The initial event in acne is the formation of comedo, a plug in the follicle, wh

ich is
termed open if a black tip is visible in the follicular orifice and closed if the
opening has not distended enough to be visible without magnification. Patients
(and their mothers) erroneously conclude that this black tip is due to dirt in t
he
follicle. Rather, it represents oxidized melanin and perhaps certain sebaceous
lipids (1,2). The earliest lesion is termed microcomedo and is clinically inappa
rent,
but is the lesion that gives rise to inflammatory acne. Microcomedones are best
visualized by harvesting them using cyanoacrylate glue (3). By this method, micr
ocomedones
are seen to be numerous on the skin of acne patients, and much less
prevalent and less robust on the skin of normal individuals.
Comedo formation begins with faulty desquamation of the follicular lining.
Instead of shedding as fine particles, the epithelium comes off in sheets that a
re
incapable of exiting through the follicular orifice, and hence a plug results. C
oncentric
laminae of keratinous material fill and distend the follicle. This process is
first detectable at the junction of the sebaceous duct and the follicular epithe
lium
and involves in distal cells later. The granular layer becomes prominent, tonofi
laments
increase, and lipid inclusions form the desquamated keratin (1,4).
Most comedones contain hairs, usually small vellus hairs, and the age of a
comedo may be reflected by the number of hairs that it contains (5). Terminal
hairs are almost never seen in comedones. It may be that the presence of a stout
hair in the follicle provides a mechanical opening that prevents comedo distenti
on.
Is it possible that the conversion of vellus to terminal hairs as acne patients
mature
is the explanation for the decrease in acne in the late teens and early 20s?
The cause of the faulty desquamation that leads to comedo formation is not
known. Comedones have been demonstrated before puberty, so activation of sebaceo
us
secretion cannot be the key event (1). Many compounds have been shown to
induce comedones in experimental systems (e.g., coal tar, sulfur, squalene, halo
genated
biphenyls, and cutting oils), but none are obviously relevant to the natural
course of acne formation (6 8). Two experimental systems exist for studying
comedo formation: the rabbit ear model and the backs of human volunteers.
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