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‫السالم‬
‫علیکم‬
Lecture no. 5
BONE HEALING & Repair
Mr. Naeem Bukhari
Lecturer, MLT, UOH
Contents
֍Introduction
֍Types of bone healing
֍Stages of bone healing
֍Regulation of bone healing
֍Factors affecting bone healing
֍Assessment
֍Complications
֍Current trends
֍Conclusion
Introduction
• Bonehealing refers to complex and sequential
events that occur to restore injured bone to pre-
injury state.
• Boneinjury remains aconstant counterpart to
human existence, we are able to cope with this
due to bone healing. Thesurgeon musttherefore
have adequate understanding of its processes,
influencing factors and complications in order to
achieve optimum outcome.
Typesof bone healing
⸙ Healing by callus formation (indirect, secondary)
⸙ Healing by direct union(primary)
Stagesof bone healing
• Healing by callus formation
– Haematoma formation
• Occursimmediately
– Inflammation and cellular proliferation
• 8hrs to 1-2weeks
• Migration of inflammatory cells(macrophages,
neutrophils, platelets)
• Elaboration of cytokines, growth factors,other
mediators
• Proliferation and differentiation of mesenchymalstem
cells, migration of fibroblasts andosteoclasts
• neovascularization
Stagesof bone healing
• Healing by callus formation
– Callus formation
• 2-3wks to 4-8wks
• Osteoclasts mop up deadbone
• Collagen matrix formation
• Osteoid deposition andmineralisation
• Formation of wovenbone
– Consolidation
• Weeksto 2-3mnths
• Lamellar bone formation
• Remaining gapsfilled by lamellar bone
Stagesof bone healing
• Healing by callus formation
– Remodelling
• 2mnths to years
• Guided by stress exposure
• Osteoclasts are responsible
• Healing by direct union
– Occursin fractures where ends arecompressed,
with intervening space<500microns
– No callus formation
– Gaphealing – occurs if spaceis200-500microns
– Contact healing – occurs if spaceis<200microns
HAEMATOMA INFLAMMATION CALLUS CONSOLIDATION REMODELLING
Regulation of fracturehealing
• Local factors
– TGF-B
– PDGF
– FGF
– IGF
– VEGF
– BMP
– Cytokines
• Systemicfactors
– Hormones
Regulation of fracturehealing
• TGF-B
– Promotes proliferatn & diff of stem cells
– Stimulates collagen synthesis
• PDGF
– Stimulates T1collagen synth by osteoblast
– Stimulates osteoclast resorption
• FGF
– Stimulates fibroblast proliferation
– Stimulates angiogenesis
• VEGF
– Stimulates angiogenesis
Regulation of fracturehealing
• IGF
– Stimulates bone collagen & matrixsynthesis
– Inhibits bone collagendegradation
• BMP
– Osteoinductive
– Stimulates diff of osteoprogenitors toosteoblasts
• Cytokines
– IL-1,6 stimulate bone resorption
– Chemotaxis and regulation of inflammatorycells
Regulation of fracturehealing
• Systemicfactors
– Growth hormone – acts viaIGF
– Thyroid hormones – increase bone resorption
– Oestrogen – minimises bone resorption
Factors influencing bone healing
• Local
– Typeof bone
– # pattern
– # site
– Soft tissuedevitalisation
– Soft tissue interposition
– Blood supply
– Infection
– Irradiation
Factors influencing bone healing
• Systemic
– Malnutrition
– DM
– Drugs– NSAIDs,steroids, cytotoxics
– Tobacco use
– Thyroid disorders
– Vitamin deficiency
– CNStrauma
– HIV
Assessmentof fracture healing
• Clinical
• Radiological
Complications
• Malunion
• Delayed union
• Non-union
• Infection
• Post-traumatic arthritis
• Growth abnormalities
Current trends
• rBMP
– Delivered locally at 10-1000x naturalexpression
– Enhance# healing
– Decreaseinfection in GAIIIa & b#s
– Useful in recalcitrantnon-unions
• Pulsedelectromagnetic field (PEMF)
– Usedin treatment of nonunions
• Low-intensity pulsed ultrasound (LIPUS)
– Increasesgene expression, enhances blood flow,
enhances remodelling
– Reversesanti-angiogenic effect of nicotine
Conclusion
• Despite major advancement in understanding
of bone healing, problems/complications still
continue to arise.
• More research is needed in this all-important
area if these problems are to be satisfactorily
prevented or overcome
Bone healing and Repair

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Bone healing and Repair

  • 1. ‫السالم‬ ‫علیکم‬ Lecture no. 5 BONE HEALING & Repair Mr. Naeem Bukhari Lecturer, MLT, UOH
  • 2. Contents ֍Introduction ֍Types of bone healing ֍Stages of bone healing ֍Regulation of bone healing ֍Factors affecting bone healing ֍Assessment ֍Complications ֍Current trends ֍Conclusion
  • 3. Introduction • Bonehealing refers to complex and sequential events that occur to restore injured bone to pre- injury state. • Boneinjury remains aconstant counterpart to human existence, we are able to cope with this due to bone healing. Thesurgeon musttherefore have adequate understanding of its processes, influencing factors and complications in order to achieve optimum outcome.
  • 4. Typesof bone healing ⸙ Healing by callus formation (indirect, secondary) ⸙ Healing by direct union(primary)
  • 5. Stagesof bone healing • Healing by callus formation – Haematoma formation • Occursimmediately – Inflammation and cellular proliferation • 8hrs to 1-2weeks • Migration of inflammatory cells(macrophages, neutrophils, platelets) • Elaboration of cytokines, growth factors,other mediators • Proliferation and differentiation of mesenchymalstem cells, migration of fibroblasts andosteoclasts • neovascularization
  • 6. Stagesof bone healing • Healing by callus formation – Callus formation • 2-3wks to 4-8wks • Osteoclasts mop up deadbone • Collagen matrix formation • Osteoid deposition andmineralisation • Formation of wovenbone – Consolidation • Weeksto 2-3mnths • Lamellar bone formation • Remaining gapsfilled by lamellar bone
  • 7. Stagesof bone healing • Healing by callus formation – Remodelling • 2mnths to years • Guided by stress exposure • Osteoclasts are responsible • Healing by direct union – Occursin fractures where ends arecompressed, with intervening space<500microns – No callus formation – Gaphealing – occurs if spaceis200-500microns – Contact healing – occurs if spaceis<200microns
  • 8. HAEMATOMA INFLAMMATION CALLUS CONSOLIDATION REMODELLING
  • 9.
  • 10. Regulation of fracturehealing • Local factors – TGF-B – PDGF – FGF – IGF – VEGF – BMP – Cytokines • Systemicfactors – Hormones
  • 11. Regulation of fracturehealing • TGF-B – Promotes proliferatn & diff of stem cells – Stimulates collagen synthesis • PDGF – Stimulates T1collagen synth by osteoblast – Stimulates osteoclast resorption • FGF – Stimulates fibroblast proliferation – Stimulates angiogenesis • VEGF – Stimulates angiogenesis
  • 12. Regulation of fracturehealing • IGF – Stimulates bone collagen & matrixsynthesis – Inhibits bone collagendegradation • BMP – Osteoinductive – Stimulates diff of osteoprogenitors toosteoblasts • Cytokines – IL-1,6 stimulate bone resorption – Chemotaxis and regulation of inflammatorycells
  • 13. Regulation of fracturehealing • Systemicfactors – Growth hormone – acts viaIGF – Thyroid hormones – increase bone resorption – Oestrogen – minimises bone resorption
  • 14. Factors influencing bone healing • Local – Typeof bone – # pattern – # site – Soft tissuedevitalisation – Soft tissue interposition – Blood supply – Infection – Irradiation
  • 15. Factors influencing bone healing • Systemic – Malnutrition – DM – Drugs– NSAIDs,steroids, cytotoxics – Tobacco use – Thyroid disorders – Vitamin deficiency – CNStrauma – HIV
  • 16. Assessmentof fracture healing • Clinical • Radiological
  • 17. Complications • Malunion • Delayed union • Non-union • Infection • Post-traumatic arthritis • Growth abnormalities
  • 18. Current trends • rBMP – Delivered locally at 10-1000x naturalexpression – Enhance# healing – Decreaseinfection in GAIIIa & b#s – Useful in recalcitrantnon-unions • Pulsedelectromagnetic field (PEMF) – Usedin treatment of nonunions • Low-intensity pulsed ultrasound (LIPUS) – Increasesgene expression, enhances blood flow, enhances remodelling – Reversesanti-angiogenic effect of nicotine
  • 19. Conclusion • Despite major advancement in understanding of bone healing, problems/complications still continue to arise. • More research is needed in this all-important area if these problems are to be satisfactorily prevented or overcome