Recent retrospective evidence has underlined the possibility of preventing psoriatic arthritis (PsA) onset in patients suffering from psoriasis (PsO) by using systemic treatments , particularly biologics [1, 2]. However, there are some conflicting data stating the opposite, with a greater risk of PsA among biologics users [3]. Importantly, none of these analyses highlighted any difference in terms of arthritis prevention in PsO among the various systemic therapies, apart from the study by Singla et al. [4]. In detail, these authors retrospectively evaluated the electronic health record database of PsO patients to assess the risk of incident inflammatory arthritis after initiation of biological therapies over a mean time span of 2.4 years, finding the risk of developing inflammatory arthritis to be significantly lower in patients under treatment with IL12/23 inhibitors (adjusted HR 0.58, 95% CI 0.43–0.76) or IL-23 inhibitors (0.41, 0.17–0.95) compared to patients treated with TNF inhibitors, while no significant difference was observed between IL-17 inhibitors (0.86, 0.54–1.38) and TNF inhibitors. However, it is well known that such retrospective observational epidemiological studies on drug effects may be influenced by two main limitations, protopathic bias (i.e., dermatologists were treating presumed psoriatic arthritis—PsA) and confounding by indication (i.e., dermatologists tended to use more TNF inhibitors in suspected PsA compared to IL-12/23 inhibitors) [5]. Besides, there are other possible patient-related variables that have not been considered by such studies possibly affecting their findings; thus, only a stratification according to these factors would ensure a reliable evaluation of biologics efficacy in reducing the likelihood of developing arthritis. In this regard, it is of utmost importance to underline that patient-related risk factors may impact in a different way in terms of timing of PsA development. Indeed, based on the recently released EULAR (European League Against Rheumatism) points to consider on PsO to PsA transition, it is possible to identify a phase of “psoriasis at higher risk for PsA” that is typified by medium- to long-term risk factors (average of 7–12 years before PsA onset), including severe skin involvement, nail psoriasis, obesity and familial history for PsA, and a phase of “subclinical PsA” encompassing short-term risk factors (average of 1–3 years before PsA onset), including arthralgia and imaging evidence of synovio-entheseal inflammation (Fig. 1) [6, 7]. Based on the above, we strongly believe that only prospective studies designed according to a precise stratification of the above-mentioned risk factors and considering their temporal impact on PsA development [8] may clarify whether biologics prevent the transition toward a clinical PsA. In this regard, we recently published a case series focusing on the “subclinical PsA” stage, showing the possibility to “reverse” such a phase (with improvement/remission of arthralgia and/or synovio-entheseal inflammation on imaging) using guselkumab [9]. However, prospective controlled trials on large samples are needed to confirm these preliminary data.

Fig. 1
figure 1

Transition from psoriasis to clinical psoriatic arthritis (PsA) goes through two stages: (1) “psoriasis at higher risk for PsA,” including patients with a medium-/long-term risk (average of 7–12 years) of developing PsA (i.e., those with severe skin involvement, nail psoriasis, obesity, and/or familial history for PsA); (2) “subclinical PsA,” including patients with a short-term risk (average of 1–3 years) of developing PsA (i.e., those with arthralgia and/or imaging evidence of synovio-entheseal inflammation). Such phases precede “clinical PsA,” which may present with three main patterns, including “peripheral,” “oligoarthritis,” and “articular erosions”

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