title: [Secondary osteoporosis or secondary contributors to bone loss in fracture. Therapeutic intervention of rheumatoid arthritis bone loss].
abstract: In rheumatoid arthritis (RA) , the osteoclast pathway is activated by abnormal immune conditions accompanied by chronic inflammation resulting in periarticular osteoporosis and local bone destruction around joints. In addition, multiple factors lead to systemic osteoporosis, including reduced physical activity and pharmacotherapies such as steroids. These conditions cause decreased bone mineral density and bone quality, and expose patients to an increased risk of fracture. When treating patients with RA osteoporosis, it is important to improve systemic osteoporosis using anti-osteoporotic agents, and to suppress fracture risk by controlling inflammation (which is associated with periarticular osteoporosis and bone destruction) with a combination of disease-modifying anti-rheumatic drugs or biological agents.
authors.affiliation: Department of Orthopaedic Surgery, The University of Tokyo Hospital, Japan.
authors.forename: Kumiko
authors.initials: K
authors.lastname: Ono
authors.forename: Satoru
authors.initials: S
authors.lastname: Ohashi
authors.forename: Sakae
authors.initials: S
authors.lastname: Tanaka
mesh_terms: D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000188:drug therapy*; D015519:Bone Density / Q000187:drug effects*; D050723:Fractures, Bone / Q000150:complications / Q000188:drug therapy*; D006801:Humans; D010024:Osteoporosis / Q000150:complications / Q000188:drug therapy*
chemical_list: D018501:Antirheumatic Agents