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A significant statistical difference was found between the incidence of intraepithelial elastic fibers in keratoacanthoma and squamous cell carcinoma arising in actinic keratosis (P < 0.001). There was no significant difference when keratoacanthoma was compared to adenoid squamous cell carcinoma (P = 0.13) and de novo squamous cell carcinoma (P = 0.73). However, in keratoacanthoma intraepithelial elastic fibers were found in areas of pseudoepitheliomatous hyperplasia and in the central keratin plug, as well as in areas of infiltrating, peripheral keratinocytes. In adenoid squamous cell carcinoma and de novo squamous cell carcinoma, the intraepithelial elastic fibers were found only in areas of atypical epithelial cells at the margin of the neoplasm. Intracytoplasmic glycogen was found to be statistically more abundant in keratoacanthoma than in squamous cell carcinoma arising in actinic keratosis (P < 0.001), adenoid squamous cell carcinoma (P < 0.001), and in de novo squamous cell carcinoma (P < 0.001)

Sex hormone binding protein analyses were performed on six keloids, the adjacent skin, and on six simple scars. A high level of androgen binding (510 to 1149 Fm/mg of cytosol protein) was found in the keloids. The estrogen and progesterone binding activities were low. Para-keloid tissues were found to have androgen binding of 177 to 476 Fm/mg of cytosol protein. Once again, estrogen and progesterone binding activities were low. In six simple scars, androgen binding was less than 1/10 of that found in the keloids (37 to 60 Fm/mg of cytosol protein); estrogen and progesterone binding was so low that it was almost undetectable. We believe this data suggests that localized hyperandrogen metabolism may play a causal or at least contributory role in the pathogenesis of keloids.