[Expectation for alleviation of joint destruction in rheumatoid arthritis by new molecular targeting pharmaceutics including anti-rankle antibody].
Molecular signals of RANK/RANK/OPG, essentially required in osteoclast differentiation, have been shown to pertain to joint destruction in rheumatoid arthritis (RA) . In rodent adjuvant arthritis systemic administration of OPG did not prevent inflammation, but effectively reduced joint destruction preserving peri-arthritic bone mass. In clinical trial anti-RANKL antibody (Denosumab) injection once in every 6 months alleviated the worsening of joint erosion in hands for a year in patients with RA. Although RANKL/RANK signals have not been confirmed as the exclusive causative factor to joint destruction and bone loss, a new horizon may be brought about by Denosumab in the treatment of RA.
Nakamura
Toshitaka
T
Department of Orthopedics, School of Medicine, University of Occupational and Environmental Health.
D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D061067:Antibodies, Monoclonal, Humanized; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000209:etiology*; D016723:Bone Remodeling; D002454:Cell Differentiation; D000069448:Denosumab; D006801:Humans; D010010:Osteoclasts / Q000166:cytology; D010024:Osteoporosis / Q000188:drug therapy / Q000209:etiology; D053245:RANK Ligand / Q000008:administration & dosage / Q000276:immunology* / Q000502:physiology; D015398:Signal Transduction
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D053245:RANK Ligand; D000069448:Denosumab