The restoration of surface integrity and continuity of the skin after wounding, with a tissue strength approaching normal.
Phases of Wound Healing
Begins at the time of the wounding
Lasts 24-48 hours
Transient vasoconstriction caused by platelets via TXA-2 (Thromboxane A2). This slows blood flow to aid in hemostasis.
Platelets form thrombus.
Clotting factors are activated.
Vasodilation that is prostaglandin and histamine mediated
Increased blood flow supplies cells and substrates for wound healing
Macrophages and neutrophils remove necrotic tissue, debris, and bacteria
Macrophages secrete TGF-B which attracts fibroblasts
Lasts 2-4 weeks
Fibroblasts, attracted by TGF-B, move into the wound
Fibroblasts produce collagen and extracellular matrix to replace the platelet/fibrin plug
During the proliferative phase, the collagen is randomly laid down. This changes in the remodeling phase.
Macrophages and fibroblasts replace the random collagen with more orderly and extensively cross-linked collagen (mostly Type I) as in normal skin.
The scar will achieve 80% of the strength of regular skin.
Local Factors that Impede Wound Healing
Systemic Factors that Impede Wound Healing
Smoking and Delayed Healing
Smoking causes vasoconstriction by nicotime, which reduces blood to the area.
Additionally, it causes atherosclerosis.
Additionally, the carbon monoxide shifts oxyhemoglobin curve to the left, impairing oxygen delivery to the tissues.
Histologically, increased amounts of collagen and ECM, but not organized.
Histologically, whorls of fibroblasts arranged around vessels. May get worse with surgery.
Heavy genetic influence.
Often affects darker-skinned patients.