Starup-Linde Jakob, Hygum Katrine, Langdahl Bente Lomholt
Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark.
Steno Diabetes Center North Jutland, Aalborg University Hospital, Aalborg, Denmark.
Endocrinol Metab (Seoul). 2018 Sep;33(3):339-351. doi: 10.3803/EnM.2018.33.3.339.
Type 2 diabetes (T2D) is associated with an increased risk of fracture, which has been reported in several epidemiological studies. However, bone mineral density in T2D is increased and underestimates the fracture risk. Common risk factors for fracture do not fully explain the increased fracture risk observed in patients with T2D. We propose that the pathogenesis of increased fracture risk in T2D is due to low bone turnover caused by osteocyte dysfunction resulting in bone microcracks and fractures. Increased levels of sclerostin may mediate the low bone turnover and may be a novel marker of increased fracture risk, although further research is needed. An impaired incretin response in T2D may also affect bone turnover. Accumulation of advanced glycosylation endproducts may also impair bone strength. Concerning antidiabetic medication, the glitazones are detrimental to bone health and associated with increased fracture risk, and the sulphonylureas may increase fracture risk by causing hypoglycemia. So far, the results on the effect of other antidiabetics are ambiguous. No specific guideline for the management of bone disease in T2D is available and current evidence on the effects of antiosteoporotic medication in T2D is sparse. The aim of this review is to collate current evidence of the pathogenesis, detection and treatment of diabetic bone disease.
2型糖尿病（T2D）与骨折风险增加相关，这在多项流行病学研究中已有报道。然而，T2D患者的骨矿物质密度增加，从而低估了骨折风险。常见的骨折风险因素并不能完全解释T2D患者中观察到的骨折风险增加。我们认为，T2D患者骨折风险增加的发病机制是由于骨细胞功能障碍导致骨转换率降低，进而引起骨微裂纹和骨折。硬化蛋白水平升高可能介导了低骨转换，并且可能是骨折风险增加的一个新标志物，不过仍需进一步研究。T2D患者肠促胰岛素反应受损也可能影响骨转换。晚期糖基化终末产物的积累也可能损害骨骼强度。关于抗糖尿病药物，噻唑烷二酮类药物对骨骼健康有害，与骨折风险增加相关，而磺脲类药物可能因导致低血糖而增加骨折风险。到目前为止，其他抗糖尿病药物的作用结果尚不明确。目前尚无针对T2D患者骨病管理的具体指南，且关于抗骨质疏松药物在T2D患者中作用的现有证据较少。本综述的目的是整理有关糖尿病骨病发病机制、检测和治疗的当前证据。
