Wednesday, November 10, 2010

What Causes Acne? Part 2

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Although the underlying root cause of acne vulgaris is a genetic predisposition, the disease process has several components; one of which, is retention hyperkeratosis (the rapid production of skin cells retained within a follicle). The follicle we are referring to is what many people commonly know as a pore. It contains sebaceous glands (oil glands), and is lined with epithelial cells (skin cells). There are several popular hypotheses, which help us to understand what causes the acceleration of desquamated skin cells to build up within the follicle, creating follicular plugs.

The three hypotheses of retention hyperkeratosis have one common thread. Androgens. Androgens, are commonly known as male hormones such as testosterone, dihydroepiandrosterone (DHEA), dihydroepiandrosterone sulfate (DHEA-S).

In acne prone individuals, androgens initiate the process of retention keratosis. In addition, girls and boys may begin developing comedonal acne (plugged follicles) as early as age 6 (this is due to ongoing development within a region of the adrenal glands responsible for producing specific androgens). There is a correlation between the degree of comedones in prepubescent girls and their circulating DHEA-S levels. Finally, those with malfunctioning androgen receptors within their sebaceous glands are less likely to develop acne.

While the hypotheses give us insight, the exact cause of retention hyperkeratosis is unknown. Retention hyperkeratosis is one of several factors in the disease pathway of acne vulgaris.

Stay tuned for “What Causes Acne? Part 3”