Figure 1-. Progression of Acute Wound Healing in Skin.

(A) Immediately after wounding, a fibrin clot forms to plug the damaged tissue. (B) For several days after injury, local release of tissue damage signals leads to the recruitment of neutrophils and monocytes/macrophages from circulation to prevent infection and phagocytose dead cells and debris. Recent evidence suggests that nearby tissue-resident lymphocytes can also mobilize to wound margins during this time period. (C) As inflammation resolves, keratinocytes at the wound margins proliferate, migrate, and differentiate to re-epithelialize the injury site and restore barrier integrity. Granulation tissue forms in the wound bed and is vascularized by angiogenesis of nearby blood vessels. Myofibroblasts accumulate in granulation tissue and contract to draw the wound closed. The influx of lymphocytes into the wound reaches its peak, and macrophage polarization shifts from pro-inflammatory to pro-reparative states. (D) After the wound closes, cellularity of the wound bed decreases and a scar forms through a combination of collagen deposition, cross-linking, and remodeling. This process strengthens the wound site at the expense of regenerating normal dermis.