Biology Of Tooth Movement.docx

BIOLOGY OF ORTHODONTIC TOOTH MOVEMENT CONTENTS 1- Introduction 2-The periodontium •

Gingiva

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Cementum

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Periodontal ligament

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Alveolar bone

3-History of studies pertaining to tooth movement 4- Classification of tooth movement 5- Bilological considerations 6-Orthodontic tooth movement 7-Tissue response to periodontium 8-Hyalinisation 9-ResorptionSignaling molecules in orthodontic tooth movement 10-Types of tooth movement 11-Signaling molecules in orthodontic tooth movement 12-Types of tooth movement 13-Phase of tooth movement 14-Theories of tooth movement 15-Piezoelectric theory 16-Bone bending theory 17-Pressure-Tension theory 18-Orthodontic force 19-Clinical considerations

20-Factors affecting tooth movement 21-Surgical enhancement of tooth movement 22-Iatrogenic effects of tooth movement 23-Future of orthodontic tooth movement 24-Conclusion 25-References

INTRODUCTION  Orthodontic treatment is based on the principle that if prolonged pressure is applied to a tooth, tooth movement will occur as the bone around the tooth remodels.  Tooth movement involves a cascade of tissue reactions and is a result of several complicated and highly organized interactions at molecular level.

THE PERIODONTIUM-It Includes the tissues supporting and investing teeth.    

Gingiva Periodontal ligament Cementum Alveolar bone

PERIODONTAL LIGAMENT  Soft, specialized, unique connective tissue  Situated b/w the cementum covering the root of the tooth & the bone forming the socket wall  Width ranges from 0.15 to 0.38 mm which varies with the location of the tooth and the age of the patient  Principle function is to support teeth in their sockets and at the same time permit them to withstand the considerable masticatory forces Groups of periodontal fibers  Alveolar crest group  Horizontal group  Oblique group  Apical group  Interradicular group CEMENTUM  First demonstrated in 1835 by two pupils of Purkinje. 

Layer of calcified tissue covering the dentin of the root.

 Specialized connective tissue avascular and has no innervations.

 physical and chemical properties similar to bone. Functions of cementum  Primary function – furnish a medium for attachment of collagen fibers that bind the tooth to the alveolar bone.  Also serves as a major reparative tissue for root surfaces  Root damages ( minor fractures , resorptions) can be repaired by deposition of new cementum ALVEOLAR BONE  That bone of the jaws which contains the sockets for the teeth is known as alveolar bone.  Consists of  an outer cortical plate  A central spongiosa  bone lining the alveolus referred to as the bundle bone (provides attachment for the PDL fiber bundles) Based on the arrangement of collagenous matrix. 1)Immature Bone: 

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

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Bundle Bone: is a functional adaptation of lamellar structure to allow attachment of Sharpey's fibers.

2)Mature Bone : Lamellar Bone:  Strong, highly organized, well-mineralized tissue. Adult human bone is almost entirely of this remodeled variety.  The full strength of lamellar bone that supports an orthodontically moved tooth is not achieved until approximately 1 year after completion of active treatment.

Composite Bone:  An osseous tissue formed by the deposition of lamellar bone within a woven bone lattice.  An important intermediary type of bone in physiologic response to orthodontic loading. BONE MODELING AND REMODELING Wolff’s Law as stated in 1892“Every change in the form and function of bone or of their function alone is followed by certain definite changes in their internal architecture, and equally definite alteration in their external conformation, in accordance with mathematical laws.” Both trabecular and cortical bone grow, adapt, and turn over by means of two fundamentally distinct mechanisms: Modeling and Remodeling. Because bone is a relatively rigid material, incapable of internal expansion or contraction, changes in osseous structure are via cell-mediated resorption and formation. In Bone modeling, independent sites of resorption and formation change the form (i.e., shape or size or both) of a bone. In other words it is a process of uncoupled resorption and formation. In bone remodeling a specific, coupled sequence of resorption and formation occurs to replace previously existing bone. Bone modeling is the dominant process of facial growth and adaptations to applied loads such as head gear, RPE, and functional appliances. Modeling changes can be seen on cephalometric tracings, but remodeling events are apparent only at the microscopic level. HISTORY OF ORTHODONTIC TOOTH MOVEMENT  Celsus- first advocated about use of mechanical forces to evoke tooth movement  1728 Fauchard - bone moves out of the way of pressure  1888 Farrar – bone responds to mechanical loads  Sandtedt ( 1904 to 1905 ) first investigated the phenomenon of tooth movement by histological examination of supporting structures.He found that the under gentle pressure, bone resorption took place on the pressure side and bone deposition on the tension side  Oppenheim’s( 1911 ) experiments further supported the conclusions made by Sanstedt

 In 1932, Schwarz concluded from his experiments that the most favorable tooth movement was produced by forces not greater that capillary blood pressure, such forces being insufficient to collapse the capillaries in the PDL 

Reiten (1951) & Kvam (1971) carried out a series of experiments on dogs and human subjects to determine the tissue reaction during tooth movement and discovered changes in the cellular level including the phenomenon of hyalinization.

 Storey (1973)-concluded from his experiments about the orthodontic forces RESPONSE TO NORMAL FUNCTION  During masticatory function, the teeth and PDL structures are subjected to heavy intermittent forces tooth contacts last for 1 second or less ; forces are quite heavy , ranging from 1-2kg while soft substances are being chewed , up to as much as 50 kg against a more resistant object.  When a tooth is subjected to such type of heavy load ,quick displacement of the tooth within PDL space is prevented by incompressible tissue fluid present in PDL space. Instead the force is transmitted to the alveolar bone, which bends in response. CLASSIFICATION OF TOOTH MOVEMENT Physiologic tooth movement  Eruption  Drifting Pathologic tooth movement  Periodontal Pathology  Oral pathologies ( Cysts, Tumors etc ) Orthodontic tooth movement  Tooth Movement under external clinical forces ORTHODONTIC TOOTH MOVEMENTNo great difference exists between the tissue reactions observed in physiologic and those observed in orthodontic tooth movement. However, since the teeth are moved more rapidly during treatment as compared to physiologic tooth movement, the tissue changes elicited during orthodontic forces are consequently more marked and extensive. (Rygh and Brudvik 1995).

 Storey & Smith (1952)-observed same finding in their experiments  Proffit (2007), Ren et al (2003)-suggested that optimal force may differ for each tooth and for each individual patient.  If force is more than optimum “Suffocation of strangualated periodontium’’  Optimum orthodontic force has the following characteristics Produces rapid tooth movement.  Minimal patient discomfort.  Lag phase of tooth movement is minimal.  No marked mobility of the teeth being moved Tissue Response in Periodontium: The most dramatic remodelling changes incident to orthodontic tooth movement occur in the PDL. Application of a continuous force on the crown of the tooth leads to tooth movement within the alveolus that is marked initially by narrowing of the periodontal membrane, particularly in the marginal area. If the duration of movement is divided into an initial and a secondary period, direct bone resorption is found notably in the secondary period, when the hyalinized tissue has disappeared after undermining bone resorption. During the crucial stage of initial application of force, the tissue reveals a glass like appearance in light microscopy, termed hyalinization. Hyalinization: •

It is a form of tissue degeneration characterized by formation of a clear, eosinophilic homogenous substance.

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A hyalinized zone is a local cell free area of over compressed periodontal tissue. The conventional pathologic process of hyalinization is an irreversible one; however, hyalinization of the periodontal ligament is a reversible process.

 Presence of hyalinised area indicates that the ligament is non functional and therefore bone resorption cannot occur. Elimination of hyalinised tissue occurs by two mechanisms 1-Resorption of alveolar bone by osteoclasts differentiating in the peripheral intact periodontal membrane and in adjacent marrow spaces.

 2-Invasion of cells and blood vessels from the periphery of compressed zone by which necrotic tissue is removed by the process of enzymatic action and phagocytosis. 

Greater the forces, the wider are the area of hyalinization and smaller hyalinization area when less force is used. Frontal Resorption-

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When forces applied are within physiological limits, resorption is seen in alveolar plate immediately adjacent to ligament . This kind of resorption is known as Frontal Resorption. Undermining Resorption

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When extreme forces are applied to teeth resulting in crushing or total compression of PDL leading to regressive changes , and formation of hyalinized zone so the bone cant resorb in frontal portion adjacent to teeth and the bone resorption occurs in the adjacent marrow spaces and in the alveolar plate behind and above the hyalinized areas .This kind of resorption is known as Undermining resorption or rearward resorption. PHASES OF TOOTH MOVEMENT

 Storey inferred from his animal studies and graphed analyses that,  “In general, each curve has three phases: the first, where rapid movement takes place through the periodontal ligament space; the second, where movement occurs relatively slowly, or not at all, with the heaviest forces; and finally a stage where teeth begin to move rapidly……” • • •

1-The Initial Phase: There is mechanical displacement of the tooth following deformation of supporting bone within the periodontal membrane space. This movement may be a crown tipping or a bodily movement, and is frequently a combination. Tissue compression and bone deformation in this phase, which ordinarily lasts 6-8 days , can result in rapid movement. 2-The Lag Phase:

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According to Reitan , this is the plateau or hyalinization stage in which little or no tooth movement occurs.

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It is characterized by cell free zones on the pressure side of the root and undermining resorption on the periodontal side of the alveolar wall.

This stage usually lasts from 1-3 weeks. 3-The Post-Lag Phase: There occurs a mechanical displacement of tooth associated with cellular activity of resorption and deposition. This may be any type of tooth movement and may be rapid or slow. It occurs spontaneously at the conclusion of the hyalinization period or lag phase without additional force input. SIGNALING MOLECULES  Main component of phospholipids of cell membrane released due to action of phospholipase enzyme Prostaglandins,Leukotrienes and Thromboxanes  Von Euler (1934)  Production is regulated by phospholipase A2 and COX  Role of PGE1 and E2 in stimulating bone resorption (klein & raisz 1970,Lee 1990)  PGI2 & TXA2-increase osteoclastic activity in rats (Guston et al,2004) First messenger binds to special receptors on cell membrane and produces secondary messenger which interacts with cellular enzymes and evokes response. SECOND MESSENGER SYSTEM  Cyclic nucleotide pathway  Phosphatidyl Inositol dual signaling pathway 1-CYCLIC AMP SIGNALING PATHWAY  Cyclic AMP Protein kinase A regulates bone resorption mediated by cathepsin K in cultured mouse osteoclasts (Park et al,2006)  Cyclic GMP action mediated through cGMP dependent protein kinase plays key role in synthesis of nucleic acids and proteins (Davidovitch,1995) 2-PHOSPHATIDYL INOSITOL DUAL SIGNALING PATHWAY  Phospatidyl inositol 4,5 biphosphate undergoes hydrolysis and forms,

 Inositol 4,5 biphosphate,Releases calcium ions from intracellular stores biphosphate,it undergoes phosphorylation and  Ins (1,3,4,5) P4 is formed,controls entry of calcium at plasma membrane,  Activation of cGMP and IP leading to expression of transcripor factor growth response gene 1  Elevated in osteoblasts involved in response to mechanical stretch (Dolce et al,1996) VITAMIN D •

Active form of Vitamin D

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Maintains calcium homeostasis(Collins & Sinclair,1988)(Takano-Yamamoto et al,1992

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Stimulates bone mineralisation and osreoblast cell differentiation (Kate et al)

THEORIES OF TOOTH MOVEMENT These are the basis of the two major theories of Orthodontic tooth movement•

Pressure Tension Theory by Schwarz

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Blood flow theory by Bien

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Bone bending Piezoelectric theory 1-PRESSURE TENSION THEORY

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Most accepted theory of tooth movement,relies on chemical rather than electric signals as the stimulus for cellular differentiation and tooth movement.Sustained pressure causes tooth to shift position within the periodontal space.

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Schwarz hypothesized that the “PDL space is a continuous hydrostatic system, and forces applied to this environment by means of mastication or orthodontic appliances create a hydrostatic pressure that would be, in accordance with Pascal's law, transmitted equally to all regions of the PDL’’.

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According to Schwarz , whenever a tooth is subjected to an orthodontic force , it results in areas of pressure and tension.

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The area of periodontium in the direction of tooth movement is under pressure while the area opposite to tooth movement is under tension.

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Paravascular osteogenic response in tension zone of PDL (Masella & Meister,2006)

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Areas of pressure show bone resorption while areas of tension show bone deposition (Mostafa et al )

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

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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.

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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 2-PIEZOELECTRIC THEORY

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Farrar(1988) first noted deformation or bending of interseptal alveolar walls. He related tooth movement to change in bone metabolism controlled by the electric signals that are produced when the alveolar bone flexes and bends.

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Baumrind (1969) conducted the experiment in rats.

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Grimm (1972) in humans.

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Bassett (1962)-bioelectric signals.

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Zengo et al (1974) in dogs.

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Davidovitch et al (1980), suggested a physical relationship between mechanical and electrical perturbation of bone

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Piezoelectricity : phenomenon observed in many crystalline materials in which a deformation of the crystal structure produces a flow of current as electrons are displaced from one part of the crystal lattice to another .

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example-

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Collagen

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Hydroxyapetite crystal

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Collagen hydroxyapetite interface

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Due to migration of electrons within the crystal lattice as it is distorted by pressure, electrons migrate from one location to another and an electric current is observed

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Crystal is stable as long as the force is maintained. When force is released, crystal returns to its original shape & a reverse flow of electrons is seen

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Hence a rhythmic activity would produce a constant interplay of electric signals, whereas occasional application and release of force would produce only occasional electric signals

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Piezoelectric signals have two unusual characteristics-

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Quick decay rate-when a force is applied, piezoelectric signal is produced. This electric charge quickly dies away to zero even though the force is maintained

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When the force is released, electron flow in the opposite direction is seen

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When force of greater magnitude and duration is applied , interstitial fluid in the PDL space gets squeezed out and moves towards the apex and cervical margins and results in decreased tooth movement.This effect is known as Squeeze film effect by Bien.

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Alteration in chemical environment at the site of vascular stenosis due to decreased oxygen level in compressed areas as compared to tension area.

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Vascular stenosis & aneurysms formation

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blood gases escape into interstitial fluid,

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favourable for resorption

GENETIC CONTROL MECHANISMS •

Several Genes, linked to mechanical activation of bone, produce enzymes such as glutamate/aspartate transporter (GLAST), inducible nitric oxide synthetase (iNOS) and prostaglandin G/H synthetase (PGHS-2). Inducible gene products compose an intricate series of edocrine, paracrine, and autocrine mechanisms for controlling bone modeling. -Parathyroid Hormone (PTH) and PTH-related protein (PTHrP) enhance expression of insulin-like growth factor I (IGF-I). Other products secreted

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Osteocalcin

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Osteonectin

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Osteopontin

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RANKL (receptor activator of nuclear factor kappa B ligand )

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Macrophage colony stimulating factor ( M-CSF )

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osteoprotegerin (OPG)

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- Receptor activator of nuclear factor kappa ligand (RANKL) and Osteoprotegerin (OPG) are regulators of bone metabolism

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RANKL promotes osteoclastogenesis

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OPG inhibits osteoclastogenesis

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Expression of RANKL and OPG in human PDL cells was measured by Zhang et al (2004)

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V In situ hybridization under conditions of physiologic tooth movement in rats demonstrated site-specific expression of mRNAs for osteonectin(Osn), osteocalcin (Ocn), and osteopontin (Opn) (JHC-1994).

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In response to orthodontic force, Opn mRNA is elevated within the tissue by 12hrs and can be demonstrated at 48hrs by in situ hybridization in >50% of osteoclasts and >87% of osteocytes in the interdental septum of maxillary molars (JBMR1999).

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Msx1 is a regulator of bone formation during development and postnatal growth. It is involved in the control of neural crest cell migration but also appears to be important for bone modeling activity.

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Vit D3 down regulated the expression of OPG and upregulated the expression of RANKL

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Prostaglandins are released when cells are mechanically deformed, at molecular level Focal adhesion kinase (FAK) appears to be mechanoreceptor in PDL cells,and its compression is leads to release of PgE2

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Concentration of receptor activator of nuclear factor kappa ligand(RANKL) AND Osteoprotegrin(OPG) in gingival crevicular fluid increase during tooth movement, which suggests that PDL cells under stress may induce the formation of osteoclasts through upregulation of RANKL. CLINICAL CONSIDERATIONS

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Factors Influencing Orthodontic tooth movement-

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Force

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Drugs/medications

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Systemic diseases

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Age of Patient ON THE BASIS OF DURATION OF FORCE

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Continuous

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Interrupted

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Intermittent CONTINUOUS FORCEIt is an active orthodontic force that decreases little in magnitude between appointment periods. Continuous forces are expected to bring about direct resorption of the root socket.

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Eg-light wire appliance INTERMITTENT FORCE

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An active orthodontic force that decays to zero magnitude or nearly so prior to the next appointment.

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For an appliance to deliver intermittent force, appliance components should have high stiffness and initial activation should be twice the expected corresponding soft tissue deformation. It is an active orthodontic or orthopaedic force that is inactive for intervals of time between appointments. INTERRUPTED FORCE

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It exhibits cyclic,long term magnitude pattern.

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eg-force exerted by an extra oral appliance worn at night only EFFECTS OF DRUGS ON TOOTH MOVEMENT Orthodontic Tooth Movement enhancers

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Vitamin D administration enhances tooth movement

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Direct injection of prostaglandin into the PDL has shown to increase the rate of tooth movement ( Painful ) Orthodontic Tooth Movement Depressors

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Bisphosphonates ( used for Tt of osteoporosis eg. Alendronate )

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Prostaglandin Inhibitors ( eg. Indomethacin used for arthritis treatment )

PROSTAGLANDINS •

Play an important role in the cascade of signals that lead to tooth movement

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Two categories of drugs affect prostaglandin activity :

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Corticosteriods and NSAIDS (interfere with prostaglandin synthesis)

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Other agents with mixed agonistic and antagonistic effects on various prostaglandins NSAIDS

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Acetominophen(Tylenol)- is the preferred ‘over-the-counter’ medication for orthodontic patients because it acts on the CNS and does not interfere with localized inflammatory processes.

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NSAIDS are effective orthodontic analgesics, but they may reduce the rate of tooth movement, and they should not be administered for long periods of time to orthodontic patients.

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Several other drugs can affect prostaglandin level and therefore could affect the response to orthodontic tooth movement

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Eg-Amytryptiline,Quinine,Procaine Misoprostol, a prostaglandin E1 analogue, has been used to enhance orthodontic tooth movement in rats (AJODO-2002).

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At a dose of 10μg/day for 14 days, oral misoprostol increased the amount of orthodontic tooth movement in all the experimental groups compared with the appliance control group.

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These results indicate that oral Misoprostol can be used to enhance the rate of tooth movement with less risk of increased root resorption than PGE2. Osteoporosis

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A problem faced by many post menopausal Females & also aging individuals of both sexes

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Medication

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Estrogen ( older women ) Bisphosphonates

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They are synthetic analogues of pyrophosphate that bind to hydroxyapatite in bone.

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Act as specific inhibitors of osteoclast-mediated bone resorption.

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Eg. Alendronate

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Physicians of older women on these drugs and who require orthodontic treatment should be consulted regarding the possibility of switching over to estrogen, at least temporarily. OTHER DRUGS AFFECTING TOOTH MOVEMENT

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Tricyclic antidepressants ( doxepin, amitriptyline, imipramine)

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Anti-arrhythmic agents ( procaine )

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Anti malarial drugs ( quinine, quinidine, chloroquine)

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Methyl Xanthines

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Anticonvulsant drug phenytoin

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Some tetracyclines ( doxycycline ) inhibit osteoclast recruitment. EFFECTS OF SYSTEMIC DISEASE ON TOOTH MOVEMENT 1-Cardiovascular diseases

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Infective endocarditis 2-Bleeding Disorders

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Haemophilia

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Neutropenia

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Polycythemia vera

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Anaemia

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Thallasemia 3-Haematological malignancies(Leukemia) 4-Respiratory disorders

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Asthma

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OSA

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Cystic fibrosis

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Allergy and nasal obstruction 5-Disorders of skeletal system

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Arthritis

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Bone tumors 6-Endocrinal disorders

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Diabetes Mellitus

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Hypothyroidism

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Parathyroid gland disorder

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Growth hormone disorder

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Estrogen 7-Nervous system

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Epilepsy

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Psychiatric disorder

It is of prime importance to include a detailed medical history of the patient during the diagnosis phase of the orthodontic treatment. A sound knowledge of the effect of different regularly used drugs and systemic diseases will aid the clinician to take the required precautions and in turn make the orthodontic treatment as efficient as possible SURGICAL ENHANCEMENT In 19th century Hullihan , the pioneer American oral surgeon experimented with moving teeth after making cuts in alveolar bone In mid century German surgeon Kole revived the idea that cuts between teeth could produce faster tooth movement Surgical Techniques More recently, rapid tooth movement after corticotomy has come to be viewed as a demineralization/remineralization phenomenon that produces a regional acceleration of

bone remodeling that allows faster tooth movement rather than movements of blocks that contains teeth as done previously The surgical approach has been broadened into Accelerated Osteogenic Orthodontics(AOO) by adding areas of decortications over facial surfaces of alveolar bone that are then covered with particulate bone grafting material. This adds modeling to remodeling after local injury. PROPOSED APPROACHES FOR FASTER TOOTH MOVEMENT •

Vibration of the teeth

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Application of light to alveolar process

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Application of therapeutic ultrasound to teeth and adjacent structures

1-AcceleDent vibratory system(OrthoAccelTechnologies,Inc,Houston,TX)

induce piezoelectric currents, based oh high frequency vibration (30Hz) to teeth for approx 20 mins. and stimulates quick remodeling 2- Phototherapy (Biolux) It uses light with an 800-850 nm wavelength that penetrates soft tissue and “infuses light energy directly into the basal bone’’. IATROGENIC RESPONSE OF SUPPORTING TISSUES IN ORTHODONTICS Various Clinical, Radiological and Histological investigations have been conducted from time to time to assess the damage to root substance and supporting tissues. Damage to Periodontal Tissues 1-Gingival Inflammation: The initial and most important factor causing gingival inflammation is bacterial plaque at the gingival margin. Patients with fixed appliances have increased retention sites for microbial samples and therefore significantly higher total numbers of Strep. mutans and Lactobacilli.  A greater plaque index; tendency for bleeding; increased pocket depth and greater interproximal loss of attachment have been observed more frequently for molars with orthodontic bands 2-Root resorption

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Orthodontic force application - evoke excessive resorption of root cementum, proceeding into the dentin, eventually shortening the root length—a process called root resorption.

 Ottolengui (1914) and Ketcham (1927) - first to report severe root resorption associated with orthodontic tooth movement.  It is an undesirable and the least predictable sequelae of orthodontic treatment.  Jarabak and Fizzell - analyzing the effect of force systems during mechanotherapy concluded that the magnitude of an orthodontic force and rigid fixation of the archwire to the brackets could be considered the most important factors predisposing a tooth to the root resorption  Brezniak and Wasserstein classified root resorption according to its severity. Cemental /surface resorption : where only the outer layers are resorbed, to be fully regenerated or remodeled later . Dentinal resorption : with repair, where the cementum and the outer layers of dentin are resorbed, and are repaired along with morphological alterations . Circumferential root resorption : where full resorption of the hard tissue components of the root apex occurs, resulting in root shortening. 3-Pulpal reactions  Conflicting results for correlation of pulpal changes incident to orthodontic force.  Some reports suggested permanent damage to pulpal tissue from orthodontic force, but others claimed no significant long-lasting effects on the dental pulp.  Labart et al demonstrated increased pulpal respiration rate in rat incisor pulp (1-2 times more than controls),orthodontic stress for 72 hours  Mostafa et al : congested and dilated blood vessels, and edema of pulpal tissue in their histologic observations.  The progression of the inflammatory process in human pulp fibroblasts stimulation by neuropeptides and production of inflammatory cytokines, such as IL1, IL-3, IL-6, and TNF. 4-Alveolar Bone Loss:  Compressed gingiva in extraction sites (between teeth that have moved together) can produce a long-lasting epithelial fold, or invagination.

 Surrounding connective tissue- loss of collagen, mechanical forces employed can cause sub lethal damage and stimulates hyperplasia  may aggravate a pre-existing plaque induced gingival lesion and cause loss of alveolar bone and periodontal attachment. Experimental studies in the Beagle dogs also have shown that it is possible for orthodontic tipping forces to shift a supragingivally located plaque into a sub gingival position, resulting in the formation of infrabony pockets. (JCP 1977) 5-Marginal Bone Recession: It is the displacement of the soft tissue margin, apical to the CEJ, with subsequent exposure of the root surface. This is associated with localized plaque induced inflammatory lesions and sometimes in combination with orthodontic therapy. Alterations occurring the gingival dimensions and marginal tissue position in conjunction with orthodontic therapy are related to the direction of tooth movement. Labial and Buccal movements results in reduced facial gingival dimensions, whereas an increase is observed after lingual movement.  With respect to orthodontic treatment, this implies that as long as tooth is moved exclusively within the envelope of the alveolar process, the risk of harmful side effects in the marginal tissue is minimal, irrespective of the dimensions and quality of the soft tissue (JCP 1981,87).] POSTTREATMENT STABILITY Not all orthodontically achieved changes remain stable, although the question of relapse is related to the objective of treatment.  Retention is designed to maintain the occlusion during remodelling of the periodontal tissues and further aging of the occlusion, i.e. the transitional changes in growth, dentoalveolar development and muscular adaptation. Retention is thus a continuation of orthodontic treatment. If orthodontic tooth movement has not been followed by re-modelling of the supporting tissues, the tooth tends to return to its former position. Correct positioning of the entire tooth and good intercuspation are the main contributors to eventual stability. CONCLUSION

Rapid advances in all biological fields have enabled us to better understand the mechanisms involved in orthodontic tooth movement.  This growing body of knowledge illuminate useful paths in clinical orthodontics and assist us in identifying and discarding harmful methods of mechanotherapy and also will move orthodontics closer to the goal of being optimal, where teeth are moved efficiently, without causing discomfort to the patient or damage to the teeth and their supporting tissues.  Future orthodontics will increasingly become biologically correct and, consequently, patient-friendly REFERENCES  Reitan K. Tissue behavior during orthodontic tooth movement.Am J Orthod 1960;46: 881-90.  Reitan K. Some factors determining the evaluation of force is orthodontics. Am J Orthod 1957; 43:32-45.  Schwarz AM. Tissue changes incident to orthodontic tooth movement. Int J Orthod 1932;18: 331-52.  Proffit WR. Biologic basis of orthodontic therapy. In: Proffit WR, Fields HW, editors. Contemporary orthodontics. 4TH ed. St Louis: Mosby; 2009  Baumrind S. A reconsideration of the property of the pressure tension hypothesis. Am J Orthod 1969;55:12-22.  The Periodontal Ligament: a unique, multifunctional connective tissue, Periodontolgy 2000, Vol 13, 1997, 20-40  Contemporary Orthodontics, William R. Profitt, 3rd edition  Oral Anatomy, Histology & Embryology, B.K.B. Berkovitz, 3rd edition  Oral Histology, Ten Cate, 6th edition  Inflammation, Henry Towbridge, 5th edition    Farrar JN. Irregularities of the teeth and their correction. Vol 1.New York: DeVinne Press; 1888. p. 658.

 Grimm FM. Bone bending, a feature of orthodontic tooth movement. Am J Orthod 1972;62:384-93.  Krishnan V, Davidovitch Z. Cellular, molecular, and tissue-level reactions to orthodontic force. Am J Orthod Dentofacial Orthop 2006;129:469.e1-32.    

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