The roles of architecture and estrogen depletion in microdamage risk in trabecular bone
The roles of architecture and estrogen depletion in microdamage risk in trabecular bone
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DOI：
10.1016/j.jbiomech.2016.08.009
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发表时间：
2016-10-03
影响因子：
2.4
通讯作者：
Niebur, Glen L.
中科院分区：
文献类型：
--
作者：
Kreipke, Tyler C.;Garrison, Jacqueline G.;Niebur, Glen L.
骨量或骨密度不足以区分个体的骨折风险。骨质量的其他指标，如微结构特征和骨组织特性，包括损伤的存在，可能会改善对骨折风险的诊断。微损伤和微结构是骨小梁质量的两个相互依赖的方面，在补偿骨密度后，一些微结构的变化与损伤风险密切相关。本研究采用去卵巢绵羊模拟绝经后骨质疏松症模型，探讨微结构和雌激素缺乏对骨小梁微损伤易感性的影响。采用一系列压缩和扭转超载的方法，研究股骨远端松质骨微损伤的形成倾向。卵巢切除对该解剖部位的微结构影响很小。微损伤与骨体积分数和结构模型指数(SMI)相关，卵巢切除增加了对这些参数的敏感性。后者可能是由于作为应力集中的吸收腔增加或骨组织特性改变所致。先前存在的损害也与新的损害地层相关。然而，顺序加载主要产生新的裂纹，而不是扩展现有的裂纹，这表明先前存在的微损伤通过将载荷转移到先前未受损的骨小梁而导致进一步的骨损伤，而骨小梁随后会受到损伤。SMI显示，从板状到杆状的骨小梁的转变决定了这种转变，可能是骨骼的一个特征，它已经倾向于通过受损的微结构积累更大程度的损害。(C)2016爱思唯尔有限公司。保留所有权利。
Bone quantity, or density, has insufficient power to discriminate fracture risk in individuals. Additional measures of bone quality, such as microarchitectural characteristics and bone tissue properties, including the presence of damage, may improve the diagnosis of fracture risk. Microdamage and microarchitecture are two aspects of trabecular bone quality that are interdependent, with several microarchitectural changes strongly correlated to damage risk after compensating for bone density. This study aimed to delineate the effects of microarchitecture and estrogen depletion on microdamage susceptibility in trabecular bone using an ovariectomized sheep model to mimic post-menopausal osteoporosis. The propensity for microdamage formation in trabecular bone of the distal femur was studied using a sequence of compressive and torsional overloads. Ovariectomy had only minor effects on the micro architecture at this anatomic site. Microdamage was correlated to bone volume fraction and structure model index (SMI), and ovariectomy increased the sensitivity to these parameters. The latter may be due to either increased resorption cavities acting as stress concentrations or to altered bone tissue properties. Pre-existing damage was also correlated to new damage formation. However, sequential loading primarily generated new cracks as opposed to propagating existing cracks, suggesting that pre-existing microdamage contributes to further damage of bone by shifting load bearing to previously undamaged trabeculae, which are subsequently damaged. The transition from plate-like to rod-like trabeculae, indicated by SMI, dictates this shift, and may be a hallmark of bone that is already predisposed to accruing greater levels of damage through compromised microarchitecture. (C) 2016 Elsevier Ltd. All rights reserved.