Cell biological process during real tooth movement.pptx

cell biological process during orthodontic tooth movement

1. Cell biological process during orthodontic tooth movement Guided by: Dr Rajan K Mahindra Dr Rakesh Mohode Dr Govind Suryavanshi Presented by- Sneha Shah

2. Contents Process of hyalinization. How osteoclast recruited at site of resorption. Process of alveolar bone resorption. Changes occurring on the trailing side.

3. Cell biological process during initial phase and hyalinisation Tooth moves at a rate of 10µm/s in first few seconds Subsequent 20 seconds -1µm/s Thereafter at 0.1µm/s Stabilizes within 5hrs

4. Process of hyalinization

5. Orthodontic Force Blood vessel in pdl are occluded, causing hypoxic condition Cell death through loss of cell membrane integrity. Uncontrolled release of cell organelle and debris into ECM Necrotizing tissue initiate an inflammatory response through IL-1 β & PGE2 IL-1 β & PGE2 attract leucocytes & nearby phagocytes Cell eliminate dead cell and debris ECM changes by protein denaturation that means Secondary & tertiary structures of collagen type I are lost but their primary structures remain Protein can no longer perform their function and a gelatinous substance is formed This process is called Hyalinization & is mediated by enzymes from Matrix Metalloproteinase Family (MMP-1, MMP-8,MMP-13)

6. At the leading side Continuous mechanical stress Removal of necrotic tissue is accompanied by an influx of differentiating fibroblasts which secrete new ECM Periodontal tissue subjected to mechanical stress express Periostin , an ECM protein New ECM contain type III collagen instead of type I collagen VEGFs are synthesized and secreted by variety of cells such as mast cells, macrophages and fibroblasts Circulating VEGFs bind to VEGF receptors on endothelial cell trigger the pathway leading to angiogenesis restoring vasculature of PDL After the hyalinized tissue is completely removed, tooth is again surrounded by a vital PDL

7. Cell biological process during tooth movement

8. Orthodontic force Induces negative strain at leading side and positive strain at trailing side Results in strain of periodontal fibroblast Integrins by which fibroblast are attached to the ECM can act as a force transducer Fluid flow in PDL & canalicular network in the alveolar bone is induced Fluid flow induces strain in the cell membrane of fibroblasts, osteoblast, & osteocyte Osteoblast and periodontal fibroblast contribute to activation of cells by integrin mediated strain transmission to the cytoskeleton & subsequent induction of expression of a variety factors & cytokines These factors such as FGF, IGF-1, IL-1 α, IL- β ,IL-6& TNF α Mediate the differentiation of precursors into osteoblast and osteoclast ,

9. How are osteoclast recruited at the site of resorption ?

10. Myeloid precursor Differentiate into Monocyte Osteoclast precursor Further differentiation of osteoclast dependent on the RANKL secreted by fibroblast & osteoblast Osteoclast precursor express RANK RANKL binds to RANK to form mononuclear osteoclasts, characterized by the expression of Tartarate Resistant Acid Phosphatase(TRAP) Mononuclear osteoclast fuses to become multinuclear osteoclasts Binding of OPGs to RANKL inhibits the binding of RANKL to RANK on the osteoclast precursor .Thus hampers the differentiation and functioning of osteoclasts Strain affects both the secretion of RANKL & OPG MCS-F

11. Resorption of alveolar bone For functioning of osteoclast they should be attached to mineralised bone matrix through α V β 3 integrin This is only possible when the osteoblasts, osteoid& non-mineralized bone matrix covering the surface of alveolar bone are removed. ECM of the osteoid is degraded through the action of MMP’s (MMP1, 8 , 13 &14) Osteoblast disappear by apoptosis induced by binding of TNF-α to its receptor TNFR1&TNFR2 Combined osteoblast apoptosis &ECM degradation leads to exposure of mineralized bone matrix which serves as landing site for osteoclasts

12. Osteoclasts moves by chemotaxis & attach the bone by α V β3 integrin , connecting osteoclast to RGD peptides in bone matrix Upon adhesion to bone osteoclast polarize & reorganize their cytoskeleton to generate a ring like F-actin rich structures sealing zone that isolates howship’s lacunae from the surroundings Inside the sealing zone ruffled border is formed Isolated area becomes acidic through influx of H+ ATPase mediated proton pump this favours dissolution of bone minerals In addition, the lysosomal enzyme, CathepsinK , &MMP -9 are secreted into howship’s lacunae

13. Trailing side PDL is widened Accompanied by positive strain in the ECM Acute inflammatory reaction Results in increase in IL-1 β , IL-10, PGE2 &TGF- β Subsequent increase in OPG and decrease in RANKL by osteoblast and fibroblast

14. No. of fibroblast increase the secretion of collagen type I and type III New sharpey’s fibre are formed Osteoblast deposit bone Expression of MMP is downregulated & TIMP is upregulated thus ECM breakdown is inhibited Finally FGF-2 & VEGF growth factor involved in the development of vascular elements are upregulated

15. Diagnosis and Management of Malocclusion And Dentofacial Deformities, O.P. Kharbanda, Third Edition.Contemporary Orthodontics, William R. Proffit . Sixth Edition Biological Mechanisms of Tooth Movement- JaapC . Maltha , Vinod Krrishnan , Anne Marie Kuijpers-Jagtman .

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