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Why do people with diabetes have a higher risk of fragile bones?

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A new expert review has examined why people with both type 1 and type 2 diabetes face a higher risk of bone fragility and fracture.

The International Osteoporosis Foundation (IOF) Working Group review published in the journal Nature Reviews Endocrinology confirmed that fracture risk is increased not just in type 1 diabetes, but also in the more common type 2 diabetes.

Although bone mineral density (BMD) is decreased in type 1 diabetes, BMD in type 2 is often normal or even slightly elevated compared with an age-matched control population, the researchers said. However, in both types of the condition, bone turnover is decreased and the bone material properties and microstructure of bone are altered — the latter particularly when there are microvascular complications.

The reasons for the bone fragility in diabetes are complex, and include hyperglycaemia, oxidative stress, and accumulation of advanced glycation endproducts that compromise collagen properties, increase marrow adiposity, release inflammatory factors and adipokines from visceral fat, and potentially alter the function of osteocytes (bone cells).

Additionally, treatment-induced hypoglycaemia, certain antidiabetic medications with a direct effect on bone and mineral metabolism (such as thiazolidinediones, or TZDs), as well as an increased propensity for falls, all contribute to increased fracture risk.

The longer the duration of the disease, the higher the risk of diabetes complications, including bone health complications, the researchers noted.

Use of insulin has also been associated with an increased risk of fractures, although it is not clear whether this is because insulin use is a marker of the severity and/or longer duration of the disease or whether it could be due to the occurrence of hypoglycaemic events that cause falls.

Professor Serge Ferrari, chair of the IOF Bone and Diabetes Working Group and Professor at the Geneva University Hospital, Switzerland, commented:

“Currently, no guidelines exist on how and at which stage of the disease to initiate anti-osteoporotic medication in patients with diabetes mellitus. Medications with a neutral or favourable effect on bone metabolism, such as metformin and incretin-based treatments, are preferable. In contrast medications like TZDs should be used with caution.”

Professor Massimo Massi Benedetti, senior programmes advisor at the International Diabetes Federation (IDF) and member of the IOF Working Group, welcomed the review.

“It is important that health professionals are aware that fragility fractures are a severe complication of diabetes,” he said. “Prevention strategies in the treatment of diabetes are to be implemented from the early stage of the disease, while the risk of fractures needs to be evaluated on a routine basis in the population at risk in order to minimise the effect of the clinical factors that have been identified as the possible cause of higher frequency of bone fractures in diabetes. With increasing clinical awareness, ongoing research and the development of specific new drugs we are hoping that there will be new opportunities to improve bone health in people with diabetes in the future.”