Define Wound Healing. Describe its types and complications.

The Concept

A wound is any break in the normal structure and continuity of a tissue. Wound healing is the body's response to that injury — a remarkably organised, overlapping cascade of cellular and biochemical events whose goal is to restore the barrier and, as far as possible, the function of the tissue. It is important to understand that these 'phases' are not separate boxes that finish one after another; they overlap continuously, and a problem in an early phase (say, ongoing infection prolonging inflammation) holds up every later phase. Understanding the sequence explains almost everything about why wounds heal well or badly.

Phase 1 — Haemostasis (immediate)

The moment a vessel is cut, it constricts to limit blood loss, and platelets stick to the exposed collagen of the damaged wall, aggregating into a platelet plug. The coagulation cascade then lays down fibrin, converting the plug into a stable clot. This clot does two jobs at once: it stops the bleeding, and it forms a temporary scaffold along which the repair cells will later migrate. Crucially, activated platelets also release growth factors (PDGF, TGF-β) that summon inflammatory cells — so haemostasis is not merely 'stopping bleeding', it is the trigger that starts the whole healing programme.

Phase 2 — Inflammation (0–3 Days)

Neutrophils arrive first, over the first day or two, to kill bacteria and clear debris. From about day 2–3 the macrophage takes over and becomes the key orchestrating cell of healing: it phagocytoses dead tissue and bacteria, and secretes the growth factors (PDGF, TGF-β, VEGF, FGF) that call in fibroblasts and drive new blood-vessel formation. This is why inflammation is a double-edged sword — too little (as in immunosuppression or steroid use) means poor debridement and weak signalling, while too much or too prolonged (as with persistent infection or a foreign body) traps the wound in this phase and prevents it moving on.

Phase 3 — Proliferation (3–21 Days)

Now the wound is rebuilt. Fibroblasts migrate in and synthesise collagen (initially the weaker type III) and ground substance. At the same time, new capillaries sprout (angiogenesis), and together the new vessels and collagen form granulation tissue — the red, granular, slightly bleeding tissue seen in an open healing wound; its redness is simply the many capillary loops, and healthy granulation is the essential bed on which a wound epithelialises or accepts a skin graft. Epithelial cells then migrate across the surface from the wound edges and any surviving skin appendages (epithelialisation), and specialised contractile fibroblasts (myofibroblasts) draw the wound edges together (contraction), shrinking the defect.

Phase 4 — Maturation / Remodelling (3 Weeks – Up to 1 Year)

The wound is now closed but weak. Over months, the disorganised type III collagen is progressively replaced by stronger, cross-linked type I collagen, and the fibres reorganise along the lines of mechanical stress. This is why a wound keeps gaining strength long after it looks healed — yet even a fully mature scar regains only about 70–80% of the original tissue's tensile strength. The scar also becomes paler and flatter as its excess capillaries regress.

Types of Wound Healing

How a wound heals depends chiefly on how much tissue is lost and whether the edges can be brought together:

The logic is simple: apposed edges (primary) have almost no gap to bridge, so healing is quick with a neat scar; an open wound (secondary) must laboriously fill a defect with granulation and pull itself closed, which takes longer and scars more.

Factors That Impair Healing — and WHY

Local factors act right at the wound:

• infection prolongs inflammation and consumes resources
• a foreign body is both a mechanical barrier and a nidus for infection
• ischaemia/poor blood supply starves the wound of the oxygen collagen synthesis needs
• tension or movement repeatedly disrupts the fragile new tissue
• a haematoma separates the edges and is an ideal culture medium
• previous irradiation damages the local fibroblasts and blood vessels.

Systemic factors act through the whole patient:

• malnutrition deprives the wound of the protein needed for collagen and of key cofactors (vitamin C for cross-linking, zinc for enzymes)
• diabetes mellitus impairs healing on several fronts (microangiopathy, poor perfusion, neutrophil dysfunction, and high glucose feeding bacteria)
• corticosteroids and immunosuppression blunt the inflammatory phase and directly suppress collagen synthesis (an effect partly reversed by vitamin A)
• smoking, anaemia, advanced age, malignancy, jaundice and uraemia all reduce the wound's capacity to repair.

Complications of Healing

Healing can go wrong by being excessive — producing a hypertrophic scar or keloid — or deficient — producing a chronic non-healing ulcer or wound dehiscence. Secondary healing across a joint can cause a disabling contracture, and a long-standing scar or chronic ulcer can rarely undergo malignant change into a Marjolin's ulcer (a slow-growing squamous cell carcinoma).

Wound strength never exceeds about 80% of the original tissue.

• Four overlapping phases: haemostasis (clot + growth factors) → inflammation (macrophage is key) → proliferation (granulation, collagen III, epithelialisation, contraction) → remodelling (collagen III→I, strength rises to ~80% over months).
• Healing types: primary (apposed, fine scar), secondary (open, granulation + contraction, more scar), tertiary (delayed primary closure).
• Collagen synthesis needs oxygen + vitamin C — explains why ischaemia, smoking, anaemia and scurvy impair healing.
• Local factors: infection, foreign body, ischaemia, tension, haematoma; systemic: malnutrition, diabetes, steroids, smoking.
• Complications: excess (keloid/hypertrophic), deficient (ulcer/dehiscence), contracture, Marjolin's ulcer.