THE HAIRLESS MOUSE and PHOTOAGING

Photoaging, a term coined in the mid 1980s (Kligman and Kligman, 1986) to denote the gross and microscopic skin changes resulting from chronic sun exposure, is not a new concept. The first documentation of these changes came from the late 19th century dermatologists Unna and Dubreuilh who recognized the devastating effects of sunlight when they compared the skin of farmers and sailors to that of indoor workers. Because severely actinically damaged people look far older than their chronologic age with their multitudes of wrinkles and excrescences, their yellowed, nodular, leathery skin, the term “premature aging” was long used to describe the condition. By contrast, photophobes in their nineties can have smooth, unblemished skin showing only some laxness and deepening of expression lines. Recent research has shown that photoaged and chronically aged skin are distinctly different (Braverman and Fonferko, 1982a,b; Lavker, 1979; Gilchrest. 1984). Contr,asts between the two conditions have been reviewed by Kligman (1989). Underlying the visible aspects of photoaging is damage to the elastic fibers, collagen and glycosaminoglycans (GAG)* of the dermis. The microvasculature and other structural elements of the skin suffer as well. The evolution of these changes requires decades of sun exposure (Kligman, 1969). Aside from ethical reasons, systematic study of photoaging in humans would be impractical. For example, Shellow and Kligman (1968) failed to produce elastosis in humans after UV-B irradiation for up to a year. Thus, an animal model, in which the process is accelerated, is desirable.