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Journal of Diabetes Research
Volume 2016, Article ID 6969040, 5 pages
Review Article

Sweet Bones: The Pathogenesis of Bone Alteration in Diabetes

Department of Physiology, College of Medicine, University of Dammam, P. O. Box 2114-31451, Dammam, Saudi Arabia

Received 17 July 2016; Accepted 15 September 2016

Academic Editor: Ilias Migdalis

Copyright © 2016 Mohammed Al-Hariri. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Diabetic patients have increased fracture risk. The pathogenesis underlying the status of bone alterations in diabetes mellitus is not completely understood but is multifactorial. The major deficits appear to be related to a deficit in mineralized surface area, a decrement in the rate of mineral apposition, deceased osteoid surface, depressed osteoblast activity, and decreased numbers of osteoclasts due to abnormal insulin signaling pathway. Other prominent features of diabetes mellitus are an increased urinary excretion of calcium and magnesium, accumulation of advanced glycation end products, and oxidative stress leading to sweet bones (altered bone’s strength, metabolism, and structure). Every diabetic patient should be assessed for risk factors for fractures and osteoporosis. The pathogenesis of the bone alterations in diabetes mellitus as well as their molecular mechanisms needs further study.