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Increased bone resorption mediated by osteoclasts causes various diseases such as osteoporosis and bone erosion in rheumatoid arthritis (RA). Osteoclasts are derived from the monocyte/macrophage lineage, but the precise origin remains unclear. In the present study, we show that the purified CD16 -  human peripheral blood monocyte subset, but not the CD16 +  monocyte subset, differentiates into osteoclast by stimulation with receptor activator of NF-κB ligand (RANKL) in combination with macrophage colony-stimulating factor (M-CSF). Integrin-β3 mRNA and the integrin-αvβ3 heterodimer were only expressed on CD16 -  monocytes, when they were stimulated with RANKL + M-CSF. Downregulation of β3-subunit expression by small interfering RNA targeting β3 abrogated osteoclastogenesis from the CD16 -  monocyte subset. In contrast, the CD16 +  monocyte subset expressed larger amounts of tumor necrosis factor alpha and IL-6 than the CD16 -  subset, which was further enhanced by RANKL stimulation. Examination of RA synovial tissue showed accumulation of both CD16 +  and CD16 -  macrophages. Our results suggest that peripheral blood monocytes consist of two functionally heterogeneous subsets with distinct responses to RANKL. Osteoclasts seem to originate from CD16 -  monocytes, and integrin β3 is necessary for osteoclastogenesis. Blockade of accumulation and activation of CD16 -  monocytes could therefore be a beneficial approach as an anti-bone resorptive therapy, especially for RA.

Identification of a human peripheral blood monocyte subset that differentiates into osteoclasts.