Abstract
Osteoporosis is now generally considered as a complication of diabetes mellitus (DM). Higher HbA1c level and presence of diabetic vascular complications and insulin use are associated with higher risk of fractures, indicating detrimental effects of chronic hyperglycemia on bone. Because bone mineral density does not seem to be affected by glycemic control, this chapter reviews the influence of abnormal glucose metabolism on bone and diabetes-associated factors causing impaired bone strength mainly from clinical studies. Results of human histomorphometrical studies and longitudinal metabolic bone marker studies indicate that bone turnover may not be generally suppressed in DM. With hyperglycemia bone resorption seems to be stimulated, whereas bone formation may be suppressed. Vitamin D deficiency is common in DM, which may or may not be associated with secondary hyperparathyroidism, could not account for such changes in bone turnover. Animal and in vitro studies support this concept. Hyperglycemia per se or via the accumulation of advanced glycation end products (AGEs) appears to stimulate osteoclasts while suppressing osteoblasts, and perhaps mesenchymal stem cells as well as osteocytes. AGE accumulation in bone matrix also compromises mechanical strength. More clinical longitudinal studies would be needed to further elucidate the influence of hyperglycemia in the development of osteoporosis associated with DM.
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Okazaki, R., Inoue, D. (2016). Mechanism for the Development of Bone Disease in Diabetes: Abnormal Glucose Metabolism. In: Inaba, M. (eds) Musculoskeletal Disease Associated with Diabetes Mellitus. Springer, Tokyo. https://doi.org/10.1007/978-4-431-55720-3_4
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