MDacne
Acne is basically caused by the interplay of a genetic tendency, hormonal changes (increased sensitivity to androgens or increased androgens) and external triggers. Acne vulgaris is thought to have a familial cause in half of the cases. Identical (monozygotic) twins show the same tendency for acne; however, dizygotic twins do not show the same risk for acne.
Acne is not an infectious disease. Today, it is recognized as an inflammatory process in which the skin overreacts to a special bacterium, Propionibacterium acnes. (p. acnes) that lives in our sebaceous glands. (skin oil glands).
The acne bacteria break down the triglycerides in the sebum break down to free fatty acids. These free fatty acids attract inflammatory cells and induce the ductal epithelium to secrete pro-inflammatory cytokines (interleukin [IL]-1, IL-6, IL-8, IL-10, IL-12 and tumour necrosis factor alpha [TNFα]).
The inflammatory reaction continues by means of a type IV immune reaction to one or more antigens in the follicle. This inflammatory process causes hyperkeratinization of the opening of the sebaceous gland, leading in turn to a keratin plug (the comedone). Further proliferation of the bacteria in the clogged sebaceous gland, with the progression of the inflammatory process, leads to the typical red acne pimple.
In summary, acne is caused by a complex interplay that involves increased sensitivity to androgens and increased androgen levels, changes in sebum lipid composition, P. acnes overgrowth, and local pro-inflammatory cytokines that cause epithelial hyperproliferation.
Read more:
New finding in acne pathogenesis
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