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Wound healing2



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  • http://www.pilonidal.org/aftercare/wound_healing_indepth.php
  • Fibroblasts are connective tissue that synthesise and secrete collagen and growth factors (angiogenesis and endothelial cells proliferation)
  • Fibroblasts are connective tissue that synthesise and secrete collagen and growth factors (angiogenesis and endothelial cells proliferation)
  • Fibroblasts are connective tissue that synthesise and secrete collagen and growth factors (angiogenesis and endothelial cells proliferation)


  • 1. Wound Healing Karen Gordon
  • 2. Wound healing or “Cicatrisation”• Definition – A healing process which leaves a scar (i.e. a cicatrix).• Pathology – Contraction of fibrous tissue, formed at a wound site by fibroblasts, reducing the size of the wound but causing tissue distortion and disfigurement. Once thought to be due to contraction of collagen but now known to be due to cellular activity.
  • 3. • Tissue repair after injury – Skin – Other organ• Skin – Normal protective barrier against environment • Epidermis and dermis in steady state equilibrium – Once normal protective barrier broken • Physiological process of wound healing starts immediately
  • 4. The 4 phases of wound healingWound consists of filling gap created by tissuedestruction followed by restoration of structuralcontinuity of injured part through 4 phases ofhealing:• Haemostasis• Inflammation• Proliferation• Remodelling
  • 5. Haemostasis• Immediately after injury to prevent blood loss• Clotting – Vasconstriction – Platelet activation and aggregation of platelets to form fibrin clots – Coagulation• Mediators of vasoconstriction induced by – Serotonin, thromboxane A2 and endothelin-1 • Released by platelets and the endothelium • Bind to and act on receptors on smooth muscle of arterioles to cause vasoconstriction
  • 6. Haemostasis• Platelet (thrombocyte) activation stimulated by – Von Willebrand factor • Binds to glycoprotein platelet receptors • Released by endothelium – Collagen • Exposed in subendothelium – Thrombin, an enzyme • Activated by coagulation cascade• Platelets when activated – Change shape and display GPIIb/IIa receptors – Allow aggregation and bind to fibrin – Plug then formed in ruptured blood vessels
  • 7. Haemostasis• Other factors released that initiate wound healing – Platelet-derived growth factor • Stimulates cell division • Formation of new cells to close wound • Promoted angiogenesis – Adenosine diphosphate and thromboxane A2 • Stimulate production of GPIIb/IIIa receptors • Promotes platelet aggregation and clot formation• Final phase of haemostasis – Coagulation cascade forms mesh (fibrin + platelets) which traps rbcs
  • 8. Inflammation• Lasts 2-4 days after injury• Vasodilatation for movement of mediators• Neutrophils released to kill bacteria• Macrophages and monocytes phagocytose • Clean and scavenge bacteria, foreign particles and necrotic debris • Prepare site for healing• Macrophages release factors to stimulate proliferative process • Cause migration and cell division • Stimulate capillary regrowth and granulation process • Leads to attraction of fibroblasts• Clinically: wound swollen and painful • Most of pain will subside once inflammation starts resolving
  • 9. Proliferation• MARKED BY ARRIVAL OF FIBROBLASTS• Building new tissue to fill wound space – Characterised by angiogenesis, collagen deposition, granulation tissue formation, epithelialisation and wound contraction• Fibroblasts enter and grow in wound by day 3 – Connective tissue that synthesise and secrete collagen • and growth factors for angiogenesis, • promoting endothelial cell proliferation and migration – Secrete glycoproteins and collagen – Fibroblasts + endothelial cells = granulation tissue
  • 10. Proliferation• Granulation tissue formed by day 7 – Formed from macrophages, fibroblasts and new capillaries which fills damaged tissue – New capillaries leaky • Allow plasma proteins and leucocytes to leak into tissue – Clinically: Bright red, fragile (bleeds easily), moist and soft to touch with an uneven appearance• Epithelialisation – final components – Regeneration, migration, proliferation, and differentiation of epithelial cells at wound edge • Form new surface area similar to before injury – Epidermal cells migrate from wound edge and provide cover for new tissue
  • 11. Proliferation• Clinically at the end of proliferation: oedema diminishes (as WCC move away) and wound blanches (small vessels thrombose and degenerate)
  • 12. Remodelling and maturation• Overlaps with proliferation phase• 3 weeks tp up to 6-18 months• Remodelling of collagen fibres – Along tension lines – Cells no longer needed removed by apoptosis – Scar tissue• Clinically: scar tissue becomes avascular• Tensile strength 80% by end of 3 months• Nerve endings re-grow as tissues rearrange• Patients may feel tugging, tightness, tension, itching as new tissue stabilises
  • 13. Remodelling and maturation• Complex• Susceptible to interruption and failure• Can lead to non-healing chronic wounds – Factors contributing to this • Diabetes • Venous or arterial disease • Old age • Infection