The pathogenesis of hidradenitis suppurativa involves an interplay of genetics, hormones, infection, and social, immunological and mechanical factors. In terms of genetics, no single gene has been associated with the disease. However, familial occurrences of HS resembling an autosomal dominant-like inheritance pattern have been reported. As a result of the hormonal role, post-pubertal individuals seem to be mostly affected. There is a correlation between the disease in females and the onset of menarche. It is rarely seen before puberty or after menopause. Also, HS flares correlate with menstruation and are associated with an increased organ sensitivity to low levels of androgens, as there is no increased androgen production in HS. Antiandrogen methods of therapy have been shown to be effective forms of treatment in HS in both males and females (Margesson and Danby 2014).

Historically, bacterial infections were thought to be the cause of HS but there is now a general consensus that infection plays a limited role. It appears to have a role solely in the development of relapsing lesions as a secondary infection (Margesson and Danby 2015). If there is an acute worsening of HS or lack of usual response to therapy, a bacterial culture may be performed to evaluate for secondary infection.

HS, classified as a follicular disorder, involves the plugging/occlusion of the folliculopilosebaceous units in the skin. Immunologically, this leads to activation of the innate immune system. After the follicles are clogged, they rupture into the dermis with the contents released causing an inflammatory response. This response leads to abscess formation and may also allow secondary bacterial infection. As the abscesses heal and recur, fistulous tracts may form.

As a follicular disorder, HS is often associated with other follicular disorders in what is termed the “follicular occlusion tetrad.” Pilonidal cyst, dissecting cellulitis of the scalp and acne conglobata have established associations with HS and form the other three parts of the tetrad of follicular occlusion disorders. A patient with HS will typically have two of these disorders. It is also important to note that HS also carries an association with acne vulgaris as well as obesity and smoking.

The folliculopilosebaceous units are weak structurally in HS and are prone to rupture by trauma. This further contributes to the disease as a mechanical factor that accounts for the location of lesions in intertriginous areas. Social factors such as smoking, diet and the use of the drug lithium also contribute to HS by increasing follicular clogging. Obesity and nicotine have also been implicated specifically (Margesson and Danby 2015).