Skin Anatomy, Physiology, and the Phases of Wound Healing
Skin architecture
The epidermis is avascular and stratified: keratinocytes build the barrier, melanocytes provide pigment, and Langerhans cells contribute immune surveillance. The dermis holds type I collagen, elastin, fibroblasts, vessels, and nerves; the hypodermis supplies cushioning, insulation, and fat. Functions include barrier protection, thermoregulation, sensation, vitamin D synthesis, and immune defense. Age, steroids, diabetes, malnutrition, and ischemia thin the epidermis, flatten the dermal-epidermal junction, reduce perfusion and collagen synthesis, and slow every healing phase.
The four phases
- Hemostasis (minutes to hours): vasoconstriction, platelet plug, fibrin clot.
- Inflammation (days 0-4, occasionally to 6): neutrophils then macrophages debride and signal; mild redness and serous exudate are expected.
- Proliferation (roughly day 3-21): angiogenesis, fibroblast collagen (type III), beefy-red granulation, epithelialization advancing about 0.5-1 mm/day from wound edges, and contraction by myofibroblasts.
- Maturation (3 weeks to 1-2 years): type III collagen is replaced by type I, water content falls, and tensile strength climbs, but only to about 80% of unwounded skin, never 100%.
Traps
Questions blur granulation (bumpy, beefy red), slough (yellow, stringy), and eschar (leathery, black). Prolonged inflammation, not simply a red wound, signals infection, bioburden, or trauma. Healing by secondary intention granulates and contracts and is never reverse staged. Primary closure is a clean, apposed wound; tertiary (delayed primary) closure is deliberate closure after contamination is controlled.
Rule of thumb
Time the phases with 4 days, 3 weeks, 2 years. A wound is only about 20% as strong as intact skin at 3 weeks, so suture lines can dehisce with coughing or lifting.