The microvessels in hypertrophic scars, keloids and related lesions: a review.
The healing of a deep surface wound in humans begins with the formation of granulation tissue and includes a marked microvascular regeneration, initially in an inflammatory milieu. The inevitable sequel is usually a hypertrophic scar or keloid in which there is significant microvascular occlusion. The occlusion begins in the granulation tissue and is the result of an excess of endothelial cells. Several other examples of fibroses contain significant microvascular occlusion. The evidence demonstrates that hypertrophic scars and keloids are hypoxic, undoubtedly due to the microvascular occlusion. Hypoxia may stimulate excessive production of collagen, which forms the bulk of these lesions, from fibroblasts and myofibroblasts. The origin of the new fibroblast remains undetermined. The current evidence suggests it is probably not the pericyte. Resident or peripheral fibroblasts, endothelial cells or undifferentiated cells from the growing tips of microvessels are possibilities. Differential degeneration, or apoptosis, of the fibroblasts, pericytes and microvessels occurs from granulation tissue through hypertrophic scarring. Compartmentalization of fibroblasts between lateral microvascular branches probably accounts for nodule formation. Differential degeneration of the lateral microvessels may account for increases in collagen nodule growth and ultimate size. Hypertrophic scars and keloids may be resolved through light topical pressure maintained over time. Under such treatment, fibroblasts, pericytes and endothelial cells degenerate, probably at a rate greater than that which occurs normally. As degeneration or apoptosis continues the nodules and scar become more avascular and more hypoxic, prompting fibroblast death and release of lysosomal enzymes important for maturation. An alternative treatment, particularly of the granulations, would be to control excessive endothelial (microvascular) or fibroblast proliferation or collagen synthesis. To this end, determination of endothelial or fibroblast cell phenotype for possible antibody targeting may be mandatory.
Kischer
C W
CW
Department of Anatomy, University of Arizona, College of Medicine, Tucson.
D002921:Cicatrix / Q000473:pathology* / Q000628:therapy; D006801:Humans; D007627:Keloid / Q000473:pathology*; D008833:Microcirculation / Q000473:pathology / Q000648:ultrastructure; D014945:Wound Healing