Fast Five Quiz: What Do You Know About Acne?

William James, MD; Robert A. Schwartz, MD, MPH

Disclosures

October 05, 2016

The pathogenesis of acne vulgaris is multifactorial. The key factor is genetics. Acne develops as a result of an interplay of the following four factors:

1. Release of inflammatory mediators into the skin

2. Follicular hyperkeratinization, with subsequent plugging of the follicle

3. Follicular colonizationby Propionibacterium acnes

4. Excess sebum production

Research has shown that inflammatory responses actually occur before hyperkeratinization. Cytokines produced by CD4+ T cells and macrophages activate local endothelial cells to up-regulate inflammatory mediators, such as VCAM-1, intercellular adhesion molecule 1 (ICAM-1), and human leukocyte antigen (HLA)-DR in the vessels around the pilosebaceous follicle.

Follicular hyperkeratinization involves increased keratinocyte proliferation and decreased desquamation, leading to sebum- and keratin-filled microcomedones.

For more on the pathophysiology of acne, read here.

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