Wound Healing and Tissue Repair
The four phases
Hemostasis comes first (vasoconstriction, platelet plug, fibrin clot; seconds to minutes). Inflammation follows (neutrophils, then macrophages; roughly days 1 to 4, up to a week in clean wounds). Proliferation overlaps it (fibroblasts lay down type III collagen, angiogenesis builds granulation tissue, keratinocytes migrate across the wound bed, and myofibroblasts contract the wound; roughly day 4 to week 3). Maturation or remodeling is the longest phase, converting type III to type I collagen and reorganizing the matrix; it can run 3 weeks to 1 to 2 years, and the scar never regains more than about 80 percent of original tensile strength.
Acute versus chronic
Acute wounds progress on schedule. Chronic wounds stall, usually locked in a prolonged inflammatory phase with elevated proteases (MMPs), diminished growth factor activity, senescent cells, and biofilm. Healing can occur by primary intention (approximated edges), secondary intention (left open to fill with granulation, contract, and epithelialize), or tertiary intention (delayed closure after infection or contamination is controlled).
Traps in questions
Candidates are often asked which phase predominates at a given time, or whether a description represents acute or chronic healing. A beefy red, pebbled wound bed signals proliferation, not infection. Systemic factors that blunt healing include ischemia, diabetes, malnutrition, corticosteroids, immunosuppressants, smoking, and advanced age; local factors include pressure, shear, moisture imbalance, and bioburden. A stalled wound is not automatically infected.
Rule of thumb
The 4-week rule: a wound that has not reduced in area by roughly 30 percent at 4 weeks of appropriate care warrants reassessment of the plan, the diagnosis, or the presence of biofilm and occult infection.