INTRODUCTION: Type 1 diabetes (T1D) is an autoimmune disease with chronic hyperglycemic state, which incidence has been globally rising during the past decades. Besides the well-known diabetic complications such as retinopathy, nephropathy and neuropathy, T1D is characterized also by poor bone health. The reduced bone mineralization, quality and strength lead to vertebral and hip fractures as the most important clinical manifestations. Suppressed bone turnover is the main characteristic of T1D-associated bone disorder. RESULTS: This is thought to be due to hyperglycemia, hypoinsulinemia, autoimmune inflammation, low levels of insulin-like growth factor-1 and vitamin D. Young age of T1D manifestation, chronic poor glycemic control, high daily insulin dose, low body mass index, reduced renal function and the presence of diabetic complications are clinical factors useful for identifying T1D patients at risk of reduced bone mineral density. Although the clinical risk factors for fracture risk are still unknown, chronic poor glycemic control and the presence of diabetic complications might raise the suspicion of elevated fracture risk in T1D. In the presence of the above-mentioned risk factors, the assessment of bone mineral density by dual-energy X-ray absorptiometry and the search of asymptomatic vertebral fracture by vertebral fracture assessment or lateral X-ray radiography of thorax-lumbar spine should be recommended. CONCLUSION: There is no consensus about the treatment of diabetic bone disorder. However, the improvement of glycemic control has been suggested to have a beneficial effect on bone in T1D. Recently, several experiments showed promising results on using anabolic pharmacological agents in diabetic rodents with bone disorder. Therefore, randomized clinical trials are needed to test the possible use of the bone anabolic therapies in humans with T1D.
INTRODUCTION:Type 1 diabetes (T1D) is an autoimmune disease with chronic hyperglycemic state, which incidence has been globally rising during the past decades. Besides the well-known diabetic complications such as retinopathy, nephropathy and neuropathy, T1D is characterized also by poor bone health. The reduced bone mineralization, quality and strength lead to vertebral and hip fractures as the most important clinical manifestations. Suppressed bone turnover is the main characteristic of T1D-associated bone disorder. RESULTS: This is thought to be due to hyperglycemia, hypoinsulinemia, autoimmune inflammation, low levels of insulin-like growth factor-1 and vitamin D. Young age of T1D manifestation, chronic poor glycemic control, high daily insulin dose, low body mass index, reduced renal function and the presence of diabetic complications are clinical factors useful for identifying T1D patients at risk of reduced bone mineral density. Although the clinical risk factors for fracture risk are still unknown, chronic poor glycemic control and the presence of diabetic complications might raise the suspicion of elevated fracture risk in T1D. In the presence of the above-mentioned risk factors, the assessment of bone mineral density by dual-energy X-ray absorptiometry and the search of asymptomatic vertebral fracture by vertebral fracture assessment or lateral X-ray radiography of thorax-lumbar spine should be recommended. CONCLUSION: There is no consensus about the treatment of diabetic bone disorder. However, the improvement of glycemic control has been suggested to have a beneficial effect on bone in T1D. Recently, several experiments showed promising results on using anabolic pharmacological agents in diabetic rodents with bone disorder. Therefore, randomized clinical trials are needed to test the possible use of the bone anabolic therapies in humans with T1D.
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