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Journal of Osteoporosis
Volume 2015 (2015), Article ID 174186, 8 pages
Review Article

Type 1 Diabetes and Osteoporosis: From Molecular Pathways to Bone Phenotype

1Department of Medicine, Western University, London, ON, Canada
2Division of Endocrinology and Metabolism, St. Joseph’s Health Care, 268 Grosvenor Street, London, ON, Canada N6A 4V2

Received 17 November 2014; Accepted 9 March 2015

Academic Editor: Manuel Diaz Curiel

Copyright © 2015 Tayyab S. Khan and Lisa-Ann Fraser. 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.


The link between type 1 diabetes mellitus (DM1) and osteoporosis, identified decades ago, has gained attention in recent years. While a number of cellular mechanisms have been postulated to mediate this association, it is now established that defects in osteoblast differentiation and activity are the main culprits underlying bone fragility in DM1. Other contributing factors include an accumulation of advanced glycation end products (AGEs) and the development of diabetes complications (such as neuropathy and hypoglycemia), which cause further decline in bone mineral density (BMD), worsening geometric properties within bone, and increased fall risk. As a result, patients with DM1 have a 6.9-fold increased incidence of hip fracture compared to controls. Despite this increased fracture risk, bone fragility remains an underappreciated complication of DM1 and is not addressed in most diabetes guidelines. There is also a lack of data regarding the efficacy of therapeutic strategies to treat osteoporosis in this patient population. Together, our current understanding of bone fragility in DM1 calls for an update of diabetes guidelines, better screening tools, and further research into the use of therapeutic strategies in this patient population.