26dkou363 10.3205/26dkou363 urn:nbn:de:0183-26dkou3633 Meeting Abstract Schäfer Schäfer Nicole N

Dept. of Orthopedic Surgery, Experimental Orthopedics, Centre for Medical Biotechnology (ZMB) Bio Park 1, University of Regensburg, Regensburg, Deutschland

author Pann Pann Patrick P

Dept. of Trauma Surgery, University Hospital Regensburg, Regensburg, Deutschland

author Rudolph Rudolph Matthias M

Center for Applied Tissue Engineering and Regenerative Medicine (CANTER), University of Applied Sciences Munich, München, Deutschland

author Péré Péré Nicolas N

Center for Applied Tissue Engineering and Regenerative Medicine (CANTER), University of Applied Sciences Munich, München, Deutschland

author Clausen-Schaumann Clausen-Schaumann Hauke H

Center for Applied Tissue Engineering and Regenerative Medicine (CANTER), University of Applied Sciences Munich, München, Deutschland

author Böhm Böhm Markus M

Dept. of Dermatology, University of Münster, Münster, Deutschland

author Grässel Grässel Susanne S

Dept. of Orthopedic Surgery, Experimental Orthopedics, Centre for Medical Biotechnology (ZMB), Bio Park 1, University of Regensburg, Regensburg, Deutschland

author German Medical Science GMS Publishing House

Düsseldorf

610 20261020 engl This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). M0659 363 Deutsche Gesellschaft für Orthopädie und Unfallchirurgie Deutsche Gesellschaft für Orthopädie und Orthopädische Chirurgie Deutsche Gesellschaft für Unfallchirurgie Berufsverband für Orthopädie und Unfallchirurgie Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2026) Grundlagenforschung | Osteoarthrose Berlin 20261020 20261023 DKOU26_Abs_772 TextObjectives and questions: Osteoarthritis (OA) is a progressive inflammatory disease characterized by cartilage degradation and joint-wide structural damage. To investigate its pathogenesis, the murine destabilization of the medial meniscus (DMM) model serves as highly relevant proxy for human OA due to its cross-species biomechanical similarities. The neuropeptideα-melanocyte-stimulating hormone (α-MSH) exhibits potent anti-inflammatory and chondroprotective properties, primarily through the melanocortin 1 receptor (MC1R). This study evaluated whether intra-articular supplementation with the stable analog NDP-α-MSH or the derivative KdPT can modulate anti-inflammatory and senescence-associated pathways to delay OA progression.Material and methods: OA was induced in 12-week-old male wild type (C57Bl/6J) mice via destabilization of the medial meniscus (DMM) surgery, with sham-operated mice serving as controls. Animals received intra-articular injections of NDP-α-MSH, KdPT, or PBS at 1, 4, 8, and 12 weeks post-surgery. After 8 and 16 weeks post DMM/Sham surgery, evaluation included nighttime locomotion monitoring, histological assessment of cartilage degradation, and immunohistochemical analysis of MC1R- and TUNEL-positive chondrocytes. Additionally, cartilage stiffness was quantified via atomic force microscopy (AFM), and systemic inflammatory markers were measured using Luminex multiplex ELISA.Results: DMM surgery induced significant cartilage degradation, which was markedly inhibited by NDP-α-MSH and KdPT treatment 16 weeks post-surgery compared to PBS controls. While MC1R-positive chondrocytes decreased in NDP-α-MSH treated DMM mice relative to sham controls, plasma levels of pro-inflammatory markers (CRP, IL-1β, IL-6, IL-18) were significantly reduced in the NDP-α-MSH group at 8 and 16 weeks post-surgery. Furthermore, KdPT administration resulted in greater total distance moved and longer moving times, yet it significantly reduced average locomotor velocity, indicating a pattern of persistent but slower-paced exploration compared to other treatment groups.Discussion and conclusions: These findings demonstrate that intra-articular applied α-MSH analogs effectively mitigate cartilage loss and systemic inflammation following joint destabilization. The reduction in circulating cytokines and the preservation of joint integrity suggest that targeting melanocortin signaling offers a viable therapeutic strategy for disease-modifying OA treatment. 0 0 0 0