Abstract
In rheumatoid arthritis (RA), cells within the inflamed synovium and pannus elaborate a variety of cytokines, including tumor necrosis factor (TNF) alpha, interleukin (IL)-1, IL-6, and IL-17, that contribute to inflammation, and may directly affect bone. The receptor activator of NF-kappaB (RANK) ligand/RANK/osteoprotegerin pathway plays a critical role in regulating osteoclastogenesis in articular bone erosions in RA. Proinflammatory 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, the authors discuss the current understanding of pathogenic mechanisms of bone erosion in RA and examine current therapeutic approaches to prevent this damage.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
