title: [Mechanism of the bone destruction in rheumatoid arthritis].
abstract: Rheumatoid arthritis (RA) is characterized by the presence of inflammatory synovitis accompanied by cartilage and bone destruction. Histological examination of RA pannus shows a number of osteoclasts on the surface of the destructed bone. RA synovial tissues produce a variety of proinflammatory cytokines and growth factors that may increase osteoclast formation, activity, and/or survival. Synovial fibroblasts from RA patients express high levels of RANKL, which is essential for the differentiation of osteoclasts, and therefore, RANKL can be a good therapeutic target of joint destruction in RA.
authors.affiliation: Department of Orthopaedic Surgery, The University of Tokyo.
authors.forename: Masaki
authors.initials: M
authors.lastname: Nakamura
authors.forename: Sakae
authors.initials: S
authors.lastname: Tanaka
mesh_terms: D001172:Arthritis, Rheumatoid / Q000503:physiopathology*; D002352:Carrier Proteins / Q000502:physiology; D005347:Fibroblasts / Q000502:physiology; D006801:Humans; D008562:Membrane Glycoproteins / Q000502:physiology; D010010:Osteoclasts / Q000502:physiology; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D013583:Synovial Membrane / Q000166:cytology
chemical_list: D002352:Carrier Proteins; D008562:Membrane Glycoproteins; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; C505686:TNFRSF11A protein, human; C505688:TNFSF11 protein, human