Rationale
Local bone destruction and osteoporosis in rheumatoid arthritis (RA) is mediated by the interaction of the receptor activator of nuclear factor kappa B (RANK) with its ligand (RANKL) and osteoprotegerin (OPG). Effector cells – osteoclasts – are generated upon the contact between RANK-positive (RANK+) pre-osteoclasts with RANKL expressed on the surface of osteoblasts or inflammatory cells [1]; a role of the soluble form of RANKL (sRANKL) in synovial fluid (SF) or serum in the osteoclast maturation has also been discussed. We have previously reported higher local production of OPG and sRANKL in RA active joints in comparison with their serum concentration, lower local and systemic concentrations of OPG in RA patients in comparison with those suffering from osteoarthritis (OA) and no difference in SF-sRANKL levels between RA and OA groups [2].