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. Author manuscript; available in PMC: 2018 Feb 1.
Published in final edited form as: Expert Opin Biol Ther. 2016 Nov 30;17(1):119–128. doi: 10.1080/14712598.2017.1263614

Figure 2. Mechanisms of DMab action in inhibiting osteoclast differentiation.

Figure 2

(A) Osteoclast precursors (OCPs) are present in bone marrow, circulation and inflamed joints. OCPs express RANK and c-Fms receptors on their cell surfaces. Binding of RANK to RANK ligand (RANKL) and c-FMS to M-CSF, respectively, are essential for the initiation of RANKL-dependent OC differentiation. (B) Through binding to RANKL, DMab blocks engagement with its receptor, RANK on OCPs and inhibits the subsequent activation and maturation of OCPs. Consequently, DMab decreases bone resorption and fosters an overall increase in bone mineral density (BMD).