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Bone, sweet bone—osteoporotic fractures in diabetes mellitus

Abstract

Diabetes mellitus adversely affects the skeleton and is associated with an increased risk of osteoporosis and fragility fractures. The mechanisms underlying low bone strength are not fully understood but could include impaired accrual of peak bone mass and diabetic complications, such as nephropathy. Type 1 diabetes mellitus (T1DM) affects the skeleton more severely than type 2 diabetes mellitus (T2DM), probably because of the lack of the bone anabolic actions of insulin and other pancreatic hormones. Bone mass can remain high in patients with T2DM, but it does not protect against fractures, as bone quality is impaired. The class of oral antidiabetic drugs known as glitazones can promote bone loss and osteoporotic fractures in postmenopausal women and, therefore, should be avoided if osteoporosis is diagnosed. A physically active, healthy lifestyle and prevention of diabetic complications, along with calcium and vitamin D repletion, represent the mainstay of therapy for osteoporosis in patients with T1DM or T2DM. Assessment of BMD and other risk factors as part of the diagnostic procedure can help design tailored treatment plans. All osteoporosis drugs seem to be effective in patients with diabetes mellitus. Increased awareness of osteoporosis is needed in view of the growing and aging population of patients with diabetes mellitus.

Key Points

  • Type 1 and type 2 diabetes mellitus are associated with an increased risk of osteoporotic fractures

  • Bone formation and osteoblast function are impaired in patients with type 1 diabetes mellitus

  • BMD is increased but bone quality is reduced in patients with type 2 diabetes mellitus

  • Glitazones might promote bone loss and should be avoided in patients with osteoporosis

  • Comorbidities guide the selection of specific osteoporosis therapies

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Figure 1: Skeletal complications of diabetes mellitus.
Figure 2: Skeletal effects of pharmacological treatments for T2DM.
Figure 3: Impaired osteogenesis in T1DM.

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Acknowledgements

C. Hamann and L. C. Hofbauer are supported by grants from Elsbeth Bonhoff Foundation. C. Hamann and L. C. Hofbauer and K.-P. Günther are supported by Center for Regenerative Therapies Dresden seed grants. L. C. Hofbauer is also supported by Deutsche Forschungsgemeinschaft Transregio-67, project B2.

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C. Hamann and L. C. Hofbauer researched the data for and contributed equally to writing of the article. All authors provided a substantial contribution to discussions of the content and reviewed and/or edited the manuscript before submission.

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L. C. Hofbauer has worked as a consultant for Amgen, Merck and Novartis. He has received research grants from Amgen, Novartis and Nycomed. He has received hororaria from Amgen, Lilly, Merck, Novartis and Nycomed. The other authors declare no competing interests.

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Hamann, C., Kirschner, S., Günther, KP. et al. Bone, sweet bone—osteoporotic fractures in diabetes mellitus. Nat Rev Endocrinol 8, 297–305 (2012). https://doi.org/10.1038/nrendo.2011.233

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