code-Proteins of GFs, BMPs,TGFßOsteoblast differentiation & proliferation – separate genes

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GF genes (embryonic stage)- TGFß, fibroblast GF-1, Indian Hedgehog

Other genes-NO synthetase, ProstaglandinG/H synthetase, glutamate/asparate transporter

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Lipoprotein receptor-related protein 5-(LRP5)- modifies osteoblast formation & increasing bone massHomeobox genes ( specialized DNA sequence in exons of many regulatory genes)-

Msx 1- key regulator of bone development & modelingMsx 2-Regulates Cbfa1 expressionHox A-2-Controls 2nd branchial arch patterning

- Suppresses Cbfa1 & bone formation

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Neurotransmitters

Physiologic orthodontic force

PDL fibres release calcitonin gene related peptide (CGRP) and substance P .

These neurotransmitters serve as vasodiators

Induce bone formation by osteoblasts proliferation and osteoclasts inhibition

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Osteoclastic Activity

Rate limiting agents for oeteoclast differentiation and functionOstoeprotegrin(OPG)Cathepsin K Chloride channel 7

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Tooth movement is a highly conserved physiological mechanism for continuous adaptation of the dentition. Orthodontic tooth movement is a biomechanical exploitation of the physiologic mechanisms for developing and maintaining optimal occlusal function. The tooth continues to move until it achieves equilibrium with natural and applied loads.

CONCLUSION

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There are grounds for cautious optimism that we may now be near the end of the search for the ultimate laws of nature.

Stephen W. Hawking

THANK YOU

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