The block on the left shows a cross-section of skin: the thin outer stratum corneum (pale), the epidermis beneath it, the thicker dermis with its vessels, and the fatty hypodermis at the base. A gap cut through all three upper layers is the wound; small drifting spheres above the surface are moisture molecules and pathogens testing the barrier — how many get through depends on how intact the stratum corneum is.
The wound itself closes through four real phases, each with its own colour of agent filling the gap: platelets forming a clot (hemostasis, red-brown), immune cells clearing debris (inflammation, orange), fibroblasts and new capillaries building granulation tissue (proliferation, pink), and finally collagen realigning into mature scar (remodeling, pale). Progress through each phase is gated on the previous one finishing, matching the real overlapping-but-ordered cascade.
TEWL ∝ (1 − barrier_integrity)²
gap(t+dt) = gap(t) − closure_rate(phase) · rate · dt
P(pathogen breach) ∝ (1 − barrier_integrity) · (wound_open ? 3 : 1)
- Wound width — how deep the cut runs; a wider gap takes proportionally longer for granulation tissue to bridge.
- Healing rate — speeds or slows the whole cascade, standing in for factors like nutrition, age and blood supply.
- Barrier integrity — how intact the stratum corneum is elsewhere on the skin; low integrity (as in eczema or after sunburn) raises transepidermal water loss (TEWL) and lets more particles breach even where there's no wound.
- Trigger infection — spikes inflammation and briefly stalls closure, mirroring how a contaminated wound extends the inflammatory phase before proliferation can resume.
Real-world relevance: this is why intact barrier function matters even away from a wound (chronic barrier damage drives conditions like atopic dermatitis) and why wound care protocols exist to keep a healing wound clean — reinfection resets the clock on an already time-ordered process.