Bone microarchitecture, biomechanical properties, and advanced glycation end-products in the proximal femur of adults with type 2 diabetes.
Bone microarchitecture, biomechanical properties, and advanced glycation end-products in the proximal femur of adults with type 2 diabetes.
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DOI：
10.1016/j.bone.2018.05.030
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发表时间：
2018-09
期刊：
影响因子：
4.1
通讯作者：
Bouxsein ML
中科院分区：
文献类型：
--
作者：
Karim L;Moulton J;Van Vliet M;Velie K;Robbins A;Malekipour F;Abdeen A;Ayres D;Bouxsein ML
骨骼脆弱是2型糖尿病（T2D）的主要并发症，但对T2D骨骼脆弱的机制了解甚少。骨折风险的增加被认为是由于晚期糖基化终产物（AGEs）的积累导致骨微结构恶化或骨质量差。我们通过临床研究来确定：1)T2D骨是否改变了骨微结构、AGEs和骨生物力学特性，2)骨AGEs与骨生物力学特性相关，3)血清AGE水平反映了骨中的AGE水平。为此，我们收集了接受全髋关节置换术的T2D （n = 20）和非糖尿病（n = 33）受试者的血清和股骨近端标本。股骨颈切片采用微计算机断层扫描（microCT）成像，循环参考点压痕测试，并定量测定AGE含量。从股骨头取下小梁核心，用微ct成像并进行单轴无侧限压缩试验。t2dm患者的HbA1c更高（+23%,p≤0.0001），但与非糖尿病患者相比，皮质组织矿物质密度、皮质孔隙度或小梁微结构没有差异。循环参考点压痕显示，t2dm皮质骨的蠕变压痕距离（+18%,p≤0.05）和压痕距离增加（+20%,p≤0.05）大于非糖尿病患者，但其他压痕变量无差异。除了屈服应力外，两组患者的骨小梁力学性能相似，屈服应力在t2dm患者中往往低于非糖尿病患者。血清戊苷和血清总AGEs在两组间无差异。在t2dm患者中，骨皮质而非骨小梁的AGEs往往更高（21%,p = 0.09）。血清AGEs和戊sidine与皮质骨和小梁骨AGEs呈正相关。我们的研究提供了关于成人T2D患者的生物力学特性和AGEs的新数据，这些数据需要更好地理解糖尿病骨骼脆性的机制。
Skeletal fragility is a major complication of type 2 diabetes mellitus (T2D), but there is a poor understanding of mechanisms underlying T2D skeletal fragility. The increased fracture risk has been suggested to result from deteriorated bone microarchitecture or poor bone quality due to accumulation of advanced glycation end-products (AGEs). We conducted a clinical study to determine whether: 1) bone microarchitecture, AGEs, and bone biomechanical properties are altered in T2D bone, 2) bone AGEs are related to bone biomechanical properties, and 3) serum AGE levels reflect those in bone. To do so, we collected serum and proximal femur specimens from T2D (n = 20) and non-diabetic (n = 33) subjects undergoing total hip replacement surgery. A section from the femoral neck was imaged by microcomputed tomography (microCT), tested by cyclic reference point indentation, and quantified for AGE content. A trabecular core taken from the femoral head was imaged by microCT and subjected to uniaxial unconfined compression tests. T2D subjects had greater HbA1c (+23%, p ≤ 0.0001), but no difference in cortical tissue mineral density, cortical porosity, or trabecular microarchitecture compared to non-diabetics. Cyclic reference point indentation revealed that creep indentation distance (+18%, p ≤ 0.05) and indentation distance increase (+20%, p ≤ 0.05) were greater in cortical bone from T2D than in non-diabetics, but no other indentation variables differed. Trabecular bone mechanical properties were similar in both groups, except for yield stress, which tended to be lower in T2D than in non-diabetics. Neither serum pentosidine nor serum total AGEs were different between groups. Cortical, but not trabecular, bone AGEs tended to be higher in T2D subjects (21%, p = 0.09). Serum AGEs and pentosidine were positively correlated with cortical and trabecular bone AGEs. Our study presents new data on biomechanical properties and AGEs in adults with T2D, which are needed to better understand mechanisms contributing to diabetic skeletal fragility.
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