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Pathways for Bone Loss in Inflammatory Disease

  • Skeletal Biology (D Burr, Section Editor)
  • Published:
Current Osteoporosis Reports Aims and scope Submit manuscript

Abstract

Chronic inflammation including autoimmune disease is an important risk factor for the development of osteoporosis. Receptor activator of nuclear factor-κB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) play a central role in osteoclast differentiation and function, and the molecular pathways by which M-CSF and RANKL induce osteoclast differentiation have been analyzed in detail. Proinflammatory cytokines directly or indirectly regulate osteoclastogenesis and bone resorption providing a link between inflammation and osteoporosis. Tumor necrosis factor-α, interleukin (IL)-1, IL-6, and IL-17 are the most important proinflammatory cytokines triggering inflammatory bone loss. Inhibition of these cytokines has provided potent therapeutic effects in the treatment of diseases such as rheumatoid arthritis. Further investigation is needed to understand the pathophysiology and to develop new strategies to treat inflammatory bone loss. This review summarizes new data on inflammatory bone loss obtained in 2011.

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  1. Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Krankenhausstraße 12, 91054, Erlangen, Germany

    Tobias Braun & Georg Schett

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  1. Tobias Braun
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  2. Georg Schett
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Correspondence to Georg Schett.

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Braun, T., Schett, G. Pathways for Bone Loss in Inflammatory Disease. Curr Osteoporos Rep 10, 101–108 (2012). https://doi.org/10.1007/s11914-012-0104-5

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