In rheumatoid arthritis, cells within the inflamed synovium and pannus elaborate a variety of cytokines, including TNFα, IL-1, IL-6 and IL-17, that contribute to inflammation, and may directly impact bone. The RANKL/RANK/OPG pathway plays a critical role in regulating osteoclastogenesis in articular bone erosions in RA. Pro-inflammatory cytokines can modulate this pathway, and may also affect the ability of the osteoblast to repair bone at sites of articular erosion. In this review, we discuss the current understanding of pathogenic mechanisms of bone erosion in RA and examine current therapeutic approaches to prevent this damage.