Figure 3.

Scheme of different stages of cutaneous wound repair in rats: A, B and C: The first 12- 24 hours after injury is defined by the platelet plug and blood clot formation. Inflammatory cells invade the blood clot triggering acute inflammatory response. Furthermore, blood elements and vasoactive amines extravasate from locally damaged blood vessels within the dermis. Vascular permeability is temporarily increased to allow neutrophils, platelets and plasma proteins to infiltrate the wound. Coagulation then occurs as platelets aggregate with fibrin. D, E and F: After 48–72 h, macrophages replace polymorphonuclear neutrophils as the principal inflammatory cell. Together, polymorphonuclear neutrophils and macrophages remove debris from the wound, release growth factors, and begin to reorganise the extracellular matrix. The proliferation phase begins at about 72 h as fibroblasts, recruited to the wound by growth factors released by inflammatory cells, begin to synthesise collagen. The new tissue is called granulation tissue. Keratinocytes proliferate at the wound edge and migrate down the injured dermis and above the provisional matrix. 1–2 week after injury the wound is completely filled with granulation tissue. Fibroblasts have transformed into myofibroblasts, leading to wound contraction and collagen deposition. The wound is completely covered with a neoepidermis. Modified from Steven R. Beanes et el., 2003.

Barati et al. Diagnostic Pathology 2013 8:120   doi:10.1186/1746-1596-8-120
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