The prevention of fragility fractures in diabetic patients

Patients with diabetes mellitus (DM) are at greater risk of fractures mostly due to not only extraskeletal factors, such as propensity to falls, but also to bone quality alteration, which reduces bone strength. In people with DM, insulin deficit and hyperglycemia seem to play a role in determining bone formation alteration by AGE accumulation which directly influences osteoblast activity. Although there are conflicting data in the literature, adequate glycemic control with hypoglycemic treatment may be an important element in preventing bone tissue alterations in both type 1 and type 2 DM. Diabetes status is a predictive of future hip and major osteoporosis fractures independently of BMD and FRAX probability. Attention should be paid to the use of thiazolidinediones, especially in older women, because the direct negative effect on bone could exceed the positive effect of glycemic control. Systematic screening for complications and fall prevention efforts, along with calcium and vitamin D repletion and adequate physical activity, represents the mainstay of fracture prevention in DM patients. All anticatabolic drugs (raloxifene, bisphosphonates, denosumab) seem to be effective in DM patients. On the basis of pathophysiological evidence that suggests low bone formation in DM patients, osteoanabolic therapies such as teriparatide might represent an important therapeutic option for DM patients with severe osteoporosis and/or multiple fractures. The search for better methods for the identification of fragility fracture risk in the growing population of adult and elderly subjects with DM might be considered a clinical priority which could improve the prevention of fracture in DM patients.