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Our current understanding of the pathogenesis of the disease is incomplete. This review aims to identify available treatment options in HS and discuss the pharmacological mechanisms through which such agents function. Identifying common pathways may inform our understanding of the pathogenesis of HS as well as identify future therapeutic targets. The pharmacological mechanisms implicated in topical therapies, antibiotic, hormonal, systemic immunomodulatory and biologic therapies for HS are discussed. Significant differences exist between agents and implicated pathways in therapy for mild and severe disease. This is an expression of the possible dichotomy in inflammatory pathways (and treatment responses) in HS. Studies involving monoclonal antibodies provide the greatest insight into what these specific mechanisms may be. Their variable levels of clinical efficacy compared with placebo bolsters the suggestion that differential inflammatory pathways may be involved in different presentations and severity of disease. Nuclear factor kappa B (NF-\u03baB), tumor necrosis factor (TNF)-\u03b1 and other innate immune mechanisms are strongly represented in treatments which are effective in mild to moderate disease in the absence of scarring or draining fistulae, however complex feed-forward mechanisms in severe disease respond to interleukin (IL)-1 inhibition but are less likely to respond to innate immune inhibition (through NF-\u03baB or TNF-\u03b1) alone. It is unclear whether IL-17 inhibition will parallel TNF-\u03b1 or IL-1 inhibition in effect, however it is plausible that small molecule targets (Janus kinase1 and phosphodiesterase 4) may provide effective new strategies for treatment of HS.<\/jats:p>","DOI":"10.1177\/2040622319830646","type":"journal-article","created":{"date-parts":[[2019,3,1]],"date-time":"2019-03-01T04:30:54Z","timestamp":1551414654000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":70,"title":["Topical, systemic and biologic therapies in hidradenitis suppurativa: pathogenic insights by examining therapeutic mechanisms"],"prefix":"10.1177","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5042-3632","authenticated-orcid":false,"given":"John W.","family":"Frew","sequence":"first","affiliation":[{"name":"Laboratory of Investigative Dermatology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jason E.","family":"Hawkes","sequence":"additional","affiliation":[{"name":"Laboratory of Investigative Dermatology, The Rockefeller University, New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James G.","family":"Krueger","sequence":"additional","affiliation":[{"name":"Laboratory of Investigative Dermatology, The Rockefeller University, New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2019,3,1]]},"reference":[{"key":"bibr1-2040622319830646","doi-asserted-by":"publisher","DOI":"10.12788\/j.sder.2017.017"},{"key":"bibr2-2040622319830646","doi-asserted-by":"publisher","DOI":"10.1111\/bjd.16101"},{"key":"bibr3-2040622319830646","doi-asserted-by":"publisher","DOI":"10.1111\/bjd.15441"},{"key":"bibr4-2040622319830646","doi-asserted-by":"publisher","DOI":"10.1001\/jamadermatol.2014.691"},{"key":"bibr5-2040622319830646","doi-asserted-by":"publisher","DOI":"10.1111\/bjd.14038"},{"key":"bibr6-2040622319830646","doi-asserted-by":"publisher","DOI":"10.1111\/jdv.12966"},{"key":"bibr7-2040622319830646","doi-asserted-by":"publisher","DOI":"10.2147\/CCID.S93619"},{"key":"bibr8-2040622319830646","author":"Frew JW","year":"2018","journal-title":"F1000Res"},{"key":"bibr9-2040622319830646","doi-asserted-by":"publisher","DOI":"10.1080\/13543784.2018.1412430"},{"key":"bibr10-2040622319830646","doi-asserted-by":"publisher","DOI":"10.1080\/09546634.2017.1395806"},{"key":"bibr11-2040622319830646","doi-asserted-by":"crossref","unstructured":"Frew JW, Hawkes JE, Krueger JG. 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