Psoriasis is a primary clinical risk factor for the development of psoriatic arthritis (PsA), with severe skin disease, nail involvement, and obesity further increasing risk. While clinical examinations and screening tools help diagnose PsA, no specific treatment has yet been proven to prevent or delay its onset. Thus, early detection remains critical for preventing long-term joint damage in this at-risk patient population.

Patients with PsA can present with a variety of signs and symptoms involving multiple clinical domains. PsA can affect both small and large joints and can present in several recognizable clinical patterns, with many patients showing overlap or evolving from 1 pattern to another over time. One of the most common patterns is asymmetric oligoarthritis, which involves few joints (often <5), with an uneven distribution between the 2 sides of the body. Other common patterns are symmetric polyarthritis resembling rheumatoid arthritis and distal interphalangeal–predominant PsA. Some patients present with enthesitis or axial involvement, while other patients predominantly have skin and nail involvement. Axial disease, dactylitis, and enthesitis are important clinical domains of PsA and may occur alongside peripheral arthritis. Dactylitis and enthesitis each affect approximately 30% to 40% of patients with PsA, while axial involvement is less commonly reported. Dactylitis causes a diffusely swollen “sausage-like” digit, while enthesitis causes inflammation where tendons or ligaments attach to bone, commonly at the Achilles tendon or plantar fascia. Finally, the rarest form of PsA is arthritis mutilans, which is a severe destructive phenotype.

What I think is particularly interesting is that psoriasis acts as a window into the at-risk population for PsA, and this is something that we do not normally see with other rheumatic diseases. Approximately 30% of patients with psoriasis will eventually develop PsA. The question is: Can we identify those individuals with psoriasis who may be at highest risk for developing PsA? We know that patients with nail involvement, more severe psoriasis, psoriasis involving the scalp, inverse psoriasis, obesity, and/or a family history tend to be at higher risk for PsA.

However, joint pain in a patient with psoriasis does not automatically mean that they are at risk for PsA. This can have a variety of causes, such as osteoarthritis, a tendon injury, mechanical back pain, gout, or fibromyalgia. A good history and physical examination, including an inspection of the nails, really tell me what is going on. And if I do sense that the patient has synovitis or enthesitis, I sometimes move on to imaging with ultrasound, magnetic resonance imaging, or, less frequently, x-ray to get a better sense of whether it is mechanical or inflammatory. Questionnaires such as the Psoriatic Arthritis Screening and Evaluation (PASE) questionnaire, which we developed as a screening tool for dermatologists, and the Psoriasis Epidemiology Screening Tool (PEST) should also be embedded in patient workups to identify those who are at risk for PsA.

As a rheumatologist, the goal is to identify and treat patients early in their disease progression to prevent irreversible joint damage. However, it is one thing to say that a patient is higher risk, but it is another to say that treatment actually prevents arthritis from developing. We are now beginning to see more studies looking at the high-risk factors, but I do not think we can say that there is a specific treatment that can delay the onset of PsA or prevent it. The PAMPA study is an ongoing trial testing whether the IL-23 inhibitor guselkumab can prevent PsA or reduce musculoskeletal ultrasound abnormalities in such high-risk patients. We are waiting for the final results of this trial, but this is an example of how we are trying to get more information about what to do for these high-risk patients.

Lastly, I do want to emphasize that obesity and lifestyle can really impact a patient’s risk for PsA. For example, obesity can cause higher disease activity, worsening function, and reduced treatment response. This is because adipose tissue is metabolically active; if a person has more adipose tissue, this can amplify systemic inflammation, and we do not want this to happen. There are certain risk factors that are not modifiable for PsA, but if a patient can get their body mass index down to a level where their response to treatment is better and they are experiencing fewer comorbidities, I think that this should be part of our management. As rheumatologists, we need to educate our patients about these lifestyle factors so that they can be empowered to optimize their disease.