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Fracture classification,fracture healing

Fracture classification,fracture healing

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Fracture classification,fracture healing

  1. 1. FRACTURE CLASSIFICATION AND FRACTURE HEALING Dr. D.Tejaswi, MS (Ortho) Asst.professor Department of Orthopaedics NIMRA MEDICAL COLLEGE & HOSPITAL
  2. 2. FRACTURE • A disruption or break in the continuity of the structure of bone • Traumatic injuries account for the majority of fractures
  3. 3. HOW DOES A FRACTURE OCCUR • Injury (m.c) - Direct (soft tissue injury is common) - Indirect • Compression -impaction # • Bending -green stick /unicortical break • Tension -avulsion # • Twisting -spiral # • Repetitive stress - usually undisplaced # • Abnormal weakening –pathological #
  4. 4. CLASSIFICATION OF FRACTURES
  5. 5. • ON THE BASIS of • Etiology • Displacement • Communication with external environment • Site of fracture • Fracture morphology • Stability
  6. 6. On The Basis Of Etiology 1. Traumatic 2. Atraumatic 3. Pathological 4. Stress Fracture 5. Insufficiency fracture
  7. 7. On The Basis Of Displacement 1.Un-displaced 2.Displaced - Angulation - Translation - Rotation - Length
  8. 8. Un-displaced
  9. 9. Angulation
  10. 10. Translation
  11. 11. Rotation
  12. 12. Length
  13. 13. On The Basis Of Communication With External Environment 1.Closed Fracture 2.Open Fracture ? technically open ?
  14. 14. SITE OF FRACTURE CHILDREN ADULT 1.Epiphyseal fracture intra-articular# 2. Metaphyseal proximal / distal # 3. Diaphyseal shaft # • Upper 1/3 (proximal) • Middle 1/3 • Lower 1/3 (distal) • Junctional
  15. 15. On The Basis Of Fracture Morphology • Transverse – Spiral – Oblique – Comminuted – Impacted – Segmental – Avulsion
  16. 16. On The Basis Of Stability 1.Stable Occur when a part of the periosteum is intact across the fracture 2.Unstable Grossly displaced- Periosteum completely torn
  17. 17. Mechanisms of Bone Formation 1.Cutting Cones 2.Intramembranous Bone Formation 3.Endochondral Bone Formation
  18. 18. 1.Cutting Cones • Primarily a mechanism to remodel bone • Osteoclasts at the front of the cutting cone remove bone • Trailing osteoblasts lay down new bone
  19. 19. 2.Intramembranous (Periosteal) Bone Formation • Mechanism by which a long bone grows in width • Osteoblasts differentiate directly from preosteoblasts and lay down seams of osteoid • Does NOT involve cartilage . • It mainly forms cancellous bone.
  20. 20. 3.Endochondral Bone Formation • Mechanism by which a long bone grows in length • Osteoblasts line a cartilage precursor • The chondrocytes hypertrophy, degenerate and calcify (area of low oxygen tension) • Vascular invasion of the cartilage occurs followed by ossification (increasing oxygen tension)
  21. 21. FRACTURE HEALING
  22. 22. Fracture Healing • Types of Fracture Healing 1.Primary Healing (Direct) 2.Secondary Healing (Indirect) 3.Distraction Osteogenesis
  23. 23. 1.Primary Healing • Resembles normal remodelling of bone • Occurs only with anatomic reduction & rigid fixation. • Direct contact areas heal by cutting cones allowing passage of vessels • Gaps in reduction heal by vessel ingrowth- mesenchymal cells,osteoblasts-osteoclast cutting cones • CALLUS is not seen here
  24. 24. 2.Secondary healing • Response of periosteum / external soft tissues • External soft tissue forms bridging callus (Periosteal bridging callus) • Intramembraneous= peripheral to fracture • Endochondral= adjacent to fracture Motion enhances periosteal response
  25. 25. Stages Of Fracture Healing 1.Tissue Destruction And Hematoma Formation 2. Inflamation And Cellular Proliferation 3.Stage Of Callus Formation 4. Stage Of Cosolidation 5. Stage Of Remodelling
  26. 26. 1.Tissue destruction and Hematoma formation • 1-2 Days • Torn blood vessels- hemorrhage • A mass of clotted blood (hematoma) forms at the fracture site • Site becomes swollen, painful, and inflamed
  27. 27. 2.INFLAMATION AND CELLULAR PROLIFERATION • Within 8 hours inflammatory reaction starts. • Continued for 2-7 Days • Proliferation and Differntiation of mesenchymal stem cells. • Secretion of TGF-B , PDGF and various BMP factors.
  28. 28. 3.Callus Formation • Inflammation triggers cell division and angiogenesis • Chondrocytes secrete collagen and proteoglycans • Capillaries grow into the tissue and phagocytic cells begin cleaning debris • Granulation tissue (soft callus) forms a few days after the fracture • Fibrocartilaginous callus forms
  29. 29. 4.STAGE OF CONSOLIDATION • New bone trabeculae appear in the fibrocartilaginous callus • Fibrocartilaginous callus converts into a bony (hard) callus • Bone callus begins 3-4 weeks after injury, and continues until firm union is formed 2-3 months later
  30. 30. 5.STAGE OF REMODELLING • Excess material on the bone shaft exterior and in the medullary canal is removed • Allows the bone to assume its normal configuration and strength • Compact bone is laid down to reconstruct shaft walls
  31. 31. 3.DISTRACTION ESTEOGENESIS • Distraction Histogenesis • “A biological process of new bone formation between the surfaces of osteotomized bone segments that are separated gradually by incremental traction” • G.A. Ilizarov (1950’s) • Lengthening limbs through gradual distraction of fracture callus
  32. 32. Biology of Distraction • 1. Osteotomy/Corticotomy phase • 2. Latency phase • 3. Distraction phase • 4. Consolidation phase • 5. Remodeling phase
  33. 33. 1.Osteotomy Phase • Divides the bone into two segments • Triggers process of bone repair – Angiogenesis – Fibrogenesis – Osteogenesis
  34. 34. 2.Latency Phase • Period from bone division to onset of distraction • Inflammation and soft callus formation of the fractured bone • Soft callus formation begins 3-7 days and lasts 2-3 weeks • Latency period = 5-7 days
  35. 35. 3.Distraction Phase • Characterized by the application of traction forces to osteotomized segments • Rate : 1 mm/day • Rhythm : 0.25 mm every 6 hours 0.5 mm twice a day • Duration : 1-3 weeks
  36. 36. 4.Consolidation Phase • Cessation of traction forces to removal of distractor • Newly formed bone mineralizes and increases in bone density and strength • Duration: 3- 4 months
  37. 37. 5.Remodeling Phase • Removal of distractor to application of functional loading • Formation of lamellar bone
  38. 38. FACTORS AFFECTING FRACTURE HEALING
  39. 39. Depends Upon----- 1.Fracture Type 2.Gap Condition 3.Fixation Rigidity 4.Loading 5.Biological Environment
  40. 40. Biological factors • Age • Comorbid medical conditions • Functional level • Nutritional status • Vascular injury • Hormones • Growth factors • Health of soft tissse envelope • Sterility • Smoking • Local pathological conditions • Extent of bone loss
  41. 41. Mechanical factors Level of energy affected Extent of bone loss Soft tissue attachment Stability / undue mobility Anatomic location of fracture
  42. 42. Growth Factors • Transforming Growth Factor (TGF -β ) • Bone Morphogenetic Proteins (BMP) • Platelet-Derived Growth Factor (PDGF) Fibroblast Growth Factors (FGF) • Insulin like growth factor II (IGF-II)
  43. 43. Osteoinductive • Mesenchymal cells to osteoblasts • Regulates cartilage and bone formation in fracture callus • Induces mesenchymal cells and osteoblast to produce type II collagen • Promote cell proliferation and matrix synthesis by • chondrocytes and osteoblasts • Stimulate osteoblast or osteoprogenitor cell activity
  44. 44. • Promotes proliferation and differentiation of mesenchymal precursors for osteoblasts, osteoclasts and chondrocytes • Stimulates both enchondral and intramembranous bone formation • Induces synthesis of cartilage-specific proteoglycans and type II collagen • Stimulates collagen synthesis by osteoblasts
  45. 45. • Local Regulation of Bone Healing • Growth factors -Transforming growth factor -Bone morphogenetic proteins -Fibroblast growth factors -Platelet-derived growth factors -Insulin-like growth factors • Cytokines -Interleukin-1,-4,-6,-11, - macrophage and granulocyte/macrophage (GM) - colonystimulating factors (CSFs) and -Tumor Necrosis Factor • Prostaglandins/Leukotrienes • Hormones • Growth factor antagonists
  46. 46. Platelet-Derived Growth Factor • A dimer of the products of two genes, PDGF-A and PDGF-B • PDGF-BB and PDGF-AB are the predominant forms found in the circulation • Stimulates bone cell growth • Mitogen for cells of mesenchymal origin • Increases type I collagen synthesis by increasing the number of osteoblasts • PDGF-BB stimulates bone resorption by increasing the number of osteoclasts
  47. 47. Insulin-like Growth Factor • Two types: IGF-I and IGF-II • Synthesized by multiple tissues • IGF-I production in the liver is stimulated by Growth Hormone • Stimulates bone collagen and matrix synthesis • Stimulates replication of osteoblasts • Inhibits bone collagen degradation
  48. 48. • Cytokines - Interleukin-1,-4,-6,-11, -Granulocyte/macrophage (GM) colonystimulating factors (CSFs) and - Tumor Necrosis Factor-Stimulate bone resorption - IL-1 is the most potent
  49. 49. • Specific Factor Stimulation of Osteoblasts and Osteoclasts Cytokine Bone Formation Bone Resorption • IL-1 + +++ • TNF-α + +++ • TNF-β + +++ • TGF-α -- +++ • TGF-β ++ ++ • PDGF ++ ++ • IGF-1 +++ 0 • IGF-2 +++ 0 • FGF +++ 0
  50. 50. • Prostaglandins / Leukotrienes -Effect on bone resorption is species dependent • Prostaglandins of the E series - Stimulate osteoblastic bone formation - Inhibit activity of isolated osteoclasts • Leukotrienes -Stimulate osteoblastic bone formation -Enhance the capacity of isolated osteoclasts to form resorption pits
  51. 51. Hormones • Estrogen -Stimulates fracture healing through receptor mediated mechanism - Modulates release of a specific inhibitor of IL-1 • Thyroid hormones -Thyroxine and triiodothyronine stimulate osteoclastic bone resorption • Glucocorticoids Inhibit calcium absorption from the gut causing increased PTH and therefore increased osteoclastic bone resorption
  52. 52. • Parathyroid Hormone - Intermittent exposure stimulates Osteoblasts - Increased bone formation • Growth Hormone - Mediated through IGF-1 (Somatomedin-C) - Increases callus formation and fracture strength
  53. 53. Vascular Factors • Metalloproteinases Degrade cartilage and bones to allow invasion of vessels • Angiogenic factors • specific mitogens • Angiopoietin (1&2) Regulate formation of larger vessels and branches
  54. 54. Electromagnetic Field • Electromagnetic (EM) devices are based on Wolff’s Law that bone responds to mechanical Stress . • Exogenous EM fields may stimulate bone growth and repair by the same mechanism • Clinical efficacy very controversial • No studies have shown PEMF to be effective in “gap healing” or pseudarthrosis
  55. 55. Ultrasound • Low-intensity ultrasound is approved for stimulating healing of fresh fractures - Modulates signal transduction, -increases gene expression, - increases blood flow, -Enhances bone remodeling and -increases callus torsional strength in animal models

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