Bone disease is a serious complication to diabetes. Patients with type 1 diabetes (T1D) and type 2 diabetes (T2D) suffer from an increased risk of fracture, most notably at the hip, compared with patients without diabetes. The fracture risk is influenced by general factors; gender, age, body mass index, and diabetes specific factors; blood glucose status, fall risk, and diabetes medications. Different underlying mechanisms contribute to bone disease in patients with diabetes. Bone quality is affected by low bone turnover in T1D and T2D, and furthermore, incorporation of advanced glycation end-products, changes in the incretin hormone response, and microvascular complications contribute to impaired bone quality and increased fracture risk. The low bone turnover may be caused by several factors, among them increased levels of sclerostin and reduced levels of IGF-I. There are differences in the bone phenotypes between patients with T1D and T2D. Patients with T1D tend to have low BMD whereas patients with T2D tend to have high BMD, however, the changes in BMD do not explain the increased fracture risk in either group. Furthermore, the bone turnover is more suppressed in patients with T2D than in patients with T1D.
Diagnosis of bone disease in patients with diabetes is a challenge as current methods for fracture prediction such as bone mineral density T-score and fracture risk assessment tools underestimate fracture risk for patients with T1D and T2D.
Posthoc analyses of clinical trials on treatment modalities for osteoporosis have shown that approved medications for osteoporosis improve BMD and prevent fractures in patients with diabetes as well as in patients without.
Fractures are common in patients with diabetes and therefore prevention of osteoporosis and falls should be an integrated part of care and management of patients with diabetes.