Abstract
Chemically induced choracne may be used as a model to study the factors involved in the development of comedogenesis. Even though the activating agents in chloracne and acne vulgaris are obviously entirely different, it seems probable that the biochemical events activated in the development of comedogenesis in these two syndromes are identical. 2,3,7,7-Tetra-chlorodibenzo-p-dioxin (TCDD) is the most potent known chloracnegen discovered to date. As such, it is the most potent comedogenic agent known. In contrast to humans, in whom the skin and especially the sebaceous follicles are the primary target organs to express toxicity following exposure to this chemical, skin of laboratory animals generally does not exhibit a similar sensitivity. Known exceptions are skin of the inner surface of the rabbit ear, facial skin of monkeys, and skin of hairless, but not of haired, mice. Low-dose application of TCDD stimulates epidermal/epithelial hyperplasia/hyperkeratinization in the hairless, but not haired, mice. We have used the skin of congenic haired and hairless mice (which differ by a single mutation at the hr locus) as a model in in vivo and in vitro studies to analyze the mechanisms involved in TCDD-induced changes in skin. This paper will discuss the advantages and drawbacks of this model for studies of comedogenesis.