Acne Vulgaris Facts And Treatments

Acne vulgaris is a common skin disease that affects 60-70% of Americans (acne vulgaris could be seen as a disease of Western civilization, according to Dr. Loren Cordain) at some time during their lives. Twenty percent will have severe acne, which results in permanent physical and mental scarring. Acne vulgaris is American’s most common disease and is characterized by noninflammatory, open or closed comedones and by inflammatory papules, pustules, and nodules. Acne vulgaris affects the areas of skin with the densest population of sebaceous follicles; these areas include the face, the upper part of the chest, and the back.

Pathophysiology

The pathogenesis of acne vulgaris is multifactorial. The key factor is genetics.If both parents had acne, 3 of 4 children will have acne. If 1 parent had acne, then 1 of 4 of the children will have acne. However, similar to other genetic conditions, not every family will have the same pattern, with acne vulgaris sometimes skipping generations. What is inherited is the propensity for follicular epidermal hyperproliferation with subsequent plugging of the follicle. Additional aggravating factors include excess sebum, the presence and activity of Propionibacterium acnes, and inflammation.

Retention hyperkeratosis is the first recognized event in the development of acne vulgaris.The exact underlying cause of this hyperproliferation is not known. Currently, 3 leading hypotheses have been proposed to explain why the follicular epithelium produces cells at a rapid rate that are retained in individuals with acne.

First, androgen hormones have been implicated as the initial trigger.Comedones, the clinical lesion that results from follicular plugging, begin to appear around adrenarche in persons with acne in the T-zone area. Furthermore, the degree of comedonal acne in prepubertal girls correlates with circulating levels of the adrenal androgen dehydroepiandrosterone sulfate (DHEA-S).Additionally, androgen hormone receptors are present in sebaceous glands; individuals with malfunctioning androgen receptors do not develop acne.

Excess sebum is another key factor in the development of acne vulgaris. Sebum production and excretion are regulated by a number of different hormones and mediators. In particular, androgen hormones promote sebum production and release.Still, most men and women with acne have normal circulating levels of androgen hormones. An end-organ hyperresponsiveness to androgen hormones has been hypothesized. Androgen hormones are not the only regulators of the human sebaceous gland. Numerous other agents, including growth hormone and insulinlike growth factor, also regulate the sebaceous gland and may contribute to the development of acne.

P acnes is an anaerobic organism present in acne lesions. The presence of P acnes promotes inflammation through a variety of mechanisms. P acnes stimulates inflammation by producing proinflammatory mediators that diffuse through the follicle wall. Studies have shown that P acnes activates the toll-like receptor 2 on monocytes and neutrophils.Activation of the toll-like receptor 2 then leads to the production of multiple proinflammatory cytokines, including interleukins 12 and 8 and tumor necrosis factor. Hypersensitivity to P acnes may also explain why some individuals develop inflammatory acne vulgaris while others do not.

Inflammation may be a primary phenomenon or a secondary phenomenon. Most of the evidence to date suggests a secondary inflammatory response to P acnes. However, interleukin 1-alpha expression has been identified in microcomedones, and it may play a role in the development of acne.

United States

Acne vulgaris affects 60-70% of Americans at some time during their lives. Twenty percent have severe acne with permanent physical and mental scarring.

International

Persons of some races are affected more than others. Cystic acne is prevalent in the Mediterranean region from Spain to Iran.