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Mechanisms of Disease: is osteoporosis the obesity of bone?

Nature Clinical Practice Rheumatology volume 2, pages 35–43 (2006)Cite this article

Abstract

Osteoporosis and obesity, two disorders of body composition, are growing in prevalence. Interestingly, these diseases share several features including a genetic predisposition and a common progenitor cell. With aging, the composition of bone marrow shifts to favor the presence of adipocytes, osteoclast activity increases, and osteoblast function declines, resulting in osteoporosis. Secondary causes of osteoporosis, including diabetes mellitus, glucocorticoids and immobility, are associated with bone-marrow adiposity. In this review, we ask a provocative question: does fat infiltration in the bone marrow cause low bone mass or is it a result of bone loss? Unraveling the interface between bone and fat at a molecular and cellular level is likely to lead to a better understanding of several diseases, and to the development of drugs for both osteoporosis and obesity.

Key Points

  • Bone-marrow stromal cells can differentiate into adipocytes or osteoblasts

  • Bone-marrow adiposity increases with age in mammalian species

  • The function of fat in the bone marrow is unknown; it may be protective or detrimental

  • Increased bone-marrow fat as detected by MRI might be associated with greater fracture risk

  • The master controls over stem-cell lineage allocation are still not well defined

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Figure 1: Lineage allocation in the bone-marrow milieu.
Figure 2: (A) MRI of the radius in a 34-year-old healthy woman and (B) in a 64-year-old osteoporotic woman.

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Acknowledgements

The authors are supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases.

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Authors and Affiliations

  1. The Jackson Laboratory, Bar Harbor, ME, USA

    Clifford J Rosen

  2. Maine Center for Osteoporosis Research, Bangor, ME, USA

    Clifford J Rosen

  3. Assistant Professor of Orthopedic Surgery at Harvard Medical School and the Beth Israel Deaconess Medical Center, Boston, MA, USA

    Mary L Bouxsein

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Correspondence to Clifford J Rosen.

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The authors declare no competing financial interests.

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Rosen, C., Bouxsein, M. Mechanisms of Disease: is osteoporosis the obesity of bone?. Nat Rev Rheumatol 2, 35–43 (2006). https://doi.org/10.1038/ncprheum0070

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