OP0270 MICROSTRUCTURAL DAMAGE PROGRESSION OVER A 10-YEAR OBSERVATION PERIOD IN PATIENTS WITH PSORIATIC ARTHRITIS ASSESSED BY HIGH-RESOLUTION QUANTITATIVE PERIPHERAL COMPUTED TOMOGRAPHY: RESULTS FROM THE COMPACT STUDY
Authors: F. Fagni, K. Tascilar, L. Schuster, M. Yalcin Mutlu, S. A. Temiz, S. Bayat, O. Fitzgerald, S. R. Pennington, D. Martin, A. Kleyer, D. Simon, G. Schett
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> It is estimated that a diagnostic delay of as little as 6 months can lead to the development of joint erosions and worse long-term outcomes in PsA [1]. Structural damage is usually monitored with conventional radiography, but this lacks sensitivity for the subtle bone changes which emerge during the early stages of disease progression. High-resolution peripheral quantitative computed tomography (HR-pQCT) can identify erosive and proliferative bone changes earlier and more sensitively [2], allowing a more in-depth understanding of the process of structural damage development in PsA. <h3>Objectives:</h3> To evaluate the incidence of microstructural progression in PsA using HR-pQCT and to identify the associated clinical and therapeutic factors. <h3>Methods:</h3> Adult PsA patients fulfilling CASPAR classification criteria [3] who had at least two HR-pQCT scans performed of the distal radius and 2<sup>nd</sup> and 3<sup>rd</sup> metacarpophalangeal joints at our clinic were included in this retrospective analysis. Clinical data including treatment and disease activity were recorded. All HRpQCT scans were segmented by a blinded reader and assessed for the presence and volume of erosions and enthesophytes, volumetric bone mineral density (vBMD), bone microstructure, and biomechanical properties were assessed. Microstructural progression was defined as either the new occurrence or the increase in size of erosions and/or enthesophytes detected with HRpQCT. <h3>Results:</h3> A total of 93 PsA patients were recruited. Participants had a median (IQR) disease duration at baseline of 3.0 years (0.0-10.5) and provided a median follow-up of 39.8 (24.2-54.8) months with a maximum of 10 years. Clinical characteristics and therapy are reported in Figure 1A. Microstructural progression was observed in 32 (34.4%) patients and the progression-free survival curve is shown in Figure 1B. There were no significant differences in age, sex, follow-up duration, disease duration, or therapy between progressors and non-progressors. Regarding disease activity, progressors showed a higher mean number of tender (p&lt;0.0001) and swollen joints (p&lt;0.0001), as well as higher mean DAS28 (p&lt;0.0001) (Figure 1A). We detected significant time/DAS28 interactions, indicating faster loss of cortical and trabecular vBMD over time with increasing DAS28 (p=0.049) as well as numerically lower, thicker trabeculae with higher trabecular separation and irregularity. No significant changes emerged in biomechanical properties such as bone stiffness and failure load. A graphical illustration of the time/DAS28 interactions is shown in Figure 2A. At baseline, patients exposed to b/tsDMARDs had numerically lower vBMD compared to unexposed patients, possibly as a result of a higher disease activity. However, the temporal pattern revealed a consistently slower deterioration of both cortical and trabecular vBMD over time in patients treated with b/tsDMARD as opposed to a deteriorating pattern in the untreated. Remarkably, at 40 months, b/tsDMARD-exposed patients had a numerically higher vBMD than the unexposed, as compared to baseline. Also, the number of trabeculae remained consistently higher in patients treated with b/tsDMARDs during the entire follow-up. A graphical representation of time-therapy interactions is shown in Figure 2B. <h3>Conclusion:</h3> Micro-structural progression is frequent in patients with PsA and despite treatment can affect approximately 50% of patients within the first 2 years of follow-up. Higher disease activity over time was found to be the main determinant of bone damage, while therapy with b/tsDMARD slows bone deterioration. Thus, these data help to emphasize the critical period for the initiation of early b/tsDMARD treatment in preventing microstructural progression in PsA. <h3>REFERENCES:</h3> [1] Haroon M et al. Ann Rheum Dis. 2015. [2] Simon D, et al Arthitis Res Ther. 2018. [3] Taylor W, et al. Arthritis Rheum. 2006. <h3>Acknowledgements:</h3> This project has received funding from the Innovative Medicines Initiative 2 Joint Undertaking (JU) under grant agreement No 101007757 (HIPPOCRATES). The JU receives support from the European Union's Horizon 2020 research and innovation program and EFPIA. DS was supported by the 2022 GRAPPA Pilot Research Grant. FF was supported by the Deutsche Forschungsgemeinschaft as part of the NOTICE clinician scientist programme. <h3>Disclosure of Interests:</h3> Filippo Fagni Janssen, Galapagos, Novartis, Lilly, Koray Tascilar: None declared, Louis Schuster: None declared, Melek Yalcin Mutlu: None declared, Selahattin Alp Temiz: None declared, Sara Bayat Galapagos, Oliver FitzGerald: None declared, Stephen R. Pennington: None declared, David Martin: None declared, Arnd Kleyer: None declared, David Simon: None declared, Georg Schett Janssen.