Immune system ↗Immediate flow is reduced
Local vessel contraction and tissue pressure briefly limit blood loss while platelets contact exposed matrix.
IMMUNE / 06
Seal. Clear.
Rebuild. Remodel.
Wound phases overlap. Platelets, immune cells, vessels, epithelium, fibroblasts, matrix, nerves, and mechanical load cooperate; healing can regenerate structure, produce scar, or remain stalled.
A provisional plug forms
Adhesion and activation recruit more platelets and release mediators that connect hemostasis to inflammation and repair.
Coagulation stabilizes the seal
Thrombin-generated fibrin reinforces the plug and creates a temporary matrix for migrating cells.
Early cells decontaminate
Neutrophils remove microbes and damaged material but can extend tissue injury if activation is excessive or prolonged.
Clearance prepares the handoff
Macrophages phagocytose debris and dying neutrophils while changing mediator output toward growth, angiogenesis, and repair.
Surface cells migrate and divide
Keratinocytes or organ-specific epithelial cells move across a provisional substrate and proliferate to restore barrier continuity.
Capillaries restore supply
Endothelial sprouting and later vessel maturation provide oxygen and nutrients to metabolically active granulation tissue.
Matrix-producing cells expand
Fibroblasts migrate, proliferate, and deposit fibronectin, collagen, proteoglycans, and other extracellular components.
Contraction reduces the gap
Some fibroblasts acquire contractile features and mechanically draw wound edges inward under tissue-specific cues.
Regeneration depends on surviving niches
Resident progenitors and intact architecture can restore specialized cells; extensive destruction shifts the balance toward scar.
Early matrix is replaced
Proteases and inhibitors coordinate degradation while collagen composition, organization, and cross-linking change.
Temporary supply is pruned
As demand falls, excess capillaries regress and surviving vessels mature, reducing the redness of granulation tissue.
Mechanical capacity rises slowly
Collagen alignment and cross-linking increase tensile strength over months, but repaired tissue may not reach its original properties.
Repair can overshoot
Persistent fibroblast activation and matrix deposition can distort tissue architecture, restrict movement, or impair organ function.
Healing can stall
Infection, ischemia, pressure, edema, neuropathy, hyperglycemia, repeated trauma, malnutrition, smoking, and medicines can maintain nonhealing loops.