Wound healing involves three main phases - inflammation, proliferation, and maturation. During inflammation, hemostasis occurs within the first few hours followed by an inflammatory response involving neutrophils and macrophages over the next few days. Proliferation begins around 4-14 days as new tissue is formed through granulation, re-epithelialization, angiogenesis and collagen deposition by fibroblasts. Maturation occurs over weeks to months as remodeling and scar contraction takes place. Abnormal wound healing can result in excessive scarring like hypertrophic scars and keloids. Treatment depends on the type of abnormality but may involve pressure, silicone sheeting, steroid injections, excision and radiation. Contractures can also form from scars limiting

1. Wound HealingDr. Ranjeet Patil

2. DefinitionRegenerationReplacement of dead or damaged cells by functioning cells of same structure and functionBones, LiverRepairReplacement of dead or damaged cells by granulation tissue which matures to form scarFunction is lost-Lower order cellsSkinNoneBrain, Skeletal muscle, Cardiac muscle

3. Wound closure types PrimaryFirst-intentionClosure, the wounds are sealed immediately with simple suturing, skin graft placement, or flap closureClosure at end of a surgical procedure.SecondarySpontaneous-intention, no active intent to seal the woundCloses by re-epithelialization, contraction of the woundHighly contaminated woundTertiary Initially treated by repeated debridement, systemic or topical antibiotics, or negative pressure wound therapy for several days to control infectionSurgical intervention, such as suturing, skin graft placement, or flap design, is performed

5. WOUND-HEALING PHASESInflammationReactive phaseThe body's defences are aimed at limiting the amount of damage and preventing further injuryEschar or fibrinous exudateUpto 6 days

6. InflammationHaemostasisplatelet aggregation, degranulation, and activation of the coagulation cascadeplatelet-derived growth factor (PDGF), transforming growth factor beta (TGF), platelet-activating factor, fibronectin, and serotoninIncreased Vascular Permeability

7. InflammationInflammationPMN 24 to 48 hoursProstaglandins, complement factors, interleukin-1 (IL-1), tumour necrosis factor alpha (TNF-), TGF, platelet factor 4, bacterial productsprimary role-phagocytosis of bacteria and tissue debrisangiogenesis and collagen synthesis

8. Macrophages 48 to 96 hours – complete healingPhagocytosis Reactive oxygen species, Nitric oxide Debridement Collagenase, elastase Cell recruitment and activation Growth factors: PDGF, TGF, EGF, IGF Cytokines: TNF-, IL-1, IL-6, Fibronectin Matrix synthesis Growth factors: TGF, EGF, PDGF, Cytokines: TNF-, IL-1, Enzymes: arginase, collagenase, Prostaglandins, Nitric oxide Angiogenesis Growth factors: FGF, VEGF , Cytokines: TNF, Nitric oxide

9. T lymphocytes Less numerous than macrophagesPeak at about 1 week post injury role in wound healing is not fully defined

10. ProliferationProliferationRegenerative or reparative phaseConsists of re-epithelialization, matrix synthesis, and neovascularization to relieve the ischemia of the trauma itselfGranulation tissue4-14 days

11. Fibroblastssynthesize collagenactively carry out matrix contractionEndothelial cellsFormation of new capillaries (angiogenesis)

13. Maturation Remodelling phase Scar contraction with collagen cross-linking, shrinking, and loss of oedemaContracting or advancing edge8th day- months

14. Remodelling21 days up to 1 yearCollagen remodeling is also characteristic of this phase.Type III collagen is initially laid down, replaced by type I collagen

15. Epithelialization1st dayRapid mitotic divisionsDefect is bridgedLayering of the epitheliumKeratinisation

19. Abnormalities of Wound Healing

20. Delaying FactorsSystemic Age Nutrition Trauma Metabolic diseases Immunosuppression Connective tissue disorders Smoking Local Mechanical injury Infection EdemaIschemia/necrotic tissue Topical agents Ionizing radiation Low oxygen tension Foreign bodies

21. Excess HealingHepatic cirrhosis, Pulmonary Fibrosis, Scleroderma, Retrolental Fibroplasia, Diabetic Retinopathy, OsteoarthritisHypertrophic scarDefined as excessive scar tissue that does not extend beyond the boundary of the original incision or woundProlonged inflammatory phaseKeloidDefined as excessive scar tissue that extends beyond the boundaries of the original incision or woundAetiology is unknownBoth hypertrophic and keloid scars shows excess collagen with hypervascularity, but this is more marked in keloids where there is more type B collagen

22. TreatmentTreatment of hypertrophic and keloid scarsPressure – local moulds or elasticated garmentsSilicone gel sheeting (mechanism unknown)Intralesionalsteroid injection (triamcinolone)Excision and steroid injectionExcision and postoperative radiation (external beam or brachytherapy)Intralesionalexcision (keloids only)Laser – to reduce redness (which may resolve in any event)Vitamin E or palm oil massage (unproven)

23. ContracturesWhere scars cross joints or flexion creases, a tight web may form restricting the range of movement at the jointHyperextension or hyperflexion deformityTreatment may be simple involving multiple Z-plasties

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