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Fracture Healing.pptx
- 2. Outline • Primary Fracture Healing • Secondary Fracture Healing • Perren’s Strain Theory • Stages of Fracture Healing • Factors affecting Fracture healing • Types of Non-union • Augmenting Fracture Healing
- 4. Primary Bone Healing • Occurs when there has been Anatomical Reduction and interfragmentary compression, leading to Absolute Stability • New blood vessels grow into any small gaps that exist (gap healing) • mesenchymal cells differentiate into osteoblasts, laying down lamellar bone in small gaps and woven bone in large gaps
- 5. Primary Bone Healing • Osteoclasts form Cutting Cones that tunnel across the fracture site wherever there is contact between the bone ends or a minute gap. • Blood vessels and osteoblasts follow, laying down lamellar bone in the form of new osteons • This process of newly formed osteons bridging the gap may take many months and may be difficult to see on an X-ray • This is the same process as the remodelling phase (stage IV) of secondary bone healing
- 7. Secondary Bone Healing With Relative Stability, strain or movement at the fracture site stimulates secondary healing by two discrete processes: 1. Periosteal Bony Callus (Intramembranous Ossification): • Periosteal multipotent cells differentiate into osteoprogenitor cells, producing bone directly without first forming cartilage. • Early hard callus at the fracture site periphery, if no extensive periosteal stripping.
- 8. Secondary Bone Healing With Relative Stability, strain or movement at the fracture site stimulates secondary healing by two discrete processes: 2. Fibrocartilaginous Bridging Callus (Endochondral Ossification): • occurs simultaneously between adjacent bone ends, and within the surrounding soft tissued, involving the formation of fibrocartilage, becomes calcified then replaced by osteoid or woven bone. • dependent on some movement occurring at the fracture site (strain). • Rigid fixation inhibits the differentiation of cells and the formation of callus.
- 10. Perren’s Strain Theory • After any form of fixation or immobilization, a fracture that is loaded will undergo some degree of movement or strain. • This may be compressive, tensile, bending or torsional. • Strain at fracture site decreased with increased fracture gap or greater surface area • metaphyseal fractures (larger bone diameter) • multifragmentary or segmental fractures (overall strain shared among the individual fragments) • Fracture callus becomes increasingly stiff with time • gelatinous granulation tissue -> soft callus -> hard bony callus.
- 11. Perren’s Strain Theory • Each of these tissues is able to tolerate a different amount of strain: • Granulation tissue: up to 100 per cent. • Fibrous connective tissue: up to 17 per cent. • Fibrocartilage: 2–10 per cent. • Lamellar bone: <2 per cent.
- 12. Perren’s Strain Theory • High Interfragmentary Strain = Granulation tissue formation • as strain decreases with time cartilage and bone form • If with absolute stability = strain low • inhibits callus formation • allows direct (primary) Haversian remodelling • If fragments fixed rigidly but with a gap • primary bone healing (cutting cones) may Not be able to bridge the gap • Lack of strain = inhibits callus formation and secondary healing • May predispose to non-union. • If with relative stability • more strain-tolerant cartilaginous callus required to stiffen the fracture site before hard woven bony callus forms and replaces it (secondary healing). • A larger strain produces a bigger callus
- 13. Stages of Fracture Healing
- 14. Stage I: Hematoma Formation/Inflammation up to 1 week
- 15. Stage II: Soft Callus 1 week to 1 month
- 16. Stage III: Hard Callus 1-4 months
- 17. Stage IV: Remodelling up to several years
- 18. Factors affecting Fracture Healing
- 19. Factors affecting Fracture Healing
- 23. Augmenting Fracture Healing • Systemic Enhancement • Distant Skeletal Injury • Electromagnetic Fields • Ultrasound • Mechanical Methods
Editor's Notes
- Absolute Stability means no motion between fracture surfaces under functional load The process is very intolerant of strain (movement) at the fracture site.
- Absolute Stability means no motion between fracture surfaces under functional load The process is very intolerant of strain (movement) at the fracture site.
- Relative Stability (some controlled motion between fracture surfaces under functional load)
- Relative Stability (some controlled motion between fracture surfaces under functional load)
- Haematoma from ruptured blood vessels forms fibrin clot. Damaged tissue and degranulated platelets release signalling molecules, growth factors and cytokines. Migration of inflammatory cells into the haematoma occurs, responding to local growth factors and cytokines (IL-1, IL-6, TGF-β super-family including BMPs, PDGF, FGF, IGF). Proliferation, differentiation and matrix synthesis as haematoma is replaced by granulation tissue. Capillary in-growth (angiogenesis) and recruitment of fibroblasts, mesenchymal cells and osteoprogenitor cells. The periosteum plays an important role in this process. Cell types involved include PMNs, macrophages and then fibroblasts. At necrotic bone ends, bone resorption is mediated by osteoclasts and removal of tissue debris by macrophages.
- Increased cellularity, with proliferation, differentiation and soft callus neovascularization. Callus is a combination of fibrous tissue, cartilage and woven bone Intramembranous (bony/periosteal) callus = primary callus response: type I collagen (osteoid) laid down from periosteal osteoblasts in the cambium layer as periosteal bony callus or woven bone. This is hard callus but it does not bridge the fracture. Endochondral (fibrocartilaginous/bridging) callus = bridging external callus: multipotential cells differentiate to form chondroblasts and fibroblasts within the granulating callus, which produce the type II cartilaginous and fibrous elements of the matrix (chondroid). Chondroblasts then calcify the chondroid matrix they have produced, creating calcified fibrocartilage or soft callus. Medullary callus: this is a later process and can slowly unite the fracture if external callus fails.
- Calcified soft callus is resorbed by chondroclasts and invaded by new blood vessels. These bring with them osteoblast precursors that produce the bony (type I) elements of the matrix (osteoid) and then mineralize it to form woven bone. Soft calcified chondroid callus becomes hard mineralized osteoid callus. Bony bridging continues peripherally as subperiosteal new bone formation. At this point the fracture is united, solid and pain-free to movement.
- Once the fracture has united, the hard callus is remodelled from woven bone to hard, dense lamellar bone by a process of osteoclastic resorption followed by osteoblastic bone formation. The medullary canal reforms at the end of this process. This is the same mechanism as for direct cortical, osteonal or primary bone healing, seen following fracture fixation with absolute stability. Bone assumes a configuration and shape based on stresses acting upon it (Wolff’s law). Electric fields may play a role in Wolff’s law, with osteoclastic activity being predominant on the electropositive tension side of bone and osteoblastic activity on the electronegative compression side.
- This is defined as lack of healing of a fracture within the expected time, which varies with the bone involved, e.g. distal radial fractures are expected to heal by 6 weeks, scaphoid fractures by 8 weeks, tibial fractures by 16 ± 4 weeks and femoral fractures by 16 ± 4 weeks. The fracture is bridged by soft tissue, the characteristics of which are defined by the local blood supply and mechanical conditions (usually cartilage and/or fibrous tissue). Clinical union is defined by the absence of tenderness or motion at the fracture site with no pain on loading, while radiological union is defined as the presence of visible bridging trabeculae on three out of four cortices on X-rays. Hypertrophic non-union A good blood supply but excessive strain at the fracture site prevents progression of the callus to form bone. These usually require biomechanical stabilization to allow callus progression to bone to occur. Atrophic non-union A poor blood supply is caused by soft-tissue damage, periosteal stripping and/or fracture comminution, which may occur at the time of injury or during the exposure for internal fixation. A fracture fixed with rigid fixation (zero strain) and with the fragments distracted will also lack stimulation of callus formation. Atrophic non-unions require stabilization and biological enhancement in order to heal.
- SYSTEMIC ENHANCEMENT Several systemic approaches have been hypothesized, but none is in wide usage. Examples include IGF-1 and IGF-2, growth hormone, parathyroid hormone, vitamin D3 and prostaglandins. DISTANT SKELETAL INJURY Injury to bone marrow enhances bone healing at distant sites. Corticotomy in a long bone has a stimulatory affect on fracture healing elsewhere in the same bone. ELECTROMAGNETIC FIELDS Piezoelectric currents are produced within bone as the collagen fibres are deformed. Streaming potentials (electrokinetic currents) are produced as charged constituents of extracellular matrix flow past the mineral phase of bone as it is deformed. The endogenous electric fields produced from these processes are integral to bone homeostasis, influencing normal bone modelling and remodelling. Clinical devices use electromagnetic induction waveforms to try to reproduce these potentials and so speed up or augment fracture healing. ULTRASOUND There is good evidence that low-intensity ultrasound can affect gene expression, stimulate chondroblast and osteoblast activity, enhance blood flow, and accelerate or augment fracture healing in animal models. Pressure waves from ultrasound may also stimulate differentiating bone lining cells along the edges of a fracture. MECHANICAL METHODS Controlled axial micromotion has been shown to enhance the healing of tibial fractures.