Pro-inflammatory cytokines drive bone resorption in rheumatoid arthritis. Cytokines are amongst the most important mechanisms driving bone resorption associated to inflammation mediated by M-CSF, RANKL, TNF-α, IL-1-β, IL-6, and finally IL-17A. In RA, IL-17A is mainly produced by Th17 and mastocytes, further amplifying inflammation by enhancing pro-inflammatory cytokine production of synovial fibroblast. IL-17A also increases bone resorption by inducing RANKL production by osteoblasts and M-CSF production by synovial fibroblasts; M-CSF and RANKL are the two cytokines required to differentiate OC from different cell sources: DC, monocytes, macrophages, or bone-marrow progenitors.