The pathogenesis of hidradenitis suppurativa (HS) remains to be fully elucidated. Seminal clinical and translational investigations from the preceding 10 years have highlighted substantial variability in the contributors to inflammatory pathways involved in HS. These span from hormonal, metabolic, and microbial to genetic factors, each with potential flow on effects on immune cell polarization and subsequent clinically apparent inflammation. Understanding the heterogeneous drivers of HS and its progression may empower clinicians to take a more holistic approach in treatment planning, including addressing inflammatory comorbidities
therapeutic selection based on clinicopathological biomarkers
and appropriate patient counseling.