Erosive arthritis.docVIP

Available online /content/9/S1/S2 Review Erosive arthritis Georg Schett Department of Internal Medicine 3, University of Erlangen-Nurnberg, Krankenhausstrasse, D-91054 Erlangen, Germany Correspondence: Georg Schett, georg.schett@med3.imed.uni-erlangen.de Published: 29 June 2007 Arthritis Research Therapy 2007, 9(Suppl 1):S2 (doi:10.1186/ar2166) This article is online at /content/9/S1/S2 ? 2007 BioMed Central Ltd Abstract bone disease and increases fracture risk [1]. This tight interaction between inflammation and bone is highlighted by Inflammation and degradation of bone are two closely linked processes. Chronic inflammatory arthritis not only leads to inflam- matory bone loss but it also involves local erosion of articular bone. This osteo-destructive feature of chronic inflammatory arthritis is a major cause of disability in patients with rheumatoid arthritis. Osteoclasts are essential for the resorption of mineralized cartilage and subchondral bone in chronic arthritis. The observed up- regulation of osteoclast differentiation factors (receptor activator of nuclear factor-κB ligand [RANKL]) in the synovial membrane of chronically inflamed joints indicates that osteoclasts are abundant in this setting, leading to rapid degradation of mineralized tissue. Blockade of osteoclast formation is thus a key strategy in preventing structural damage in arthritis. Denosumab, a humanized antibody that neutralizes RANKL, is an attractive candidate agent to inhibit inflammatory bone loss. the observation that virtually all chronic inflammatory diseases, particularly rheumatic disease and chronic inflam- matory bowel disease, are associated with a high prevalence of osteoporosis and increased fracture risk [2-6]. In the case of a more localized inflammatory process, these systemic effects on bone are accompanied by local bone damage at the skelet