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Bone Disease and Diabetes

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Diabetes and Kidney Disease

Abstract

Diabetic osteopathy, one of the most recently recognized complications of diabetes mellitus, is characterized by low bone turnover, microarchitectural changes, and low vitamin D levels accompanied by a negative calcium balance – all leading to an increased fracture risk, independent of bone density which varies considerably. Although generally younger, type 1 diabetic patients usually have lower bone mineral density (BMD), primarily due to acute insulinopenia. Type 2 diabetic patients typically have insulin resistance, hyperinsulinism, and increased body weight – thus explaining the reported higher bone mass in these patients; despite the higher BMD, the accumulation of advanced glycation end products (AGEs), poor glycemic control, increased visceral fat, and several anti-diabetic drugs significantly increase bone fragility, thus explaining the paradoxically higher fracture risk despite preserved bone mass. The presence of diabetic kidney disease (DKD) aggravates bone mineral metabolism disturbances in diabetes mellitus. Patients with DKD develop more severe changes in bone and mineral metabolism and are more prone at developing adynamic bone disease. BMD and current fracture risk assessment tools underestimate fracture risk in the diabetic population, while the therapeutic management is currently limited due to scarce available data regarding bone active therapy in diabetes mellitus. The therapeutic interventions are even more limited in DKD. This chapter discusses the epidemiology, pathophysiology, and also diagnosis and treatment of diabetic osteopathy, with particular interest in the DKD-associated bone disorder.

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Bilha, S.C., Covic, A. (2022). Bone Disease and Diabetes. In: Lerma, E.V., Batuman, V. (eds) Diabetes and Kidney Disease. Springer, Cham. https://doi.org/10.1007/978-3-030-86020-2_16

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