What is the pathogenesis of acne vulgaris?

Updated: Jan 30, 2020
  • Author: Ginard I Henry, MD; Chief Editor: Gregory Gary Caputy, MD, PhD, FICS  more...
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In discussing the pathogenesis, the most common pathophysiologic condition is believed to be that of increased end-organ sensitivity to androgen stimulation. The organism Pacnes also has been demonstrated to produce a lipase that hydrolyses lipases to free fatty acids. These free fatty acids have been shown to produce inflammation in comedones when applied to rabbit ears or when injected intradermally in humans.

Additionally, P acnes may have complement activation contributions, further increasing the inflammation. Additionally, a pathophysiologic cycle occurs with respect to the keratinized layer of the sebaceous duct. In normal uninflamed ducts, the keratinized epithelium is loosely adherent and easily separates up to the skin surface as it is regenerated from deeper layers. In the acne condition, these follicular cells are cohesive and coalesce to form retention hyperkeratosis, a physical obstruction to the pilosebaceous unit. This leads to back pressure and the leakage of sebum and bacteria into the dermis across the epithelialized surface, stimulating the inflammatory response.

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