Pathophysiology

O The development of acne lesions results from four pathogenic factors: excess se-

bum production, keratinization, bacterial growth and inflammation. '

The pilosebaceous unit of the skin consists of a hair follicle and the surrounding sebaceous glands. An initial acne lesion called a comedo forms when there is a blockage in the pilosebaceous unit.8

Sebum is released by the sebaceous glands and naturally maintains hair and skin hydration. An increase in androgen levels, especially during puberty, can cause an increase in the size of the sebaceous gland and the production of abnormally high levels of sebum within those glands. This excess sebum can result in plugged follicles and acne formation.

Keratinization, the sloughing of epithelial cells in the hair follicle, is also a natural process. In acne, however, hyperkeratinization occurs and causes increased adhesiveness of the sloughed cells. Accumulation of these cells clogs the hair follicle, blocks the flow of sebum and forms an acne lesion called an open comedo or "blackhead."

Propionobacterium acnes (P. acnes), an anaerobic organism , is also found in the normal flora of the skin. This bacteria proliferates in the mixture of sebum and ker-atinocytes and can result in an inflammatory response producing a closed comedo or "whitehead." More severe acne lesions such as pustules, papules, and nodules also form with inflammatory acne and result in significant scarring if treated inadequately (see Fig. 65-2 for various stages of acne development).

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