26dkou359 10.3205/26dkou359 urn:nbn:de:0183-26dkou3597 Meeting Abstract Pfeiffer Pfeiffer Maximilian M

Klinik für Unfallchirurgie und Orthopädie, Dr. Rolf M. Schwiete Forschungsbereich für Arthrose, Frankfurt, Deutschland

author Rösch Rösch Gundula G

Klinik für Unfallchirurgie und Orthopädie, Dr. Rolf M. Schwiete Forschungsbereich für Arthrose, Frankfurt, Deutschland

author Tsai Tsai Pei-Ling PL

Goethe-Universität Frankfurt, Universitätsklinikum Frankfurt, Klinik für Psychiatrie, Psychosomatik und Psychotherapie, Frankfurt, Deutschland

author Gold Gold Maximilian M

Klinik für Unfallchirurgie und Orthopädie, Dr. Rolf M. Schwiete Forschungsbereich für Arthrose, Frankfurt, Deutschland

author Zaucke Zaucke Frank F

Klinik für Unfallchirurgie und Orthopädie, Dr. Rolf M. Schwiete Forschungsbereich für Arthrose, Frankfurt, Deutschland

author Slattery Slattery David D

Goethe-Universität Frankfurt, Universitätsklinikum Frankfurt, Klinik für Psychiatrie, Psychosomatik und Psychotherapie, Frankfurt, Deutschland

author Jenei-Lanzl Jenei-Lanzl Zsuzsa Z

Klinik für Unfallchirurgie und Orthopädie, Dr. Rolf M. Schwiete Forschungsbereich für Arthrose, Frankfurt, Deutschland Klinik für Orthopädie, Abteilung für Experimentelle Orthopädie, Ulm, 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 359 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_709 TextObjectives and questions: Chronic stress activates both the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system (SNS) and is increasingly recognized as a risk factor for osteoarthritis (OA). However, the role of local glucocorticoid and adrenergic signaling remains unclear. Therefore, we investigated the changes in adrenergic receptor (AR) and corticosterone (CORT)-converting enzyme expression linked to degeneration and inflammation in a murine model of OA.Material and methods: OA was induced in twelve-week-old male C57BL/6J mice by destabilization of the medial meniscus (DMM), with sham controls. A subset was exposed to chronic mild stress (CMS) for 4 or 12 weeks. Stress response was evaluated by measuring serum CORT and splenic noradrenaline (NE). Cartilage degeneration and synovitis were quantified using histological scoring. ARs (α2A and β2) and CORT-converting enzyme (11β-hydroxysteroid dehydrogenase-1/-2 (11β-HSD1/2)) expression in cartilage and synovium was analyzed using immunohistochemistry (IHC) and quantified as the ratio of positive cells to total cells. Ongoing analyses include glucocorticoid receptor (GR) and tyrosine hydroxylase (TH) expression. Data were analyzed using Kruskal-Wallis/Dunn's test and Spearman’s rank correlation. A p-value <0.05 was considered statistically significant.Results: Serum CORT and splenic NE increased in all CMS groups at both time points (CORT: both CMS-Sham and CMS-DMM p<0.05 at 4 and 12 weeks, NE: both CMS-Sham and CMS-DMM p<0.01 at 4 weeks, p<0.001 at 12 weeks). CMS exacerbated DMM-associated cartilage degeneration and synovitis at both 4 (cart.: p<0.05, syn.: p<0.05) and 12 weeks (cart.: p<0.01, syn.: p<0.01). No change in 11β-HSD1 expression was observed, while 11β-HSD2 decreased in CMS-Sham and DMM cartilage (both: p<0.05) and increased in DMM synovium (p<0.05) at 4 weeks, with both returning to baseline by 12 weeks. α2A-AR expression increased in CMS-Sham and CMS DMM cartilage at both 4 (both: p<0.001) and 12 weeks (both: p<0.01) and increased only in CMS DMM synovium after 12 weeks (p<0.05). β2-AR was elevated in CMS-Sham and DMM cartilage (both: p<0.05 at 4 weeks, both: p<0.01 at 12 weeks) at all time points and in the synovium of CMS-DMM mice at 12 weeks (p<0.001). Moreover, synovial β2-AR expression positively correlated with splenic NE (r=0.650, p<0.01), cartilage degeneration (r=0.518, p<0.01), and synovitis (r=0.506, p<0.01).Discussion and conclusions: CMS seems to accelerate local OA-associated processes primarily via SNS/AR-mediated mechanisms rather than HPA/glucocorticoid signaling indicated by an early loss of 11β-HSD2 (converts CORT in its inactive form) in the cartilage as well as general β2-AR dominance. Our findings underscore the potential of the β2-AR as therapeutic target in OA. 0 0 0 0