Comedone formation occurs when the pattern of keratinization inside the sebaceous follicle changes. Within the keratinocytes, these changes include the production of different keratins and a reduction in the number of lamellar granules [5]. There is also an increase in mitotic activity [6]. As a result the keratinocytes do not desquamate properly and the follicular duct is blocked. It is not known what causes these changes, but the result is a microcomedone. As further keratinized material accumulates, the follicle becomes visible from the surface as a closed comedone, or whitehead (Fig. 1). As more material accumu- |

lates, the follicle distends and open comedones, also know as blackheads are formed. The ^

black color is attributable to the oxidation of lipids as they reach the skin's surface. The ^

test methods to assess comedogenesis are designed to quantify the hyperkeratotic plugs.


The hyperkeratotic plug results in sebum accumulating in the follicilar duct and the sebaceous gland. This enables the anaerobic bacteria, P. acnes, to proliferate. The follicular

Figure 1 Examples of the different forms of comedones and acneform eruptions. (a) Closed and open comedones. (b) Papules. (c) Pustules.

duct will expand until it ruptures, releasing the bacteria and their metabolic products into the surrounding dermis. Both immunological and irritant reactions occur. In severe acne, elevated levels of anti-P. acnes antibodies are detected. Irritation may come from the fatty acids that are the result of sebaceous triglyceride digestion by bacteria. Certainly at the histological level, the classic signs of inflammation such as a neutrophilic infiltrate are observed. The consumer recognizes this as acne pustules and papules.

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