Although a recent study suggested the involvement of RANKL and osteoprotegerin (OPG) in the pathogenesis of bone-destructive disease, no study has focused on the RANKL:OPG ratio in the synovial fluid of patients with temporomandibular joint (TMJ) disorder. This communication reports on the concentrations of RANKL and OPG in synovial fluid from TMJ patients and healthy control individuals. In contrast to an unchanged concentration of RANKL, a strong decrease in the concentration of OPG was detected in the synovial fluid from patients with TMJ internal derangement. Treatment with the synovial fluid of osteoarthritis (OA) patients resulted in the high production of osteoclast-like cells from blood mononuclear cells in vitro, as well as in pit formation in dentin slices. The addition of anti-RANKL IgG or OPG attenuated OA-synovial fluid-induced osteoclast formation, suggesting that the increase in the RANKL:OPG ratio in the microenvironment of the joint has the potential to induce osteoclastogenesis in TMJ osteoarthritis.
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