Osteoclast Activation and Inflammatory Bone Diseases: Focusing on Receptors in Osteoclasts.

Abstract

Bone homeostasis depends on the balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption. An increasing number of studies have revealed that under inflammatory conditions, osteoclast overactivation is responsible for bone loss in relevant bone diseases. Multiple signaling pathways such as receptor activator of nuclear factor-kappa B ligand (RANKL) signaling are involved in osteoclast activation. These signaling pathways rely on various receptors expressed on the surface of osteoclast progenitor cells (OPCs) or osteoclasts, which are activated by their corresponding ligands and subsequently trigger intracellular signaling. Targeting of these receptors may exert an inhibitory effect on osteoclast activation and inflammatory bone diseases. In this review, we discuss osteoclast activation and receptors involved in this process. The role of these receptors in relevant bone diseases has also been discussed.