Hypertrophic scars and keloids: a review and new concept concerning their origin.
Hypertrophic scars and keloids are often the sequelae of deep injury to the skin of man. These lesions are characterized by excessive collage, in the form of discrete nodules, and an excess of microvessels, most of which are partially or totally occluded due to an excess of endothelial cells. The occlusion contributes to a measurable hypoxia. Hypertrophic scars and keloids contain elevated levels of fibronectin, immunoglobulins, other plasma proteins, histamine, type III collagen and chondroitin-4-sulfate. PO2 levels are lower than in normal skin and PCO2 levels are higher. Granulation tissue from deep injury contains predisposed patterns for nodule formation, excessive numbers of fibroblasts, high levels of fibronectin, demonstrates excessive synthesis of fibroblast products and microvascular occlusion. The likely candidate for stimulating excessive numbers of fibroblasts is fibrin polymer which persists in all granulation wounds. The stimulator for excessive synthesis activity is postulated to be related to a state of hypoxia. We propose that resolution of the lesions would be effected when microvascular patency is restored and PO2 levels returned to normal. Degradation of excess collagen would take place when collagenase and/or lysosomal hydrolases would be unmasked, activated or released. The etiology of the hypertrophic scar and keloid (and thus their resolution) is believed to be directly related to the quality of the microvessels and the leakage and deposition of blood products into the wound and lesion.
D002462:Cell Membrane / Q000648:ultrastructure; D002921:Cicatrix / Q000473:pathology*; D003094:Collagen / Q000032:analysis; D006801:Humans; D006984:Hypertrophy; D007627:Keloid / Q000473:pathology*; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D012867:Skin / Q000473:pathology* / Q000648:ultrastructure; D014945:Wound Healing
D003094:Collagen