26dkou585 10.3205/26dkou585 urn:nbn:de:0183-26dkou5852 Meeting Abstract Braun Braun Tobias T

Institute of Anatomy and Cell Biology, Paracelsus Medical University, Nürnberg, Deutschland

author Speckle Speckle Gilian G

Institute of Anatomy and Cell Biology, Paracelsus Medical University, Nürnberg, Deutschland

author Zaimidi Zaimidi Christina C

Institute of Anatomy and Cell Biology, Paracelsus Medical University, Nürnberg, Deutschland

author Rabe Rabe Alexandra A

Institute of Anatomy and Cell Biology, Paracelsus Medical University, Nürnberg, Deutschland

author Werner Werner Christian C

Institute of Anatomy and Cell Biology, Paracelsus Medical University, Nürnberg, Deutschland

author Wagner Wagner Michael M

Department of Orthopedic and Trauma Surgery, Paracelsus Medical University and Nuremberg General Hospital, Nürnberg, Deutschland

author Gögele Gögele Clemens C

Institute of Anatomy and Cell Biology, Paracelsus Medical University, Nürnberg, Deutschland

author Bail Bail Hermann-Josef HJ

Department of Orthopedic and Trauma Surgery, Paracelsus Medical University and Nuremberg General Hospital, Nürnberg, Deutschland

author Schulze-Tanzil Schulze-Tanzil Gundula G

Institute of Anatomy and Cell Biology, Paracelsus Medical University, Nürnberg, 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 585 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) Poster experimentell | Varia Berlin 20261020 20261023 DKOU26_Abs_2444 TextObjectives and questions: Many patients suffer simultaneously from osteoarthritis (OA) and diabetes mellitus type 2 (T2DM). Although OA and T2DM are obviously interrelated, the links between the pathogenesis of both diseases remains still unclear. Since the particular role of interleukin (IL)-10 and IL-24 in OA is unknown the present study focuses on the regulation of these two pleiotrophic cytokines of the IL-10 superfamily in articular chondrocytes derived from human donors with T2DM and/or OA.Material and methods: Hip and knee joint derived articular chondrocytes were isolated from human non-T2DM and T2DM donors. Samples were further divided into those derived from OA lesions or macroscopically intact cartilage. Using time lapse microscopy, scratch assays were conducted (independent experiments with chondrocytes of n=4 non diabetic and n=4 diabetic donors), and chondrocytes were monitored for initial cell adherence velocity, confluence of cell growth, and cell motility. To mimic OA, chondrocyte cultures were exposed to 10 ng/mL TNFalpha and/or 25 ng/mL C5a under 24-hour lasting normo- and hyperglycemic conditions. Subsequently, chondrocyte gene and protein expression for IL-10, IL-24 and their respective receptors were monitored. In pilot experiments, rat derived chondrocytes were stimulated with recombinant IL-24 (100 ng/mL) and analysed for collagen type 2 expression.Results: Articular chondrocytes from diabetic donors showed a lower cell confluence after 5 hours in monolayer culture. In addition, the motility was lower and wound closuring of the cell layer was significantly delayed in chondrocytes of diabetic versus non-diabetic donors. IL-10 and IL-24 were expressed on the protein level in cartilage in situ and cultured chondrocytes. Gene expression of these cytokines was higher in lesional OA cartilage compared to macroscopically intact cartilage. In cultured chondrocytes from non lesional-cartilage IL-24 was higher expressed if chondrocytes derived from diabetic compared to non-diabetic donors. Gene expression of both cytokines was induced by TNFalpha with or without C5a stimulation. The IL-10 receptor (R)-1 chain and the IL-22R1 chain, the latter belonging to one of the two known IL-24 receptors, as well as downstream suppressors of cytokine signaling 1 and 3 were induced by TNFalpha. IL-24 revealed a significant suppressive effect on collagen type 2 expression.Discussion and conclusions: Both pleiotrophic IL-10 superfamily cytokines are regulated by inflammatory OA conditions. Interestingly, IL-24 revealed differential regulation in chondrocytes of diabetic versus non-diabetic donors and could exert catabolic effects in cartilage. 0 0 0 0