ABSTRACT
Osteoclasts are derived from pluripotent stem cells in bone marrow and spleen.They play a critical role in inflammation-induced bone loss and joint destruction because in the absence of them,bone de- struction does not occur even when inflammation exists.Synovioblasts in an inflamed joint can secrete numerous inflammatory factors,including tumor necrosis factor alpha(TNF-?)and interleukin-1(IL-1)which not only induce inflammatory reactions but also elevate osteoclast formation and function indirectly or directly through promoting RANKL expression.In this wdy the inflammatory reactions are associated with bone loss and destruction. In this article,we focus on the recent progress in study of TNF-?,IL-1 and osteoclast-target therapies in management of osteoclast-mediated inflammatory bone loss.TNF-?promotes differentiation of osteoclast precursor cells in the peripheral blood and spleen,which causes a marked increase in mature osteoclasts in a diseased joint.However, IL-I supports osteoblast survival and regulates the recombination of osteoclast cytoskeleton,which further stimulates bone resorption.Since osteoclast-target therapies may inhibit osteoclast formation and function,they are becoming more and more important for inflammation-induced bone loss and joint destruction.