New Insights into the Pathogenesis of Psoriatic Arthritis

Psoriatic arthritis (PsA), a complex cutaneous and musculoskeletal disorder, displays great heterogeneity in disease onset and clinical course. 1 Distinct clinical features in PsA were outlined by Moll and Wright in 19732 and disease mechanisms differing from those identified in rheumatoid arthritis (RA), were discovered over the following50 years.3 Identification of targets in the tumor necrosis factor (TNF), IL-23-IL-17,and janus kinase/signal transducer and activation of transcription (JAK-STAT) pathways unleashed major advances in drug development and improved treatment outcomes.4 Despite these advances, disease remission is rare, and many patients cycle through biologic and targeted synthetic agents without achieving a deep treatment response. In part, this therapeutic challenge is related to the presence of inflammation in multiple disease domains in a single patient, including the peripheral joints, axial
skeleton, skin, nails, enthesitis, and dactylitis.