Acne, Oil, Bacteria and Hormones

How does Acne form ?

The exact mechanism of the development of an inflammatory acne lesion is poorly understood and unfortunately complex. With some basic high school molecular biology and microbiology, it can be appreciated and slightly understood. The formation of acne and its precursors begins with hyperstimulation of sebocytes (oil gland cells) and keratinocytes (skin cells) by androgens (male sex hormones) during puberty leading to the overgrowth and expansion of sebaceous glands and the seborrhoea (oily skin) that characterizes acne (1,2). Males suffer more severe acne due to higher levels of androgens, however, females also have androgens, which can be elevated due to access fat, as fat and cholesterol is the precursor molecule to hormones, such as androgens.

The increased sebum (oil) production leads to a deficiency of specific fatty acid, linoleic acid within the hair follicle, leading to a decrease in its barrier and protection function. This is believed to promote and maintain the growth of the human commensal (normal growing bug on our skin) bacterium, Propionibacterium acnes. This organism colonizes the follicular duct, that directs oil to the surface of the skin and contributes to the development of inflammation by stimulating immune cells and skin cells which thereby recruit other immune that kill bacteria. These cells begin producing the ‘inflammatory’ lesions mentioned above.

Overgrowth of the skin cells lining the follicle wall and reduced detachment of them, due to increased skin cell cohesion, leads to an accumulation of dead skin cells within the follicle during comedogenesis (3,4). Increased levels of the immune hormones and signals drive this process, that can also be produced from human skin cells. These signals are stimulated to be produced by skin cells when induced by P acnes, and other bacteria in order to protect from bacterial invasion. In addition, P acnes induces the production of other mediators, that subsequently diffuse into the surrounding dermis, causing the non-specific activation of other immune cells, leading to inflammation and disruption of the follicle. The follicle is subsequently invaded by T cells, which release inflammatory cytokines that result in sebum, microorganisms and keratin (skin) to be released into the dermis, damaging the skin and leading to acne like skin changes (5).

Abnormal Hormones and Acne

Women who have acne beyond there teenager years, and usually have associated pre-menstrual abnormalities and odd and irregular menstrual periods, with male features, hirsutism, may have polycystic ovary syndrome. Acne in people with abnormal hormones has numerous characteristics. Theres include persistent acne into adulthood, acne worsening before menstrual periods, abnormal cycles and menses, male features and difficulties in becoming pregnant. Acne in these people may be of any of the tupes, but usually involves the lower face, infront of the ears, jaw line and neck

References:

1. Thiboutot D, Harris G, Iles V, et al. (1995) Activity of the type 1 5 alpha-reducatse exhibits regional differences in isolated sebaceous glands and whole skin. J Invest Dermatol 105:209-214.

2. Gollnick H, Cunliffe WJ, Berson D, et al. (2003) Management of acne: a report from a Global Alliance to Improve Outcomes in Acne. J Am Acad Dermatol 49:Suppl:S1-S37.

3. Kligman AM. (1974) An overview of acne. J Invest Dermatol 62:268-287.

4. Knaggs HE, Holland DB, Morris C, et al. (1994) Quantification of cellular proliferation in acne using the monoclonal antibody Ki-67. J Invest Dermatol 102:89-92.

5. Ingham E, Eady EA, Goodwin CE, et al. (1992) Proinflammatory levels of interleukin-1a-like bioactivity are present in the majority of open comedones in acne vulgaris. J Invest Dermatol 98:895-901.