Abstract
Bone erosion is a major complication associated with rheumatoid arthritis (RA) and is a key contributing factor to the functional disability of RA patients. Tumor necrosis factor-α and interleukin-1 are well recognized as important factors causing bone erosion in RA. As such, current therapeutic regimens have relied primarily on the agents blocking the function of tumor necrosis factor-α and interleukin-1. The discovery of the receptor activator of NF-B (RANK) and its ligand (RANKL) has not only revealed an essential role for the RANKL/RANK system in arthritic bone erosion, but also indicated that the system can serve as effective therapeutic targets for arthritic bone erosion. In this review, the role of the RANKL/RANK system in bone erosion in RA, and the therapeutic agents, which are currently under development that target the system, will be discussed. Moreover, the rationale for exploring certain RANK signaling pathways as better therapeutic targets will also be discussed.
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.
