The proliferation stage consists of angiogenesis, re-epithelialization, and granulation tissue formation. The main functions of macrophages are phagocytosis of pathogens and cell debris as well as the release of growth factors, chemokines and cytokines which will push the wound healing process into the next stage. Monocytes are attracted by the inflammatory mediators and differentiate into macrophages soon after they migrate into the wound site. Several mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) are released by the neutrophils in order to amplify the inflammatory response. In the inflammatory phase, polymorphonuclear neutrophils (PMNs) are the first inflammatory cells that are recruited to the inflamed site and are present there for 2–5 days. Platelets induce the vasoconstriction in order to reduce blood loss followed by secretion of a number of inflammatory factors including serotonin, bradykinin, prostaglandins and most importantly histamine, which activate the inflammatory phase. The provisional wound matrix serves as a scaffold structure for the migration of leukocytes, keratinocytes, fibroblasts and endothelial cells. The exposed collagen also triggers platelets to begin secreting cytokines and growth factors. Clotting factors from the injured skin (extrinsic system) and aggregation of thrombocytes or platelets after exposure to collagen fibers (intrinsic system) are activated. These changes occur immediately after injury and are completed within hours. The first stage is hemostasis, which relates to the clotting cascade and the formation of a provisional wound matrix. In these four stages, there are complicated interactions within a complex network of pro-fibrotic and anti-fibrotic molecules, such as growth factors, proteolytic enzymes and extracellular matrix (ECM) proteins. Wound healing can be divided into four stages: hemostasis, inflammation, proliferation and tissue remodeling. Full size image The physiology of wound healing in the skin
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