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An update on diabetes related skeletal fragility

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Pages 193-210 | Published online: 02 Jan 2015
 

Abstract

There are several mechanisms by which diabetes could affect bone mass and strength. These mechanisms include insulin deficiency; hyperglycemia; the accumulation of advanced glycation end products that may influence collagen characteristics; marrow adiposity and bone inflammation. Furthermore, associated diabetic complications and treatment with thaizolidinediones may also increase risk of fracturing. The following article provides its readers with an update on the latest information pertaining to diabetes related bone skeletal fragility. In the authors’ opinion, future studies are needed in order to clarify the impact of different aspects of diabetes metabolism, glycemic control, and specific treatments for diabetes on bone. Given that dual energy x-ray absorptiometry is a poor predictor of bone morbidity in this group of patients, there is a need to explore novel approaches for assessing bone quality. It is important that we develop a better understanding of how diabetes affects bone in order to improve our ability to protect bone health and prevent fractures in the growing population of adults with diabetes.

Financial & competing interests disclosure

N Abdalrahman is currently supported by the Government of Libya. SC Chen is currently supported by the Yorkhill Children’s Charity and JR Wang has received generous support from the Endocrine Society. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Key issues
  • The awareness of bone as another target organ of diabetes complications remains low clinically out with the research arena.

  • Small samples sizes and problems with addressing confounding factors limit the evidence on the effect of glycemic control on bone health in diabetes.

  • Abnormalities of bone health may be present early after diagnosis.

  • Diabetic bone loss is most likely due to a complex interplay between the effects of hyperglycemia, insulin deficiency, IGF-1 deficiency, increased bone marrow adiposity, inflammation and vasculopathy on bone formation.

  • In-vitro studies support the osteogenic potential of metformin, which offers a rational prevention strategy.

  • The disparity between dual x-ray absorptiometry-derived bone mineral density and actual fracture risk highlights the limitation of dual x-ray absorptiometry as a predictor of fracture risk in conditions secondary to systemic disease.

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