Other local factors regulating bone resorption

In addition to RANKL and OPG, which are the primary regulators of bone resorption, other factors, such as inflammatory cytokines and prostaglandins, act locally to modulate osteoclast function to increase or decrease bone resorption. TNF-a and interleukin-1 beta (IL1b) are two important inflammatory cytokines that have profound proresorptive action through both RANKL-mediated and direct effects on osteoclasts. Both of these cytokines increase RANKL expression by osteoblasts. In addition, TNF-a activates NFkB and other pathways in osteoclasts that are common to RANKL signaling, and augments RANKL proresorptive effects. IL1b increases osteoclast activity and survival directly and thus also directly increases bone resorption during inflammatory diseases.18

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