title: [RANKL as a target molecule for treatment of joint destruction].
abstract: Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized progressive joint destruction. Recent studies have revealed an essential role of receptor activator of NF-kappaB ligand (RANKL) in bone destruction in RA, and therapeutics targeting RANKL has been attracting a great deal of attention.
authors.affiliation: The University of Tokyo, Department of Orthopaedic Surgery, Faculty of Medicine.
authors.forename: Sakae
authors.initials: S
authors.lastname: Tanaka
mesh_terms: D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000209:etiology* / Q000473:pathology; D016723:Bone Remodeling; D001842:Bone and Bones / Q000473:pathology; D002454:Cell Differentiation / Q000235:genetics; D015195:Drug Design; D006801:Humans; D010010:Osteoclasts / Q000166:cytology / Q000502:physiology; D053245:RANK Ligand / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D053245:RANK Ligand; D014409:Tumor Necrosis Factor-alpha