Acne is a common skin disease, typically affecting 60 percent of the population at any time. Most of the acne is seen in adolescents; however there can be a second recurrence of acne in people in their late twenties and early thirties, mostly in women.
Acne is a systemic inflammatory disease, and may be exacerbated in puberty due to the release of hormones, as well as a pro-inflammatory diet. Dermatologists classify the primary event in acne as the formation of the microcomedo, i.e., the clogging of a follicle with what is believed to be non-inflamed lesions caused by retention hyperkeratosis. However, the hyperkeratinization of the follicle is not the primary event, but the result of the release of pro-inflammatory cytokines (such as interleukin-1) in the follicular wall, resulting in increased cohesion of the cells and a clogged pore. There also may be activation of the pro-inflammatory transcription factor NFκB secondary to oxidative stress in the follicle. In addition, fatty acids within the follicle may be pro-inflammatory and may mimic active messengers similar to the pro-inflammatory platelet-activating factor.
Another causative event is the stretching of the follicular wall, caused by the impaction of exfoliated keratinocytes. This stretching can release phospholipids from the cell walls, which are broken down into pro-inflammatory fatty acid messengers. Arachidonic acid also plays a part in the inflammation as well.
Dermatologists typically use a grading system to categorize the various stages of the acne lesion. Grade One, the microcomedone, can appear as whiteheads or blackheads. Grade Two is a papule, i.e., a small pink inflamed bump. Grade Three is a pustule lesion with more visible inflammation than papule. Grade Four is a nodule or large painful solid lesion that extends deep into the skin. Grade Five is an inflamed lesion, very large and painful. It should be noted that as the follicle becomes impacted, it is often secondarily infected with propionibacteria.