Psoriasis frequently precedes psoriatic arthritis (PsA), delineating a tractable window for disease interception.This narrative review integrates mechanistic, imaging, and clinical evidence, together with expert interpretation, to examine whether effective treatment of psoriasis may modify the risk of PsA development.Converging immunopathogenic insights link skin and joint inflammation through interleukin (IL)-23/IL-17-driven pathways, enthesis-synovium crosstalk, and tissue-resident memory T-cell biology.Clinically, progression from psoriasis with arthralgia to PsA occurs in 20% of patients within 3 years, typically manifesting with peripheral, synovitis-predominant presentations.Imaging refines short-term risk stratification, with structural entheseal lesions, particularly erosions and new bone formation, representing the most consistent markers of transition.Observational data suggest that biologic therapies used for psoriasis may reduce PsA evolution, with the most consistent evidence for IL-23 pathway blockade.Metabolic factors, notably obesity and weight loss, further modify disease risk, underscoring the role of systemic inflammation and metabolic-immune crosstalk.Together, these findings support the biological plausibility of PsA prevention and justify ongoing interception trials in high-risk psoriasis populations defined by arthralgia and subclinical musculoskeletal inflammation.Robust longitudinal studies integrating biological, imaging, and pragmatic outcomes will be essential to establish causality and define scalable strategies to alter the natural history of psoriatic disease.
Abacar et al. (Sun,) studied this question.