Up to 30% of people with psoriasis develop psoriatic arthritis, and nobody can yet say which ones. This review argues the plaque is not just an inflamed patch of skin but a source of immune cells that reach the joint: T cell clones and myeloid precursors shared between skin and synovium. But arrival alone does not cause arthritis. What decides it is the stromal niche, in particular synovial fibroblasts, which act as gatekeepers.
In 670 biologic-naïve patients with active psoriatic arthritis, the oral TYK2 inhibitor deucravacitinib achieved ACR20 in 54.2% versus 34.1% on placebo at week 16, with gains in skin, function and quality of life sustained to week 52. But the pre-specified radiographic endpoint was negative, the testing hierarchy broke at enthesitis, and the claim of structural protection rests on a post hoc reanalysis.
Skin disease in PsA is not a side note to joint management — specific phenotypes (nail, scalp, palmoplantar, inverse) carry their own diagnostic and prognostic weight, and discordant skin/joint responses are a leading driver of complex-to-manage PsA. This review maps the phenotypes, the shared IL-23/IL-17/TNF pathogenesis, and how drug-class selection should follow the cutaneous pattern in front of you, not just the joint count.
A 2026 review of the psoriatic arthritis pipeline, organised around two vectors — greater precision (dual IL-17A/F blockade, engineered molecular formats, selective oral TYK2 inhibition, oral IL-23R antagonism) and moving earlier to intercept the psoriasis-to-PsA transition — alongside metabolic and dual-targeted strategies.