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. 2019 Apr 23;8:F1000 Faculty Rev-533. [Version 1] doi: 10.12688/f1000research.17296.1

Figure 3. Schematic representation of the mechanism for osteoclast development and denosumab action in rheumatoid arthritis.

Figure 3.

Pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IL-17 directly or indirectly induce receptor activator of nuclear factor-kappa B ligand (RANKL) expression in synovial fibroblasts or osteoblasts or both. RANKL stimulates osteoclast differentiation from monocyte/macrophage-lineage precursor cells, leading to bone erosion in rheumatoid arthritis. Denosumab specifically binds to RANKL and suppresses osteoclast differentiation.