Abstract
T raditional surgery for hidradenitis suppurativa (HS) consists of en bloc wide excision followed by primary closure or healing by secondary intent. A simpler technique consists of careful unroofing, exploration, and debridement of the scars, abscesses, cysts, and complex sinuses that characterize HS. Elsewhere in the Journal, van der Zee et al show us how. The following comments are directed at why this technique (which van der Zee et al refer to as ‘‘deroofing’’) succeeds when simple ‘‘incision and drainage’’ fails. The material caught beneath the epidermis in HS is not simple purulent inflammatory debris. HS is the product of genetic, mechanical, hormonal, and dietary influences. Failure of terminal differentiation of infundibular keratinocytes leads to accumulations of adherent keratinocytes plugging the duct, microcomedo development in the upper follicle, and tight occlusion of the acroinfundibulum. A genetic weakness of the glycoprotein glassy membrane support of the infrainfundibular wall is postulated as the physical defect that predisposes the pilosebaceous follicle, under the pressure of centrifugal expansion within the infundibular canal, to lose its structural integrity. Follicular contents leak out, stimulating the innate immune system. Inflammatory mediators multiply, the reaction is further inflamed, the
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