Abstract
Chronic synovial inflammation is usually accompanied by bone erosion. Due to resulting structural damage, bone erosion is a major reason for disability in RA patients. Anti-rheumatic drug therapy is focussed not only on the control of synovial inflammation but also on preserving bone from structural damage. Bone erosion in arthritis is a consequence of synovial osteoclast formation. Therapeutic approaches which interfere with synovial osteoclastogenesis and/or osteoclast activation are therefore of great interest. This review describes the mechanism of inflammatory bone loss, describes its cellular and molecular players and gives insights in current therapeutic tools to inhibit this process.
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