Acne Awareness

Causes of Acne (Etiology)

Acne vulgaris has its origin in the pilosebaceous units in the dermis.  These units, consisting of a hair follicle and the associated sebaceous glands, are connected to the skin surface by a duct (the infundibulum) through which the hair shaft passes.  On the smooth skin of the body, the hair may be very fine or entirely absents.  Because the sebaceous glands are most common on the face, back, and chest, acne tends to occur most often in these areas.  The sebaceous glands produce sebum, a mixture of fats and waxes, which maintains hydration of skin and hair.  The sebum passes to the skin surface through the infundibulum and then spreads over the skin surface to retard water loss.

At puberty there is an increase in the production of androgenic hormones in both sexes.  The increasing influx of circulatory testosterone is taken up by the sebaceous gland and converted by an enzyme, 5-alpha-reductase, to dihydrotestosterone, which is considered to be the tissue androgen responsible for the acne problem.  The sebaceous glands, under the influence of increased androgen levels, increase in size and activity producing larger amounts of sebum.  At the same time there is increased keratinization of the follicular walls.  This increased keratinization causes mechanical blockage of the sebum flow, resulting in dilation of the follicle and entrapment of sebum and cellular debris.  This lesion is a microcomedo, the initial pathologic change.

Androgens are the major stimulus to sebaceous gland development and sebum secretion.  However, patients with acne do not necessarily have higher androgen levels.  It is theorized that acne-prone patients have increased end-organ sensitivity to normal level of androgens, facilitating hypertrophic changes.

Exogenous sources of corticosteroids, both systemic and topical (Rx and OTC), may also induce the hypertrophic changes by sensitizing the follicle and producing "steroid acne".  These lesions are characterized by uniform red papules succeeded by closed comedones and finally open comedones.

Oral contraceptives with high androgenic activity also have been implicated in the production of acne.

Various drugs are known to precipitate acne eruptions, especially in individuals over age 25.  These include bromides, ethionamide, haloperidol, halothane, iodides, isoniazid, lithium, phenytoin, and trimethadione.  Cobalt irradiation and hyperalimentation (TPN) therapy also have been implicated. (2)