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Osteoporosis in Rheumatic Diseases: Anti-rheumatic Drugs and the Skeleton

Author information

Dubrovsky AM1, Lim MJ1,2, Lane NE3,4. Calcif Tissue Int. 2018 Feb 22. doi: 10.1007/s00223-018-0401-9. [Epub ahead of print]

Abstract

Author information 1 Center for Musculoskeletal Health, University of California at Davis Medical Center, Sacramento, CA, 95817, USA.

2 Division of Rheumatology, Department of Internal Medicine, Inha University Hospital, Incheon, South Korea.

3 Center for Musculoskeletal Health, University of California at Davis Medical Center, Sacramento, CA, 95817, USA. nelane@ucdavis.edu.

4 Department of Internal Medicine, University of California at Davis Medical Center, 4625 2nd Avenue, Suite 2000, Sacramento, CA, 95817, USA. nelane@ucdavis.edu.

Abstract

Osteoporosis in rheumatic diseases is a very well-known complication. Systemic inflammation results in both generalized and localized bone loss and erosions. Recently, increased knowledge of inflammatory process in rheumatic diseases has resulted in the development of potent inhibitors of the cytokines, the biologic DMARDs. These treatments reduce systemic inflammation and have some effect on the generalized and localized bone loss. Progression of bone erosion was slowed by TNF, IL-6 and IL-1 inhibitors, a JAK inhibitor, a CTLA4 agonist, and rituximab. Effects on bone mineral density varied between the biological DMARDs. Medications that are approved for the treatment of osteoporosis have been evaluated to prevent bone loss in rheumatic disease patients, including denosumab, cathepsin K, bisphosphonates, anti-sclerostin antibodies and parathyroid hormone (hPTH 1-34), and have some efficacy in both the prevention of systemic bone loss and reducing localized bone erosions. This article reviews the effects of biologic DMARDs on bone mass and erosions in patients with rheumatic diseases and trials of anti-osteoporotic medications in animal models and patients with rheumatic diseases.