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Regulation of bone destruction in rheumatoid arthritis through RANKL-RANK pathways
Sakae Tanaka, Department of Orthopaedic Surgery, Faculty of Medicine, The University of Tokyo, Tokyo 113-0033, Japan
Author contributions: Tanaka S wrote the paper.
Correspondence to: Sakae Tanaka, MD, PhD, Department of Orthopaedic Surgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. tanakas-ort@h.u-tokyo.ac.jp
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Received: July 12, 2012
Revised: November 23, 2012
Accepted: December 23, 2012
Published online: January 18, 2013
Revised: November 23, 2012
Accepted: December 23, 2012
Published online: January 18, 2013
Abstract
Recent studies have demonstrated that osteoclasts, the primary cells responsible for bone resorption, are mainly involved in bone and joint destruction in rheumatoid arthritis (RA) patients. Recent progress in bone cell biology has revealed the molecular mechanism of osteoclast differentiation and bone resorption by mature osteoclasts. We highlight here the potential role of the receptor activator of nuclear factor κB ligand (RANKL)-RANK pathways in bone destruction in RA and review recent clinical trials treating RA by targeting RANKL.
Keywords: Rheumatoid arthritis; Osteoclast; Receptor activator of nuclear factor κB ligand; Bisphosphonate; Denosumab