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OVERVIEW

Adult wound healing

  • Proceeds through several overlapping stages

    • Inflammation (days 0-6)

      • Coagulation/ haemostasis

        • Formation of thrombin-platelet plug (clot) adherent to type II collagen exposed by endothelial disruption​

        • Platelet clot is a source of growth factors (PDGF, TGF-α and –β), inflammatory vasoactive and chemotactic cytokines, fibrinogen, fibronectin, thrombospondin and von Willebrand factor

        • Fibrin-thrombin mesh traps more platelets to continue cycle

      • Inflammation​

        • Activation of mast cells and influx of neutrophils, macrophages and T-lymphocytes

        • Initial vasoconstriction followed by active vasodilatation due to inflammatory mediators

    • Proliferation (4 days to 3 weeks)

      • Re-epithelialisaton​

        • Marginal keratinocytes​ migrate over wound surface and convert into non-polarised cells expressing basal cytokeratins

        • Restitution of the basement membrane induces to cells to adopt their previous morphology and form anchoring junctions with fibronectin

      • Fibroplasia​

        • Influx of fibroblasts over fibronectin scaffold​

        • Fibroblasts synthesize type III collagen which forms granulation tissue

      • Angiogenesis​

        • Induced by VEGF​

    • Remodelling (3 weeks to 18 months)

      • When fibronectin predominates, fibroblasts actively synthesise hyaluronic acid and collagen​

        • Caeses when collagen reaches an abundant level​

      • Residual fibroblast mature into myofibroblasts and form cell-matrix and cell-cell contacts that contract the wound​

      • Type III collagen is gradually replaced by type I collagen to normal type I:III ratio of 3:1

      • Collagen becomes lamellar by activity of fibroblasts and collagenases

      • The abundant capillaries regress

      • Peak wound tensile strength is achieved at ~60 days and maximum of ~80% of unwounded skin strength

Adult wound healing

Factors affecting wound healing

  • May be attributed to a lowering of the oxygen concentration in the wound including radiotherapy and diabetes

  • Oxygen tension of more than 40mmHg augments fibroblastc activity and is required for hydroxylation of proline and lysine residues to form cross linkages in the collagen α-chain

  • Oxygen also facilitates cell-mediated killing of pathogens in the wound

  • Patient factors

    • Age​ - reduced cellular multiplication and production rate, and tensile strength and wound closure rates with age

    • Nutrition

      • Vitamin C - essential for hydroxylation of collagen​

      • Vitamin E - neutralises lipid peroxidation caused by ionising radiation

      • Minerals - zinc influences re-epithelialisation and collagen deposition

    • Systemic illness - diabetes, etc​

    • Smoking​

      • Nicotine causes tissue vasocontriction​

      • Cyanide impairs oxidative enzymes

      • Carbon monoxide impairs oxygen carrying capacity of haemoglobin

    • Drugs​

      • Steroids - impaired macrophage and fibroblast function, reduced angiogenesis and contracture​

      • NSAIDs - reduces prostaglandins

      • Chemotherapy

    • Genetic conditions - Ehlers-Danlos, progeria, etc​

  • Wound factors​

    • Infection​ - prolongs inflammatory phase

    • ​Oedema​ - reduces tissue perfusion

    • Denervation - prone to ulceration

    • Radiation

Factors affecting wound healing

Adjuncts to healing

  • Negative wound pressure

    • Unclear mechanism​

    • Reduced oedema and interstitial pressure, improved tissue oxygenation and removing inflammatory exudate/ mediators and bacteria

  • Hyperbaric oxygen

    • Increases oxygen delivery to wounds​

  • Growth factors

    • Experimental

  • Laser biostimulation 

Adjuncts to healing

Foetal wound healing

  • Regenerative process that occues with minimal of no scar formation

  • Only occurs in the skin and bone of the hoetus

  • Foetal wounds are rich in hyaluronic acid and fibronectin

  • Healing is largely controlled by fibroblasts rather than macrophages

  • Reduced levels of TGF-β, PDGF, bFGF

  • Type III collagen is deposited in a more organised manner

  • Tenascin is a modulator of cell growth and migration in foetal wounds

Foetal wound healing
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