“Preventing” Arthritis in Psoriasis Save

Prevention of the development of our systemic rheumatic diseases in individuals deemed at risk, or with some form of precursor disease process, has been a hot topic in recent years. 

We have seen a large volume of studies exploring this question in clinically suspect arthralgia/pre-RA (and sometimes RA that we are pretending isn’t RA yet!). Psoriatic arthritis has been relatively less studied in this regard despite having a more clearly obvious, in fact generally right in front of our eyes predictor of risk, in terms of skin psoriasis.

The excellent Saturday morning session on whether aggressive treatment of psoriasis can prevent psoriatic arthritis at RheumNow Live 2025 from the always compelling Dr Alexis Ogdie explored this very question.

Dr Ogdie referenced the complex interplay between various factors and the development of arthritis in individuals with psoriasis. Genetics, environmental factors, trauma, obesity, the microbiome and immune system were all highlighted as influences on the development of psoriatic arthritis. It was highlighted that this is frequently, although not always, a relatively linear process from skin psoriasis, though pre-subclinical stages perhaps with arthralgia, to frank psoriatic arthritis. The severity of skin psoriasis, obesity, and harder to explain, depression, were highlighted as key risk factors for the development of psoriatic arthritis.

To go on a slight tangent, I wonder how true or helpful this conceptualisation of psoriasis progressing linearly to arthritis in at risk patients really is. This may in turn have great relevance when we come to understand how we may be “preventing” arthritis. 

My go to psoriatic arthritis treatment resource is the excellent GRAPPA guidelines. The logic of the various domains of disease manifestations and tailoring treatment to address the individuals features appeals to me. The natural extension of this is my own conceptualisation of the umbrella term of psoriatic disease for these various manifestations. While this is very much hypothetical with not much supportive data, I view psoriatic disease as an underlying unseen entity that may then produce the various clinical manifestations such as skin disease or arthritis. The logical conclusion to this is that we are not so much trying to prevent psoriasis becoming psoriatic arthritis, we are perhaps looking at which medications may manage the earlier stages of psoriatic arthritis better.

It is therefore perhaps of little surprise that the utilisation of agents that we know also work for psoriatic arthritis to control psoriasis, would be associated with a lower rate of new diagnoses of psoriatic arthritis. 

This comes back to the same fundamental question we have in the pre-RA studies, are these agents actually preventing anything, or are they merely treating the disease before it manifests itself to us in a patient symptom at a clinical visit. I haven’t sat on the fence on this issue in pre-RA, strongly feeling that we are fooling ourselves if we think we are preventing disease, and I feel even more strongly this way in psoriasis.

One of the big difficulties with studying this is that there is huge channelling bias – if you have worse psoriasis you are more likely to get systemic treatments. This means that if you just look at raw numbers, those with psoriasis on biologic DMARDs are much more likely to get PsA. Dr Ogdie very nicely showed how there appears to be a front-loading in this process if you study it over time. Individuals with psoriasis treated with systemic agents have much higher PsA rates in the first year, but if you look at 5 years they then have lower rates of new PsA down the line.

Dr Ogdie concluded by saying that we don’t know if treatment of psoriasis prevents PsA. This is very true. It would be inconceivable to me however to think that if you have exactly the same individual and give them a biologic or not, that the biologic treated one would not be less likely to manifest arthritis symptoms. The truly interesting clinical question to answer for me is whether there is a differential rate between the different biologic DMARDs – that would potentially be game changing. There is some intriguing data from retrospective studies that IL23 blocking agents may have lower rates of PsA development than targeting other pathways. This would jive with some of the pre-clinical data suggesting that IL23 may be more important earlier in the disease process than in long-established disease. 

To a large extent however this is all conjecture, what we really need are formal studies, which Dr Ogdie also teased us about.