Physiology of tooth movement 1 /certified fixed orthodontic courses by Indian dental academy


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Physiology of tooth movement 1 /certified fixed orthodontic courses by Indian dental academy

  1. 1. Physiology of tooth movement -I INDIAN DENTAL ACADEMY Leader in continuing dental education
  2. 2. Contents - Overview of tooth supporting structures. - Response to normal functions - Biologic response to orthodontic forces - of the bone and periodontium - Clinical response, histologic response, cellular and molecular mechanisms. - Theories of tooth movement.
  3. 3. - Bone physiology bone structure, modelling and remodelling, osteoblast histogenesis and bone formation, osteoclast recruitment and bone resorption. - Wolff s law , bone metabolism - Effects of force magnitude, direction, duration decay. - Drug effects.
  4. 4. - Anchorage aspects - Deleterious effects of force on tooth movement. - Skeletal effects of force - Future applications - Conclusion
  5. 5. Tooth supporting structures Tooth movement involves changes in the periodontium depending upon the force applied. The following is a brief description of the characteristics of the normal periodontium. GINGIVA –The gingiva is differentiated into the free and attached gingiva. The connective tissue of the gingiva consisits of 60 pc of collagen fibres, 5pc of fibroblasts and 35 pc of vessels, nerves and matrix. The gingival collagen fibres exhibit cross banding with a periodicity of 700 nm.
  6. 6. - The gingival fibres which comprise the dentogingival unit are CIRCULAR FIBRES. DENTOGINGIVAL FIBRES. DENTOPERIOSTEAL FIBRES. TRANSSEPTAL FIBRES.
  7. 7. PERIODONTAL LIGAMENT – The pdl is approx 0.25mm in width, soft richly vascular and celluar connective tissue that surrounds the roots of the teeth. The major component is a network of parallel collagenous fibres inserting into the cementum of the root surface and lamina dura. The other components are cellular elements and the tissue fluids. Blood vessels and nerve endings (proprioception) are also found. The true periodontal fibres ,the PRINCIPAL FIBRES are grouped as follows.
  9. 9. CEMENTUM –it is a specialised mineralized tissue covering the root surfaces and has many features common with the bone. It contains no blood vessels ,no innervation ,does not undergo physiologic resorption but continuous deposition occurs throughout life. Primary cementum – no cells, formed during erruption. Secondary cementum - cells present, formed in response to functional demands.
  10. 10. Response to normal functions - Tissue reactions in the tooth supporting structures take place with the erruption of teeth and development of occlusion. Contrary to the relatively short erruption period the teeth and the supporting tissues have a life long ability to adapt to functional demands and drift through alveolar bone called physiologic migration. -When the teeth migrate they bring the supraalveolar fibre system with them, implying remodelling of the alveolar bone and PDL.
  11. 11. -The cells are more active on the bone side than near the root cementum. Hence major remodelling takes place near the alveolar bone. Unlike the osteoclastic resorption of bone to provide the space for tooth movements, the corresponding remodelling of the fibrous attachment is not clearly understood .But the presence of a mesh work of collagen fibres of small diameter is sufficient to explain the rapid reorganization process.
  12. 12. -A slow apposition occurs on the cementum surface throughout life, a fact that is of great importance for the resorptive mechanism in the bone and cementum. The unmineralized precementum layer has special importance as a resorption resistant coating layer thus protecting the root surface during physiologic migration. -Along with the mesio distal migration teeth also exhibit continued erruption even after full emergence , accompanying growth in alveolar height .
  13. 13. -The interest in continued erruption of teeth has taken a new turn in recent years with the introduction of implants inserted directly into the alveolar process. -The need is ever increasing for more information about the use of dental implants in young individuals, whether they should be used at all ,and if so, how and when. -Moreover tooth wear is a common occurrence and may counteract the continuous tooth erruption.
  14. 14.
  15. 15. Physiologic response to heavy pressure - During mastication teeth and PDL are subjected to intermittent heavy forces. Tooth contacts last for 1 sec or less and forces range from 2 kg to 50 kgs. In this situation quick displacement of the tooth within the PDL space is prevented by the tissue fluids and the force is transmitted to the alveolar bone which bends in response. < 1 sec –PDL fluid incompresible ,bone bends. 1-2 sec –PDL fluid expressed, tooth moves in PDL space
  16. 16. - 3 -5 sec –PDL fluid squeezes out, tissues compressed immediate pain if pressure is heavy. - Role of PDL in erruption and active stabilization of teeth. - The phenomenon of erruption makes it plain that forces generated within the PDL itself can produce tooth movement (metabolic changes in PDL). This also produces active stabilization of teeth against prolonged forces of light magnitude.
  17. 17. The current concept is that active stabilization can overcome prolonged forces of a few gms (5 -10)observed as the magnitude of unbalanced soft tissue resting pressures.
  18. 18. Response to orthodontic forces Basically no great difference exists between the tissue reactions observed in physiologic migration and those seen in orthodontic tooth movement. The changes are just more marked and extensive. Application of a continuous force on the crown of a tooth leads to its movement within the alveolus. The duration of tooth movement can be divided into an initial period and a secondary period.
  19. 19.
  20. 20. INITIAL PERIOD -In this crucial stage compression in limited areas of the pdl impedes vascular circulation and cellular differentiation causing degradation of cells and vascular structures .Degradation starts where the pressure is highest, near the bony spicules. Retardation of blood flow is followed by disintegration of vessel walls, degradation of blood elements. The tissue assumes a glass like appeareance termed HYALINIZATION.
  21. 21. Hyalinization is caused partly by anatomic and partly by mechanical factors and is almost unavoidable in the initial period of tooth movement in clinical orthodontics. It represents a sterile necrotic area generally limited to 1 or 2 mm in diameter. This process displays three stages. DEGRADATION. ELIMINATION OF DESTROYED TISSUE. REESTABLISHMENT OF A NEW TOOTH ATTACHMENT .
  22. 22.
  23. 23. - In hyalinized zones the cells cannot differentiate into osteoclasts and no bone resorption can take place. Tooth movement stops until the necrotic areas have been removed. A limited hyalinized zone is expected to persist for two weeks with the use of light forces. - Now the invasion of macrophages from the adjacent undamaged PDL helps in the elimination of the necrotic zone. Recent evidence shows invasion of multinucleated giant cells belonging to the mononuclear phagocytic system.
  24. 24.
  25. 25. - Reestablishment of the tooth attachment in the - hyalinized area starts by the synthesis of new tissue elements as soon as the degenerated tissues have been removed. The ligament space is now wider than before and rich in cells. SECONDARY PERIOD – The PDL is considerably widened and the osteoclasts attack the bone surface over a much wider area now. As long as the force is kept gentle further bone resorption is predominantly direct.
  26. 26. -A large number of osteoclasts are seen along the bone surface and the tooth movement is rapid. Extensive breakdown of the fibres takes place on the pressure side followed by complete reorganization of the fibrous system. -The main feature is the bone deposition on the tension side. Osteoblast proliferation is usually seen after 30 to 40 hours shortly after which osteoid tissue is deposited . (depends on the fibre bundles )
  27. 27. - Concomitantly with the resorption and apposition on the pdl surfaces an accompanying apposition and resorption on the spongiosa surface of the alveolar bone takes place .This tends to maintain the dimensions of the supporting bone. - Thus the orthodontic tooth movement involves many inflammation like reactions ( a process occuring in a local area when a rapid response is needed for a stress that is felt by the cells to be heavy). No unwanted sequale occurs as long as this sterile necrosis is of short duration and not complicated by local infection.
  28. 28. - Finite element in the past was used to describe stressed situations within the pdl and alveolar bone. The present study sought to determine the impact of the modelling process on the outcome of FE analyses and rate it to the current theories on tooth movement. Results demonstrate that loading of the pdl cannot be explained in simple terms of compression and tension along the loading direction. Tension in the alveolar bone was far more predominant than compression. Cattaneo, Melsen B. J Dent Res 2005
  29. 29. Theories of tooth movement The two possible control elements, biologic electricity and pressure-tension in the PDL that affects blood flow are contrasted in the two major theories of orthodontic tooth movement. Pressure tension theory –This classical theory of tooth movement relies on chemical rather than electrical signals as the stimulus for cellular differentiation and tooth movement. Chemical messengers are important in the cascade of events leading to tooth movement.
  30. 30. Sustained pressure Areas of compression, tension Blood flow alterations Changes in oxygen tension, changes in other metabolites Release of biologically active agents Stimulation of cellular differentiation activity
  31. 31. The Bioelectric Theory This theory relates tooth movement to changes in bone metabolism controlled by the electric signals that are produced when alveolar bone flexes and bends. Electric signals that might initiate tooth movement initially were thought to be piezoelectric. Piezoelectricity is a phenomenon observed in many crystalline materials. Deformation of crystal structure causes a flow of electric current due to electron displacement.
  32. 32. - These signals have two unusual characteristics. -a quick decay rate -the production of equivalent signal opposite in direction when the force is released. - The ions in the extracellular fluids interact with the electric fields generated due to bone bending and give rise to small voltages called STREAMING POTENTIALS. - Reverse piezoelectric effect can also be seen.
  33. 33. - Stress generated signals are important for the maintenance of the skeleton. Signals generated by the bending of alveolar bone during normal chewing are surely important for the maintenance of bone around teeth. - On the other hand sustained forces in orthodontics do not produce prominent stress generated signals.
  34. 34. BIOELECTRIC POTENTIALS.-These are a type of endogenous electric signals observed in bone not being stressed. Metabolically active bone cells – electronegative charges. Inactive areas – electrically neutral. - Although their purpose is unknown, cellular activity can be modified by adding exogenous electric signals.
  35. 35. - Their combined affect is noted at the cell membrane level affecting the membrane receptors and membrane potential along with cellular responses. - Electromagnetic fields can also cause the above affects. - Perhaps a fair conclusion is that even though the stress generated electric signals do not explain tooth movement ,electric and electromagnetic influences can modify the bone remodelling on which tooth movement depends.
  36. 36.
  37. 37. - Studies by Karanth, Shetty (2001) have shown that application of an electric current may alter the electrolytic environment allowing changes in the type and rate of ions that move across the cell membrane. - Changes of the flux of K, Na, Ca, Mg, Cl can mediate cellular changes. - Micropulsed electrical stimulation- can reach osteoblasts – increase cAMP, cGMP – can cause efficient remodelling- enhanced tooth movement.
  38. 38. - Tengku, Joseph (2000) incorporated a ststic magnetic field into an orthodontic appliance and noted that the tooth movement was not significantly enhanced than the controls but in contrast the root resorption was significantly increased. - Davidovitch et al (1980) studied the effects of DC electric currents on the pdl tissues. It was concluded that electric stimulation enhances cellular enzymatic phosphorylation activities in pdl tissues and may be a potent tool in accelerating bone turnover.
  39. 39. - The effect of electric-orthodontic treatment on the pdl cyclic nucleotides was studied. It was seen that teeth treated by both force and electric currents moved faster as compared to teeth treated by force alone. Anode – bone resorption ( compression side) Cathode –bone deposition ( tension side) - Hence it was concluded that orthodontic treatment can be accelerated by the use of locally applied electric currents.
  40. 40. CLINICAL RESPONSES TO ORTHODONTIC FORCES - From a clinical perspective orthodontic tooth movement has three distinct phases. DISPLACEMENT PHASE. DELAY PHASE. ACCELERATION AND LINEAR PHASE. DISPLACEMENT PHASE. –the initial reaction of the tooth to force is almost instantaneous within a fraction of a second. It reflects the immediate movement of the tooth within the viscoelastic PDL.
  41. 41.
  42. 42. - There is no extensive amounts of tissue or bone remodelling. The fluid compartments of the pdl help in the transmission and dampening of forces acting on the teeth. The magnitude of the displacement response is dependent on the root length , alveolar bone height and age. DELAY PHASE.- This phase of the tooth movement cycle is characterised by absence of clinical movement and is referred to as the delay or latency phase.
  43. 43. - Although there is no tooth movement extensive remodelling occurs in all the tooth investing tissues. The absolute amount of force applied is not as relevant as the relative force applied per unit area. - There can be partial or absolute occlusion of blood vessels. In absolute occlusion tooth movement is slower and starts approximately after 1 – 2 weeks. - Aging has been shown to effect the proliferative activity of the cells of the pdl and tooth movement subsequently during the delay phase.
  44. 44. - It has been seen that in young subjects there is faster initial tooth movement. But once the linear phase is reached the tooth movement rate becomes equal in both the groups. This indicates that the clinically observed increase in treatment time for adults can be primarily attributed to the delay phase prior to the onset of tooth movement, but the rate of migration is equally efficient once tooth movement has started. - Ren Y, Maltha. J Dent Res 2003.
  45. 45. ACCELERATION AND LINEAR PHASE.- The third phase is characterized by rapid tooth displacement Tooth movement is initiated in deference to the adaptation of the supporting pdl and alveolar bone changes. Studies have shown that following orthodontic appliance reactivation, along with the presence of activation osteoclasts a second cohort of osteoclasts can be recruited immediately. This causes immediate significant tooth movement with no greater risk of root resorption. King, Archer AJO 1998
  46. 46. - The force magnitude directly affects the rate of tooth movement. High forces used in excess of 100 gms (canine retraction) have shown to produce a lag phase of about 21 days before tooth movement. Lower forces can induce tooth translation without a lag phase at rates that are still clinically significant. Iwasaki, Nickel, Morton AJO 2000.
  47. 47. - Equally as important as magnitude, however is the timing of the force application .The force regimen has more influence on the rate of movement than the force magnitude. Light forces are more conducive to tooth movement because the cell biology system remains in a constantly responsive state .Conversely the application of intermittent forces creates a fluctuating environment of cellular activity followed by quiescence.
  48. 48.
  49. 49. CELLULAR MECHANISMS - When a force is applied the tooth moves in the direction of the force. Resorption of alveolar bone takes place and a little distance behind the alveolar wall a new bony lamella is laid. - There is transmission of mechanical influence into cellular response. - How do different cells know that they should react and in a special way? Several mechanisms have been proposed for these cellular reactions.
  50. 50. - The perturbation of pdl cells as a result of forces may change the influx of calcium and sodium ions into the cells which in turn alters the production of second messengers –cAMP and cGMP .Low levels of these may influence the differentiation of cells for bone production. - Also mechanical stress may induce localized cells to produce prostaglandins which stimulate osteoclastic bone resorption.
  51. 51. - Another mechanism can be piezoelectricity. When a long bone is bent the concave surfaces become negatively charged which is believed to stimulate bone formation. - Orthodontic forces also puts into motion both the nervous and immune systems. Increase in secondary messengers is not just solely from the direct effects of stresses but also due to endogenous signalling agents.
  52. 52. - Neurotransmitters – substance P, vasoactive intestinal polypeptide VIP, calcitonin gene related peptide CGRP and others act as from sensory nerve fibres in the pdl and supply a link between the physical stimulus and the biochemical response. - Orthodontic forces cause a marked increase in the staining intensity of interlukin 1-alpha and interlukin 1-beta particularly in osteoblasts and osteoclasts. Saito M et al AJO 1991
  53. 53. - Changes in cell shape may also play a role. There is some evidence that prostaglandins are released when cells are mechanically deformed. Prostaglandin release may be a primary rather than a secondary response to pressure .It is likely that mobilization of membrane phospholipids , which leads to formation of inositol phosphates is another pathway towards the eventual cellular response. Changes in cell shape produce effects mediated by membrane integral proteins (integrins). Sandy, Farndale AJO 1993
  54. 54. - Kaku M, Kohno (2001) have studied the effects of vascular endothelial growth factor and concluded that local administration of rhVEGF enhances the number of osteoclasts and may increase the rate of tooth movement. - AlhashimiN, Brudvik (2004) have concluded that the CD4O- CD40L interaction appears to be an active process and that force induces T-cell activation .Such activation may be involved in the induction of inflammatory mediators and bone remodelling.
  55. 55. MOLECULAR MECHANISMS - Skeletal integrity is the result of dynamic interactions between osteoblasts and osteoclasts. The rate of remodelling is dependent however on the cells of the osteoblast lineage which in addition to bone formation are also responsible for the activation and recruitment of osteoclast precursors. - However the basis of communication between these cells was unclear untill the intermediary factor was identified. It has been named as the receptor activator of nuclear factor kB ligand. RANKL
  56. 56. - Binding of RANKL to its cognate receptor, the RANK expressed on the surface of osteoclast progenitor cells leads to induction and activation of osteoclasts.( bone resorption ) - RANKL however can bind to osteoprotegerin OPG, and can inhibit activation of osteoclasts and reduce bone resorption. - This ratio of RANKL /OPG expression by osteoblasts is believed to be a key determinant of the rate of recruitment and activation of immature osteoclasts.
  57. 57. - From an orthodontic perspective , it is very likely that pressure changes in the microenvironment of the tooth socket may cause up and down regulation of the RANKL and OPG genes as a means of modullating protein production and ultimately bone remodelling. - Local mechanisms – inflammatory cytokines like interlukins , TNFs, growth factors that have biologic activities influencing individual phases of the cycle. - Endocrine mechanisms include the calciotropic hormones and the sex steroids
  58. 58. - These factors act on osteoblasts to regulate osteoblast osteoclast equilibrium and can either up- or downregulate a cascade of downstream signalling pathways that ultimately affect the expression of specific genes necessary to synthesize specific proteins involved in bone remodelling.
  59. 59.
  60. 60. - Studies by Kanzaki ,Chiba (2004) have shown that when local OPG gene transfer was done, OPG production was enhanced and osteoclastogenesis was inhibited. Local OPG gene transfer significantly diminished tooth movement. - Recent studies by Kanzaki, Chiba (2006) have shown that local RANKL gene transfer significantly enhanced osteoclastogenesis and hence lead to increased tooth movement.
  61. 61. - Tooth movement was enhanced and no systemic effects were seen. Local RANKL gene transfer might be a useful tool not only for shortening treatment time but also for moving ankylosed teeth where teeth fuse to the surrounding bone. - Wise GE, Yao S, Liu. Clin Anat 2006 have proposed that local injections of OPG may help in delaying tooth erruption.
  62. 62. References - Kanzaki H, Chiba M, Takahashi – Local RANKL gene transfer to the pdl tissues accelerates orthodontic tooth movement. Gene Thera 2006 jan5 (epub ahead of print) - Wise GE, Yao S, Liu: Injections of OPG and PMA delay tooth erruption. ClinAnat 2006;jan19-1:19-24 - CattaneoPM, Dalstra M, Melsen B: The finite element model – a tool to study orthodontic tooth movement. J Dent Res 2005 may 84:428-433
  63. 63. - Kanzaki H,Chiba M, Takahashi: Local OPG gene transfer to the pdl tissues inhibits orthodontic tooth movement.J Dent Res2004 dec 83:12:920-5 - Von Bohl M, Maltha JC .Focal hyalinization during experimental tooth movement in beagle dogs. AJO may 2004 125(5):615-23. - Alhaimi N, Fritiof, Brudvik .CD40- CD40L expression during orthodontic tooth movement in rats. AO 2004 feb 74(1) 100-5.
  64. 64. - Ren Y, Malhata JC. Age effect on orthodontic tooth movement in rats. J Dent Res 2003;82:38-42. - Karanth H S, Shetty KS. Orthodontic tooth movement and bioelectricity. Ind J Dent Res 2001 oct –dec 12,4-212-21. - Kaku M, Kohno S, Kawata. Effect of vascular endothelial growth factor on osteoclast induction during orthodontic tooth movement in mice. J Dent Res 2001 oct 80,10 1880-3.
  65. 65. - Iwasaki LR, Haack JE, Morton. Human tooth movement in response to continuous stress of low magnitude. AJO 2000;117:175-183. - Davidovitch Z et al: Electric currents, bone remodelling and orthodontic tooth movement. I and II AJO1980;jan 77:14-32 - King GJ, Archer , Zhou. Late orthodontic appliance reactivation stimulates immediate appearance of osteoclasts and linear tooth movemnt. AJO 1998;114:692-677.
  66. 66. - Nakagawa N, Kinosaki, Yamaguchi .RANK is the essential signaling receptor for osteoclast differentiation factor in osteoclastogenesis. Biochem Biophy Res Commun 1998:253;395-400. - Zengo, Pawluk, Bassett: Stress induced bioelectric potentials in the dentoalveolar complex. AJO 1973:64:17. - Roberts W, Chase ;Kinetics of cell proliferation and migration assosciated with orthodontically induced osteogenesis. J Dent Res 1981:60:174
  67. 67. - Thilander et al; Osseointegrated implants in adolescents. An alternative in replacing missing teeth? EJO 1994: 16:84. - Sandy JR, FarndaleRW, Meikle: Recent advances in understanding mechanically induced bone remodelling. AJO 1993:103;212-222 - Saito M et al: Interlukin 1 beta and PGE are involved in the response of pdl cells to mechanical stress in vivo and in vitro. AJO 1991 ,99:226
  68. 68. - Tengku BS, Joseph –Effect of a static magnetic field on orthodontic tooth movement in rats. EJO 2000 oct22 ,5 ;475-87. - Orthodontics – current principles and techniques. third edition. Graber , Vanarsdall. - Contemporary orthodontics. third edition, Proffit. - Biomechanics and esthetic strategies in clinical orthodontics. Ravindra Nanda. first edition.
  69. 69. Thank you For more details please visit