Psoriatic arthritis (PsA) represents a paradigmatic example of an immune-mediated inflammatory condition, where dysregulated interactions between innate and adaptive immunity drive multisystem pathology 1, 2, 3. Approximately 30% of patients with psoriasis develop PsA [4], with clinical manifestations spanning peripheral and axial arthritis, enthesitis, dactylitis, and spondylitis 5, 6. The spatial and temporal heterogeneity underlying these clinical outcomes of PsA reflect the dynamic interplay between Th17 tissue–resident immune cells, arthritic synovium (synovial macrophages), and osteoclasts, which leads to pannus formation and joint destruction 7, 8, 9. Persistent inflammation in PsA can lead to progressive disease if left untreated [10] — a trajectory that may be mitigated by early diagnosis and targeted therapies 11, 12.

The consequences of PsA extend beyond musculoskeletal manifestations, with patients facing heightened risks of systemic comorbidities, such as cardiovascular disease, metabolic syndrome, and extra-articular inflammatory conditions (e.g. inflammatory bowel disease) [13]. Conventional clinical measures, including the Disease Activity index in Psoriatic Arthritis (DAPSA) score, rely on joint counts and patient-reported outcomes and are suboptimal to capture subclinical inflammation in early PsA immunopathogenesis [14]. For instance, synovial T cells may drive inflammatory processes months before structural damage becomes apparent on X-rays or magnetic resonance imaging (MRI) 12, 15. Ultrasound, while useful, is limited by poor visualization of deep structures (e.g. axial skeleton) [16], operator dependency [17], and time-consuming systemic assessments [18], while MRI’s narrow field of view (FOV), low resolution for small joints, and inability to evaluate avascular entheses are known drawbacks 19, 20. Crucially, neither of these techniques directly quantify the systemic spread of immune dysregulation that defines PsA’s multisystem nature. These challenges highlight the limitations of current diagnostic frameworks and the urgent need for systemic evaluation methods capable of visualizing the proliferative-inflammatory cascade underlying PsA. Recent advances in treatment options have prompted updated recommendations from the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis, emphasizing the importance of addressing all active disease domains in individual patients and considering relevant comorbidities when selecting therapies [21].

Recently, total-body positron emission tomography (TB-PET) systems have become available that image the whole body simultaneously in a single snapshot [22]. Human imaging studies that utilize these systems have been published in the context of autoimmune arthritis [23], including PsA 24••, 25, and other conditions 26, 27, demonstrating their merits. In this review, we discuss the potential promise of these systems to evaluate the underlying pathogenesis of PsA and provide biomarkers helpful for diagnosis, therapy selection and assessing in vivo, quantitative response to treatment.