Healing and repair processes

Phases of healing

Wound healing proceeds through four overlapping phases - haemostasis, inflammation, proliferation, and remodelling - each with distinct cellular and molecular drivers
Haemostasis (minutes) - platelet plug + coagulation cascade
Inflammation (days) - neutrophils clear debris/bacteria, then macrophages take over, releasing growth factors that drive the next phase
Proliferation (days-weeks) - fibroblasts lay down collagen (type III initially), angiogenesis, re-epithelialisation, wound contraction (myofibroblasts)
Remodelling (weeks-months to years) - type III collagen replaced by stronger type I collagen, cross-linking increases tensile strength, though it never exceeds ~80% of original tissue strength

Impaired healing (chronic wounds) disproportionately affects patients with diabetes, peripheral arterial disease, venous insufficiency, and malnutrition

Chronic (non-healing) wounds are typically arrested in the inflammatory phase - persistent infection, ischaemia, or repeated trauma prevents progression to proliferation
Clinical assessment of a chronic wound should identify and correct the arresting factor rather than simply treating the wound locally

Optimise the factors that impair healing: glycaemic control (diabetes), revascularisation (arterial insufficiency), compression (venous insufficiency), nutrition (protein/vitamin C/zinc), offloading (pressure injury)
Excessive scar formation (hypertrophic scar, keloid) reflects dysregulated remodelling - keloids extend beyond the original wound margin and are more common in darker skin types

Diabetic foot ulcers, venous leg ulcers, pressure injuries, keloid/hypertrophic scarring

Healing is markedly delayed (not simply absent) by the presence of any one uncorrected factor - identifying and correcting the specific barrier is more effective than escalating local wound care alone

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