Puspitasari Melisa, Purnamasari Dyah, Setyohadi Bambang, Isbagio Harry
Department of Internal Medicine, Faculty of Medicine University of Indonesia, Cipto Mangunkusumo Hospital, Jakarta, Indonesia.
Division of Metabolism and Endocrinology, Department of Internal Medicine, Faculty of Medicine University of Indonesia, Cipto Mangunkusumo Hospital, Jakarta, Indonesia.
J ASEAN Fed Endocr Soc. 2017;32(2):90-99. doi: 10.15605/jafes.032.02.14. Epub 2017 Oct 15.
Individuals with Type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) are at increased risk for fragility fractures. Bone mineral density (BMD) is decreased in T1DM but often normal or even elevated in T2DM when compared with age-matched non-DM populations. However, bone turnover is decreased in both T1DM and T2DM. The pathophysiologic mechanisms leading to bone fragility is multifactorial, and potentially leads to reduced bone formation, altered bone microstructure and decreased bone strength. Interestingly, different antidiabetic treatments may influence fracture risk due to effects on glycemic control, triggering of hypoglycemic events or osteoblastogenesis.
1型糖尿病（T1DM）和2型糖尿病（T2DM）患者发生脆性骨折的风险增加。与年龄匹配的非糖尿病人群相比，T1DM患者的骨矿物质密度（BMD）降低，但T2DM患者的BMD通常正常甚至升高。然而，T1DM和T2DM患者的骨转换均降低。导致骨脆性的病理生理机制是多因素的，可能导致骨形成减少、骨微结构改变和骨强度降低。有趣的是，不同的抗糖尿病治疗可能由于对血糖控制、低血糖事件触发或成骨细胞生成的影响而影响骨折风险。
