Ca

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Ca

  1. 1. BONE PHYSIOLOGY,METABOLISM AND BIOMECHANICS: ( part 1): PRESENTED BY : KIRTI AGRAWAL J.R.1 DATE: 24-10-2013
  2. 2. INDEX:  Historical perspective  Ca metabolism  Ca Homeostasis  Ca conservation  Bone modeling and remodeling  Biomechanics( mechanostat theory)  specific assessment methodology  A genetic aspect( role of RANK , RANKL and OPG protien)  Types of bones
  3. 3. HISTORICAL PERSPECTIVE: IN 1947, the first modern text of bone anatomy was given by WIEMANN and SICHER REMODELING OF MINERALIZED TISSUE ,PART 1 : THE FROST LEGACY……….seminar in orthodontics IN 1960, MODERN PHYSIOLOGIC CONCEPT OF BONE WAS GIVEN BY HAROLD FROST
  4. 4. INTRODUCTION:  99%= bone+ teeth  1% = outside of skeletal  Dietary requirements: Adult: 800 m.g/ day Women during pregnancy: 1.5 g/ day Children: .8 - 1.2 g/ day Infant: 300- 500 mg/ day
  5. 5.  Sources: milk, bean , leafy vegetables,fish, cabbage, egg yolk  Absorption: duodenum
  6. 6. FACTORS PROMOTING Ca ABSORPTION:  VITAMIN D ( Ca binding protien)  Parathyroid hormone  Low( acidic)pH.  Lactose  Amino acid lysine and arginine
  7. 7. FACTORS INHIBITING THE Ca ABSORPTION:  Dietary phosphate( ideal Ca / po4 = 2: 1 )  Free fatty acid( insoluble Ca soap)  High Ph  High content of dietary fibers
  8. 8. BIOCHEMICAL FUNCTION:  MUSCLE CONTRACTION( activate ATPase , increases the interaction between actin and myosin).  BLOOD COAGULATION( factor IV)  NERVE TRANSMISSION  MEMBRANE PERMIABILITY  ACTIVATION OF ENZYME( lypase, ATPase, )  Ca as the intracellular messenger  Facilitate the release of IN SULIN , PTH, CALCITONIN)
  9. 9. Muscle contration:
  10. 10. Blood cougulation:
  11. 11. Neuro transmission:
  12. 12. PLASMA CALCIUM LEVEL:  9- 11 mg/dl
  13. 13. CALCIUM HOMEOSTASIS:  It is the process by which mineral equilibrium is maintained Instantaneous regulation Short term control Long term regulation
  14. 14. Instantaneous(rapid)regulation:  Selective transfer of Ca ions into and out of bony fluid in few seconds.  Process: Decrease in serum Ca level Stimulation of PTH hormone PTH enhances the transport of calcium ions from bony fluid into osteocytes and bone lining cells
  15. 15.  Active metabolite of vit D ( 1,25 DHCC) enhances the pumping of Ca ions from bone lining cell into extracellular fluid .  ( within the physiological limit , this mechanism supports the Ca homeostasis without resorbing bone)
  16. 16. SHORT –TERM CONTROL:  IT takes few minutes through 3 hormones: PTH, 1,25 DHCC, and calcitonin.  Calcitonin controls the hypercalcimia by suppressing the bone resorption.  PTH and DHCC : 1) Enhances the osteoclast recruitment from promonocyte precursors. 2) Increases the resorption rate of existing osteoclast. 3) It suppress the rate at which osteoblast form bone.
  17. 17. LONG TERM REGULATION:  Biomechanical factors( exercise, posture,      habits) Noncalcific hormones( sex steroid, growth hormones) Metabolic mechanism Geometric distribution Dictate mass. Mean age of bone
  18. 18. Ca CONSERVATION:  Preservation of skeletal mass.  Kidney is the primary calcium conservation organ in the body. ( it excretes the excess phosphate to minimize the loss of Ca).  Zero calcium balance is ideal metabolic state for maintaining the skeletal mass, positive Ca balance occurs during growth period( near about 10 years) negative Ca balance occurs after early adult year, progressively erode bone volume throughout life.
  19. 19.  Recommended daily allowance(RDA) of Ca : 1000-1500 mg /day.  Growing adolescents , pregnant and lactating women, post-menopausal women who are not receiving the estrogen replacement theraphy : 1500 mg / day.  Dietary products : milk mozzarella cheese swiss cheese green leafy vegetables Calcium carbonate is only 40% Ca( 500 mg of tablet provides 300 mg of Ca)
  20. 20.  Factors inhibiting the Ca conservation: kidney disease( renal osteodystrophy) Vit D3 deficiency( Ca binding protien) Liver disease
  21. 21. ENDOCRINOLOGY:  BIND RECEPTOR at the CELL SURFACE: peptide hormones( PTH, growth hormone, insulin, calcitonin)  BIND RECEPTOR at the NUCLEUS: steroid hormones( vit D, androgen, estrogen) , it is lipid soluble and passes through the plasma membrane.
  22. 22. CALCITONIN:  Secreted by PARAFOLLICULAR CELL of     thyroid gland. ACTION: antagonist to PTH IT increases the calcification by increasing the activity of osteoblast It decreases the bone resorption and increases the excretion of Ca into urine Thus decreases the blood Ca level
  23. 23. PARATHYROID HORMONE:  Low Ca level promoted the secretion of PTH.  ACTION: it bind to the membrane receptor protien on the target cells and activates adenylate cyclase to liberate cAMP.  Thus increases the blood Ca level.  That promotes the phosphorylation of protien
  24. 24. ACTION ON BONE:  It stimulates pyrophosphatase and collagenase  Demineralization of bone  It increases the blood Ca level by resorption of bone.
  25. 25. ACTION ON KIDNEY:  IT promote( the hydroxylation of 25- hydroxycholecaciferol ) the production of vit D3 in the kidney  Increases the reabsorption of Ca by kidney
  26. 26. ACTION ON INTESTINE:  Indirect action  It increases the intestinal absorption of Ca by promoting the synthesis of vit D 3
  27. 27. CHOLECALCIFEROL:  1, 25 – dihydroxy –cholecalciferol  Active form of vit D( it is not the vitamin at all; it is a hormone)  ACTION: 1) it increases the synthesis of CALCIUM BINDING PROTIEN in the intestinal cell. It increases the intestinal absorption of calcium and phosphate increases the blood calcium level 2) It also increase the Ca uptake by the bone and promote the calcification and mineralization .
  28. 28. SEX HORMONES:  ANDROGEN: 1) Increase the musculoskeletal mass 2)Increases load generated by the enhanced muscle mass.  ESTROGEN: It conserves the skeletal Ca by suppressing the frequency of bone remodeling. It protects the female skeletal from bone loss during childbearing years. Clinical implication: symptomatic osteoporosis at menopause( it enhances remodeling activation slight negative calcium balance
  29. 29.  Estrogen replacement therapy is widely recommended for Ca conservation and prevention of osteoporosis in postmenopausal women.
  30. 30. BONE MODELING AND BONE REMODELING:  In bone modeling , independent sites of resorption and formation change the form ( size and shape)of a bone.  Bone modeling is the dominant process of facial growth and adaptation.  In bone remodeling, a specific, coupled,sequence of resorption and formation occurs to replace the previously existing bone.  It is turnover of existing bone.
  31. 31.  Modeling change can be seen in the cephalometric tracing.  But remodeling can not be imaged in the clinical radiograph, it can be apparent only at the microscopic level.
  32. 32. CONTROL FACTORS FOR BONE MODELING: MECHANICAL • • • • Disuse atrophy<200 Bone maintenance 200to 2500 Physiologic hypertrophy2500to 4000 Pathologic overload>4000 ENDOCRINE • Bone metabolic hormone: PTH,vit D , calcitonin • Growth hormone: somatotropin,IGF I , IGF II • Sex steroid: estrogen and testosterone PARACRINE AND AUTOCRINE • Variety of local agents
  33. 33. CONTROL FACTORS FOR BONE REMODELING: METABOLIC MECHANICAL • ESTROGEN:increase the activation frequency • PTH: decrease the activation frequency • <1000μє: more remodeling • > 2000 μє: less remodeling
  34. 34. BIOMECHANICS: OSTEOB LAST DIFFERENTIATION Weightlessness Mechanical loading + BONE FORMATION  Mechanical loading is essential to skeletal health.  Remodeling and modeling process are related to STRAIN HISTORY, which is defined in MICROSTRAIN(μє)
  35. 35. MECHANOSTAT THEORY:  Proposed by: FROST  F and R are the modeling phenomenon that change the shape and form of bone  Reviewed by: MARTIN and BURR 1) sub threshold loading < 200μє disuse atrophy, decrease in modeling , and increase in remodeling.( ATROPHY) R>F 2)200μє <Physiologic loading<2500μє steady-state activity F=R Maintenance phase
  36. 36. 3) Load exceeding the minimal effective strain≈2500μє Hypertrophic increase in modeling Concomitant decrease in remodeling R<F 4) Pathologic overload Strain≥ 4000 μє Structural integrity of bone is threatened R>F
  37. 37. SPECIFIC ASSESSMENT METHODOLOGY::  Mineralized section:  Polarized light  Fluorescent label  Microradiography  Auto radioghaphy  Nuclear volume morphometry  Cell kinetics  Finite element modeling(FEM)  Microelectrodes
  38. 38. A GENETIC ASPECT:  The genetic mechanism is the mean of controlling the coupling of sequential resorption and formation process of bone remodeling.  a bone remodeling cycle ( A R F) completes in 151 days.  Resorption cavity requires 29 days ,which is 200 to 250 μm in diameter and 134 days (≈ 4 months )to refill it.
  39. 39. INTRAVASCULAR AND PERIVASCULAR MECHANISM OF COUPLING BONE RESORPTION AND FORMATION:  A: ACTIVATION of inflammation causes the the expression of nitrous oxide synthatase, which triggers the localized remodeling foci at the site of microdamage.  At the compression site, underlining resorption starts, necrosis of PDL, loss of cushion action of PDL, CORTICAL BONE adjacent to it exposed to high peak load
  40. 40.  R:  Exposure of collagen to extracellular fluid and Release of inflammatory cytokines( prostaglandin, interlukin1 ) attracts the T cell from the circulation to the site of microdamage.  T cell produce RANKL, which induce osteoclast histogenesis.
  41. 41.  RANKL activates the RANK receptor of preosteoclast from the circulating blood.  F: as the bone is resorbed, growth factor stimulate the preosteoblast to produce OPG protien which block the RANK receptor of osteoclast.
  42. 42.  Mononuclear cells move in and coat the scalloped resorbed surface with cementing surface.  Perivascular osteogenic cell migrate through the low cell density zone and diffenciate to the preosteoblast which divide in 2 osteoblast.  Osteoblast form new bone , filling the resorption cavity and completing the turnover process
  43. 43. CLASSIFICATION OF BONE TISSUE:  WOVEN BONE: it is relatively weak, disorgnized, and poorly mineralized.  It is the first bone, forms in response to orthodontic loading.  It causes: rapid filling osseous defect provide initial continuity for fracture strengthening a bone ,weakened by surgery
  44. 44. LAMELLAR BONE:  It is a strong, highly organized, well mineralized, and make 99% of adult human skeleton.  Strength of bone is directly related to mineral content .  Formation: primary mineralization: a mineral component ( hydroxylapatite) is deposited by osteoblast. Secondary mineralization: crystal growth occurs.
  45. 45. COMPOSITE BONE:  CANCELLOUS COMPACTION :It is an osseous tissue formed by deposition of lamellar bone within the woven bone lattice.it is known as PRIMARY OSTEON.  It is intermediary type of bone in the physiologic response to orthodontic loading.  It is the prominent osseous tissue for stabilization during early process of retention( postoperative healing).
  46. 46. BUNDLE BONE( alveolar bone proper/ lamina dura :  Functional adaptation of lamellar structure to allow attachment of tendon and ligament.  Perpendicular striations is known as SHARPEY’S FIBERS.  EXAMPLE: distinct layers of bundle bone usually are seen adjacent to PDL.

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