Abstract
The pathogenesis of hidradenitis suppurativa (HS) or acne inversa is not completely understood. Recent research has led to greater insight into the mechanisms involved in the disease. The primary defect in HS pathophysiology rests with the hair follicle. Follicular occlusion, followed by follicular rupture, and a foreign body-type immune response are necessary conditions for the development of clinical HS. A specific genetic signature and environmental factors, such as cigarette smoking, microbial colonization, and adiposity, all contribute to the HS phenotype. Translational research focused on the inflammatory mechanisms involved in HS is needed to develop novel therapeutic options for this debilitating disease.
Published Version
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