AB0099 COCULTURE OF SYNOVIAL MEMBRANE AND CARTILAGE: A POTENTIAL HUMAN EX VIVO CARTILAGE DEGRADATION MODEL. (June 2019)

• Record Type: Journal Article
• Authors: Mucke, Johanna; Warzynski, Victoria; Bleck, Ellen; Pauly, Thomas; Claßen, Tim; Schneider, Matthias; Vordenbäumen, Stefan
• Is Part Of: Annals of the rheumatic diseases. Volume 78(2019)Supplement 2
• Page Start: 1511
• Page End: 1511
• Publication Date: 2019-06
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2019-eular.2159
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: Cartilage degradation is a hallmark in both osteoarthritis (OA) and rheumatoid arthritis (RA). Ex vivo cartilage models offer the potential to study disease processes but are surprisingly rarely used. Objectives: Here we investigate the effect of synovial tissue and stimulation with TNF-α on cartilage degradation in a physiologically relevant coculture-model of synovial membrane and cartilage. Methods: Cartilage and synovial membrane were collected from patients with RA and OA who underwent joint replacement. Cartilage was cultivated either alone or with synovial membrane in medium with or without TNFα as a stimulant for up to 28 days. The explants were harvested at different time points and Safranin-O-staining was performed to visualize proteoglycan (PG) content. A scoring system from 0 (no PG content) to 3 (high PG content) was applied as a semi-quantitative measure for evaluation. Linear mixed modeling adjusted for gender and age was performed to identify factors influencing PG content. Results: Samples of 18 patients (9 OA, 9 RA) were collected. Factors associated with proteoglycan loss in cartilage were the time in culture (p=0.02), stimulation with TNF-α (p=0.0007) and coculture with synovial membrane (p=0.00002) in univariate analysis with TNF-α (p=0.0009) and coculture (p=0.001) maintaining the level of significance in multivariate analysis. (Figure 1) Conclusion: Exposure to synovial tissue and TNF stimulation drive cartilage proteoglycan loss in an ex vivo cartilage degradation model. This model may prospectively serve to investigate pathophysiologic pathways of cartilage degradation in both OA and RA. References: None Disclosure of Interests: Johanna Mucke: None declared, Victoria Warzynski: None declared, Ellen Bleck: None declared, Thomas Pauly: None declared, Tim Claßen: None declared, Matthias Schneider Grant/research support from: GlaxoSmithKline and UCB Pharma for performing the LuLa-study., Speakers bureau: Chugai, Stefan Vordenbäumen: None declared