Most Popular in:
The Practical Use of Topical Oxygen
By: Peter T. Pugliese, MD
Posted: August 22, 2008, from the September 2008 issue of Skin Inc. magazine.
page 2 of 9
The pathogenesis of acne vulgaris is characterized by four factors. Follicular epidermal hyperproliferation is the first and is associated with subsequent follicular plugging. Next is the overproduction of sebum, with the third factor being the anaerobic bacteria Propionibacterium acnes (P. acnes), which is associated with the fourth factor, inflammation. The esthetician needs to appreciate these and know how to contend with each.
Epidermal hyperproliferation. Starting with the formation of adrenal androgen before puberty, the sebaceous follicle is triggered to proliferate and is followed by the plugging of the follicle. It is believed that the adrenal hormone dehydroepiandrosterone (DHEA) is the cause of this early manifestation of acne because the appearance of comedones is first noticed during this time. It requires the presence of androgen receptors in the follicle to form a comedone, since those individuals who lack these androgen receptors or who have poorly functioning androgen receptors do not get acne.
Sebum overproduction. The second factor, the overproduction of sebum, is also related to the action of androgens. For some reason, linoleic acid is low in the follicles of people with acne, while in those mostly acne-free, it is normal. As a result of excess sebum, acneic skin tends to be oily and appear shiny.
P. acnes and inflammation. The third factor, the presence of P. acnes, is also related to the fourth factor, inflammation. Oddly, P. acnes is rarely seen in early acne lesions—the microcomedo—and is generally not found until later. Keep in mind that this organism is anaerobic and resides deep in the follicle, away from atmospheric oxygen, which it does not like. It is the P. acnes that is responsible for the inflammation seen in acne, the papule and the pustule, as well as the cyst in cystic acne. As with many bacteria, P. acnes produces mediators of inflammation that start the cascade of inflammation propagated by white blood cells, the leukocytes.
Here is a new term for you to remember: the toll-like receptor. This is a primitive defense receptor on monocytes and neutrophiles (two kinds of white cells), which, when activated, leads the cell to produce cytokines, such as Interleuken 12 (IL-12), IL-8 and tumor necrosis factor (TNF). In addition, IL-1a is also present and may be a contributing factor. Now, if you are not familiar with cytokines, you might say, “So what?”