长期存在的1型糖尿病与皮质骨机械行为缺陷和人类大腿骨基质组成的改变有关
Shannon R Emerzian1,2, Jarred Chow1, Ramina Behzad3
1Center for Advanced Orthopedic Studies, Department of Orthopedic Surgery, Beth Israel Deaconess Medical Center, Boston, MA 02215, United States.
概括
1型糖尿病 (T1D) 增加骨折的风险,由于骨质的变化. 先进的糖化最终产品 (AGEs) 和改变的矩阵组成解释了T1D患者骨强度的降低.
科学领域:
- 生物材料科学 生物材料科学
- 整形外科 整形外科 整形外科
- 内分泌学 在内分泌学.
背景情况:
- 1型糖尿病 (T1D) 与较高的关节骨折率有关,超过仅仅由骨矿物质密度降低预测的风险.
- 高度糖化最终产品 (AGEs) 的积累和骨基质组成的改变是导致这种脆弱性的潜在因素.
- 关于长期T1D患者皮层骨物质特性存在有限的数据.
研究的目的:
- 为了研究和描述皮质骨的物质行为在老年人长期T1D.
- 为了比较T1D患者和非糖尿病对照者之间的骨材料特性,AGE水平和矩阵组成.
主要方法:
- 机械测试 (4点曲,循环参考点缩,冲击微缩) 的尸体大腿骨.
- 通过拉曼光谱学量化AGE (总光AGE,托西丁,碳氧甲基氨酸[CML]) 和矩阵组成.
- 分析了20名患有T1D的老年人 (≥50岁) 和14名年龄和性别匹配的对照的样本.
主要成果:
- 与对照组相比,T1D患者的皮层骨显著减少了产后性 (-30%).
- 在T1D骨中观察到托西丁水平升高 (+17%),矿物质结晶性降低 (-1.4%),林氧化增加 (+1.9%),以及糖氨基甘油 (GAG) 含量降低 (-1.3%) .
- 多重回归分析表明,CML,原交叉链和GAG含量是强度的显著预测因素,掩盖了糖尿病状况的影响.
结论:
- 长期T1D后皮层骨中的能量吸收受损主要由AGE积累和矩阵修改来解释.
- 这些发现为1型糖尿病患者骨脆弱性背后的机制提供了新的见解.
- 针对AGE和矩阵组成可能对减轻T1D患者骨折风险至关重要.
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