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Relative Roles of Cortical and Trabecular Thinning in Reducing Osteoporotic Vertebral Body Stiffness: A Modeling Study

机译:皮质和小梁稀疏在减少骨质疏松症椎体刚度时的相对作用:造型研究

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While the effects of reduced bone density on osteoporotic vertebral strength are well known, the relative roles of cortical shell and trabecular architecture thinning in determining vertebral stiffness and strength are less clear. These are important parameters in investigating the changing biomechanics of the ageing spine, and in assessing the effect of stiffening procedures such as vertebroplasty on neighbouring spinal segments. This work presents the development of a microstructural computer model of the osteoporotic lumbar vertebral body, allowing detailed prediction of the effects of bone micro-architecture on vertebral stiffness and strength. Microstructural finite element models of an L3 human vertebral body were created. The cortex geometry was represented with shell elements and the trabecular network with a lattice of beam elements. Trabecular architecture was varied according to age. Each beam network model was validated against experimental data. Models were generated to represent vertebral bodies of age <50 years, age 50-75y and age >75y respectively. For all models, an initial cortical shell thickness of 0.5mm was used, followed by reductions in the age >75y models to 0.35mm and 0.2mm to represent cortical thinning in late stage osteoporosis. Loads were applied to simulate in vitro biomechanical testing, compressing the vertebra by 20% of its height. Predicted vertebral stiffness and strength reduced with progressive age changes in microarchitecture, demonstrating a 44% reduction in stiffness and a 43% reduction in strength, between the age <50 and age >75 models. Reducing cortical thickness in the age >75 models demonstrated a substantial reduction in stiffness and strength, resulting in a 48% reduction in stiffness and a 62% reduction in strength between the 0.5mm and 0.2mm cortical thickness models. Cortical thinning in late stage osteoporosis may therefore play an even greater role in reducing vertebral stiffness and strength than earlier reductions due to trabecular thinning.
机译:虽然骨密度降低对骨质疏松椎体强度的影响是众所周知的,但皮质壳和小梁架在确定椎体刚度和强度的相对作用的相对作用较小。这些是研究衰老脊柱的变化生物力学的重要参数,以及评估加强程序如椎体成形术对邻近脊髓的影响。这项工作介绍了骨质疏松腰椎椎体的微观结构计算机模型的发展,允许详细预测骨微结构对椎体刚度和强度的影响。创建了L3人体椎体的微结构有限元模型。皮质几何形状用壳体元件和带有梁元素的格子的小梁元件表示。短边架的架构根据年龄而变化。每个光束网络模型针对实验数据验证。产生模型以代表年龄<50岁,50-75Y年龄50-75岁和75岁的椎体。对于所有型号,使用初始皮质外壳厚度为0.5mm,然后在年龄> 75米模型中减少至0.35mm和0.2mm以表示晚期骨质疏松症的皮质稀疏。载荷用于模拟体外生物力学测试,将椎骨压缩20%的高度。预测的椎体刚度和强度随着微体系结构的进步变化而降低,刚度降低44%,强度降低43%,在50岁和年龄> 75型号之间。减少年龄> 75型模型中的皮质厚度证明了刚度和强度的大幅降低,导致刚度降低48%,在0.5mm和0.2mm皮质厚度模型之间的强度降低62%。因此,晚期骨质疏松症的皮质稀疏可能在减少椎体刚度和强度方面发挥更大的作用,而不是由于小梁稀释而减少前后的较早减少。

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