The changes of stratum corneum interstices and calcium distribution of follicular epithelium of experimentally induced comedones (EIC) by oleic acid.

Abnormal follicular keratinization is important for comedo formation in acne, but the precise mechanism is not known. A recent report about acne vulgaris suggested that an impaired water barrier function may be responsible for comedo formation, since the barrier dysfunction is accompanied by hyperkeratosis of the follicular epithelium. Furthermore, the integrity of the water barrier is crucial for the maintenance of the epidermal calcium gradient. Yet stratum corneum intercellular lipid structures, a major factor of the skin barrier function, and calcium distribution in the follicular epithelium of comedones, were not reported. To see SC intercellular lipid and calcium distribution of the follicular epithelium of comedo by electron microscopy, we applied oleic acid on the inner surface of the ear of New Zealand white rabbits to induce comedones, and then we obtained specimens and performed osmium and ruthenium tetroxide postfixation and calcium ion-capture cytochemical procedure. We found incomplete lipid bilayer structures, prominent dilatation of lacunar domains and the loss of follicular epidermal calcium gradient in experimentally induced comedones. From our results, we suggest that the permeability barrier disruption in oleic-acid-applied follicular epithelium can be induced by the changes of SC intercellular membrane structures and lacunar dilatation, and the calcium gradient is lost, so follicular epithelial proliferation and hyperkeratosis can be induced and then comedo formation occurs.