ECTS2014 Poster Presentations Arthritis and other joint diseases: translational and clinical (15 abstracts)
1Bone and Joint Research Unit, Rheumatology Division, IIS-Jiménez Díaz Foundation, Autonomous University, Madrid, Spain; 2Arthritis Research UK Pain Centre, City Hospital, University of Nottingham, Clinical Sciences Building, Nottingham, UK.
Aims: To describe different multinucleated giant cell phenotypes and their associations with synovitis in people with rheumatoid arthritis (RA) or osteoarthritis (OA), and in an experimental model of chronic arthritis.
Material and methods: A cross-sectional comparative study was performed on samples of knee synovia from age-matched patients with RA, OA, or non-arthritic post mortem (PM) controls. OA synovia were stratified by histological inflammation grade using index tissue sections. Synovia were also obtained from rabbits with antigen-induced arthritis. Synovitis was assessed by Krenn score. Histological studies employed specific antibodies against macrophage markers or cathepsin K, or TRAP enzymatic assays.
Results: More RA and inflamed OA synovia displayed multinucleated giant cells than did non-inflamed OA and PM synovia. Positive associations were found between synovitis and synovial MGC density, both in RA and OA (r=0.580, P=0.018; r=0.603, 0.038 respectively). TRAP negative/cathepsin K negative Langhans-like and TRAP positive/cathepsin K negative foreign body-like were the predominant giant cell phenotype in RA, whereas Langhans-like was the commonest multinucleated giant cell phenotype in OA. Giant cells were localized near fibrin deposits, engulfing hemosiderin and tissue debris. TRAP positive/cathepsin K positive osteoclast-like cells were only identified close to bone surfaces. Touton-like giant cells surrounded adipocyte structures. Findings from rabbits with chronic arthritis reflected those observed in RA human samples.
Conclusions: Multinucleated giant cells are associated with synovitis both in OA and in RA. Further research targeting multinucleated giant cells is required to elucidate their discrete contributions to RA and OA pathology and symptoms.