RANKL expression in chondrocytes and its promotion by lymphotoxin-α in the course of cartilage destruction during rheumatoid arthritis

We investigated the expression and localization of receptor activator nuclear factor κB ligand (RANKL) in cartilage from patients with rheumatoid arthritis (RA) relevance to degeneration. also examined role exogenous lymphotoxin (LT)-α on RANKL human chondrocytes its effect vitro osteoclast differentiation. Cartilage synovial fluid samples were obtained 45 undergoing total joint replacement surgery or puncture, including 24 osteoarthritis (OA) 21 RA. articular was by immunohistochemistry. LT-α concentrations measured using an enzyme-linked immunosorbent assay (ELISA). Normal stimulated LT-α, relative mRNA levels RANKL, osteoprotegerin (OPG), matrix metalloproteinase-9, vascular endothelial growth real-time polymerase chain reaction. Soluble protein culture media ELISA, membrane-bound cells western blotting. Co-cultures peripheral blood mononuclear (PBMCs) macrophage-colony stimulating differentiation evaluated staining for tartrate-resistant acid phosphatase. higher RA than OA samples. The population RANKL-positive that cartilage, correlated Stimulation cultured increased expression, RANKL/OPG ratio, angiogenic factors. Membrane-bound up-regulated after stimulation whereas soluble medium did not increase. PBMCs demonstrated produce induced osteoclastic PBMCs. produced may contribute destruction during could promote chondrocytes.