IN THIS ISSUE of the Archives, Suetake et al1 provide detailed results about barrier function in various types of healing wounds. While these data per se are of considerable interest, the authors also report that an abnormal permeability barrier persists over hypertrophic scars and keloids, long after reepithelialization of wounds is complete. Whereas their results do not address the potential mechanisms for the persistent functional defect, 3 possible explanations, which need not be mutually exclusive, should be considered: (1) a primary defect in the dermis of patients with hypertrophic scars and keloids leads to signals that negatively influence barrier homeostasis; (2) the excess collagen and glycosaminoglycans found in the dermis of keloids impede the ability of key nutritional ingredients, metabolic precursors, and/or growth factors to reach the epidermis; and (3) a defect in the epidermis leads to a persistent barrier abnormality, resulting in a sustained release of signaling molecules
Elias PM, Ansel JC, Woods LDC, Feingold KR. Signaling Networks in Barrier Homeostasis: The Mystery Widens. Arch Dermatol. 1996;132(12):1505–1506. doi:10.1001/archderm.1996.03890360097017
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