Patofysiologi

The initial step in the development of acne is the formation of the microcomedo. [13] Follicular keratinocytes that exhibit increased cohesiveness do not shed normally, leading to retention and accumulation. Androgens stimulate enlargement of sebaceous glands and increased sebum production, and the abnormal keratinaceous material and sebum collect in the microcomedo. This leads to a build-up of pressure, and whorled lamellar concretions develop. At this stage, a non-inflammatory comedo may be seen clinically.

This micro-environment allows the proliferation of P acnes, which is part of the normal flora of follicles. This gram-positive rod has low virulence but is capable of metabolising triglycerides and releasing free fatty acids. This metabolism, as well as its ability to activate complement, produces pro-inflammatory mediators, including neutrophil chemo-attractants. [14]

With increased pressure and recruitment of inflammatory mediators, the microcomedo may rupture and release immunogenic keratin and sebum, thus stimulating an even greater inflammatory response. Depending on the specific inflammatory cells present, suppurative pustules or inflamed papules, nodules, or cysts may develop. If a sufficient amount of inflammation and tissue damage results, post-inflammatory hyperpigmentation and scarring may result.