Abstract
Osteoprotegerin (OPG) is a key regulator of osteoclastogenesis. We investigated the presence of OPG and bone-resorbing cytokines, the potential of osteoclastic differentiation in joint fluid from failed total hip arthroplasty (THA), and the inhibitory effect of OPG on osteoclast formation in vitro induced by the joint fluid. This study aimed to clarify one important step in the cascade of periprosthetic osteolysis in the process of implant loosening. OPG levels in joint fluid in 20 cases of failed THA were significantly lower than in 15 cases of osteoarthritis (OA) (p<0.001) . The levels of bone-resorbing cytokines and interleukins (IL) -1β and IL-6 were significantly higher in failed THA joints than in OA fluid (p<0.001 and p=0.001, respectively) . Marked osteoclast formation was observed in the presence of failed THA joint fluid in the mouse coculture system, when compared to OA fluid (p<0.001) . The addition of 100 ng/ml OPG to the mouse coculture system completely inhibited osteoclast formation in the presence of failed THA joint fluid (p<0.001) . The data suggested that low levels of OPG combined with higher IL-1β and IL-6 levels represent the potential of osteoclast differentiation and activation in failed THA joint fluid. Inhibition of osteoclastogenesis in vitro by OPG suggests that a low level of OPG with elevated bone resorbing cytokines contributes to periprosthetic osteolysis via osteolytic joint fluid, thus leading to THA prosthesis loosening.
