Wound Healing

Wound healing is the body's organised response to tissue injury. After any cut, surgical incision, ulcer or open injury, a predictable sequence of events restores the protective barrier and structural integrity of the tissue. For most adult soft tissues and skin this is repair - the wound is filled with a fibrous scar - rather than true regeneration of the original organised tissue.

The process is usually described as four overlapping phases: haemostasis, inflammation, proliferation and remodelling. They are not separate, tidy steps; they blend into one another, and different parts of the same wound can be in different phases at the same time.

For the exam, three threads recur throughout this topic and are worth holding onto: the phases and their key cells (a classic basic-science viva), how a surgical wound closed by primary intention differs from an open wound healing by secondary intention, and why healing fails - the long list of local and systemic factors that examiners love, because they are exactly what you manipulate at the bedside.

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1. Haemostasis - stopping the bleeding

Within seconds of injury, damaged vessels constrict and exposed collagen activates platelets. The platelets aggregate and the clotting cascade lays down fibrin, forming a clot that both stops bleeding and acts as a provisional matrix (a scaffold) for cells to migrate along. Activated platelets also release the first wave of growth factors - notably platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) - that recruit inflammatory cells and start the repair signal.

2. Inflammation - cleaning the wound

Over the first few days, blood vessels become leaky and inflammatory cells flood in. Neutrophils arrive first (peaking at roughly 24 to 48 hours) to kill bacteria and clear debris. Macrophages then take over (peaking around days 2 to 3) and are the central orchestrating cell: they finish the clearance, then switch to a reparative phenotype and release the growth factors that drive angiogenesis and fibroblast activity. A wound that cannot move on from this phase becomes a chronic wound.

3. Proliferation - rebuilding the tissue

This is where the wound is filled in, and it has several parallel processes:

• Granulation tissue forms - the red, granular wound bed made of new capillaries plus fibroblasts in a loose collagen matrix.
• Angiogenesis - endothelial cells sprout new capillaries (driven by vascular endothelial growth factor, VEGF) to supply the metabolically active wound.
• Fibroplasia - fibroblasts migrate in and lay down type III collagen and ground substance.
• Re-epithelialisation - keratinocytes migrate from the wound edges and skin appendages across the granulation tissue to restore the surface barrier.
• Wound contraction - some fibroblasts become myofibroblasts (expressing smooth-muscle actin) and pull the wound edges together, shrinking the defect.

4. Remodelling - making the scar

The longest phase, lasting months to over a year. The disorganised type III collagen of the early scar is gradually replaced and cross-linked into stronger, better-aligned type I collagen, while excess capillaries and cells regress (the scar pales and flattens). The balance between collagen synthesis and its breakdown by matrix metalloproteinases determines the final result. Even a well-healed scar regains only about 80 percent of the original tissue's tensile strength.

A small group of growth factors are worth knowing by name, because examiners ask which cell makes them and what they do:

The collagen story is high-yield: the wound starts with type III collagen (laid down quickly but mechanically weak) and, during remodelling, this is steadily replaced by type I collagen, which is stronger and better organised. The shift in the type I to type III ratio back toward normal is a marker of a maturing, strengthening scar. Vitamin C is essential here because it is a cofactor for the hydroxylation of proline and lysine during collagen synthesis - which is why scurvy causes wound breakdown.

Tertiary intention (delayed primary closure) sits in between: the wound is deliberately left open for a few days - to let contamination, swelling or doubtful tissue viability declare themselves - and then closed surgically once it is clean and safe. This is common in contaminated trauma wounds and in compartment syndrome fasciotomies.

Examiners group these into local and systemic factors - a clean framework that scores well.

When healing goes wrong it tends to fail in one of two directions - too much scar, or no progress at all:

A chronic wound is one that has failed to heal in the expected time, typically because it is stuck in a prolonged inflammatory phase and never progresses to proliferation and remodelling. Common examples are diabetic foot ulcers, venous and pressure ulcers, and infected surgical wounds. Management aims to restart the process: debride non-viable tissue, control infection and pressure, improve blood supply, and optimise systemic factors.

Wound healing underpins almost everything in orthopaedic practice. Every surgical incision relies on it, and a wound complication after a joint replacement or fracture fixation can be the gateway to deep infection and disaster. In trauma, the decision to close a wound primarily, leave it open, or use delayed closure is a daily judgement that flows directly from these principles. In basic-science vivas, the phases, key cells and growth factors, and the local-versus-systemic list of impairing factors are classic, examinable material. And at the bedside, the things that most improve healing - good blood supply, no infection, controlled diabetes, no smoking, adequate nutrition, and a tension-free closure - are exactly the modifiable factors this topic teaches.

• Surgical site infection prevention guidance worldwide (for example WHO global guidelines and NICE in the UK) targets exactly the modifiable wound-healing factors - perioperative glycaemic control, smoking cessation, normothermia, tissue oxygenation and tension-free closure - because these protect the healing wound from breakdown and infection.
• Diabetic foot ulcer care is standardised across major bodies (such as the International Working Group on the Diabetic Foot and national diabetes societies), centred on debridement, offloading pressure, infection control, vascular assessment, and good glycaemic control - the practical application of restarting a stalled wound.
• Negative pressure wound therapy (NPWT) is widely endorsed as an adjunct for open, exuding and difficult wounds, promoting granulation and contraction; the strongest randomised evidence is in diabetic foot and complex surgical wounds.
• Across all settings the principle is the same: healing is a biological process you support rather than force - keep the wound clean, perfused and tension-free, and correct the systemic factors that hold it back.