Age-related differences in the morphology of microdamage propagation in trabecular bone.
Age-related differences in the morphology of microdamage propagation in trabecular bone.
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DOI：
10.1016/j.jbiomech.2011.08.006
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发表时间：
2011-10-13
影响因子：
2.4
通讯作者：
Guldberg RE
中科院分区：
文献类型：
--
作者：
Green JO;Wang J;Diab T;Vidakovic B;Guldberg RE
研究表明，骨小梁的微损伤密度随着年龄的增长而增加，并且与断裂韧性的降低有关。人们已经对皮质骨中的裂纹扩展进行了大量研究，但缺乏小梁骨中的数据。在这项研究中，对年轻（61.3 ± 3.1 岁）和年长（75.0 ± 3.9 岁）男性和女性股骨头小梁骨核心的严重、线性和弥漫性损伤的传播进行了检查。使用两步机械测试方案，首先通过静态单轴压缩至 0.8% 应变引发损坏，然后以 0.005 的归一化应力水平传播至 0.8% 的应变终点。将机械测试与双荧光染色技术相结合，对传播裂纹的数量和长度/面积进行量化。结果发现，与较年轻的样本相比，较老的样本达到测试终点的周期数显着减少（较年轻的样本：77372 ± 15984 个周期；较老的样本：34944 ± 11964 个周期，p=0.06）。这与老年组疲劳测试期间大量严重受损的小梁面积扩大相对应。在年轻组中，弥漫性损伤的小梁具有更大的损伤面积，这说明了有效的能量耗散机制。这些结果表明，人类骨小梁疲劳寿命与年龄相关的差异可能是由于传播的微损伤形态的差异造成的。
Microdamage density has been shown to increase with age in trabecular bone and is associated with decreased fracture toughness. Numerous studies of crack propagation in cortical bone have been conducted, but data in trabecular bone is lacking. In this study, propagation of severe, linear, and diffuse damage was examined in trabecular bone cores from the femoral head of younger (61.3 ± 3.1 years) and older (75.0 ± 3.9 years) men and women. Using a two-step mechanical testing protocol, damage was first initiated with static uniaxial compression to 0.8% strain then propagated at a normalized stress level of 0.005 to a strain endpoint of 0.8%. Coupling mechanical testing with a dual fluorescent staining technique, the number and length/area of propagating cracks were quantified. It was found that the number of cycles to the test endpoint was substantially decreased in older compared to younger samples (younger: 77372 ± 15984 cycles; older: 34944 ± 11964 cycles, p=0.06). This corresponded with a greater number of severely damaged trabeculae expanding in area during the fatigue test in the older group. In the younger group, diffusely damaged trabeculae had a greater damage area, which illustrates an efficient energy dissipation mechanism. These results suggest that age-related differences in fatigue life of human trabecular bone may be due to differences in propagated microdamage morphology.