keloids are aggressively raised dermal lesions resulting from an abnormal wound healing process. Unlike hypertrophic scars, in which the raised dermal lesions stay within the confines of the initial wound, keloids grow beyond the original wound margins. Histopathologically, keloids are characterized by keloidal collagen (thick hyalinized eosinophilic collagen fibers) with a horizontal, tongue-like advancing edge in the dermis. Keloids often begin months, perhaps up to one year, after a skin injury or inflammatory process, such as acne vulgaris, folliculitis, chickenpox, or vaccination. The pathogenesis of keloids is complex. Accumulating data implicates both local factors in the skin (tissue tension, cytokine and growth factors/receptors and their signaling pathways) as well as a genetic predisposition/contribution, including epigenetic influences. In this talk, I will summarize the pathogenesis of keloids and the pathogenesis-based treatment for keloids.

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