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Effect of Degeneration on Fluid–Solid Interaction within Intervertebral Disk Under Cyclic Loading – A Meta-Model Analysis of Finite Element Simulations

机译:循环载荷下变性对椎间盘内流固耦合的影响–有限元模拟的元模型分析

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摘要

The risk of low back pain resulted from cyclic loadings is greater than that resulted from prolonged static postures. Disk degeneration results in degradation of disk solid structures and decrease of water contents, which is caused by activation of matrix digestive enzymes. The mechanical responses resulted from internal solid–fluid interactions of degenerative disks to cyclic loadings are not well studied yet. The fluid–solid interactions in disks can be evaluated by mathematical models, especially the poroelastic finite element (FE) models. We developed a robust disk poroelastic FE model to analyze the effect of degeneration on solid–fluid interactions within disk subjected to cyclic loadings at different loading frequencies. A backward analysis combined with in vitro experiments was used to find the elastic modulus and hydraulic permeability of intact and enzyme-induced degenerated porcine disks. The results showed that the averaged peak-to-peak disk deformations during the in vitro cyclic tests were well fitted with limited FE simulations and a quadratic response surface regression for both disk groups. The results showed that higher loading frequency increased the intradiscal pressure, decreased the total fluid loss, and slightly increased the maximum axial stress within solid matrix. Enzyme-induced degeneration decreased the intradiscal pressure and total fluid loss, and barely changed the maximum axial stress within solid matrix. The increase of intradiscal pressure and total fluid loss with loading frequency was less sensitive after the frequency elevated to 0.1 Hz for the enzyme-induced degenerated disk. Based on this study, it is found that enzyme-induced degeneration decreases energy attenuation capability of disk, but less change the strength of disk.
机译:周期性负荷所致下腰痛的风险大于静态姿势长期所致的风险。椎间盘退变导致椎间盘固体结构退化和水含量降低,这是由于基质消化酶的活化引起的。退化盘的内部固液相互作用对循环载荷产生的机械响应尚未得到很好的研究。可以通过数学模型,尤其是多孔弹性有限元(FE)模型来评估圆盘中的流固耦合。我们开发了一种鲁棒的圆孔多孔弹性有限元模型,以分析在不同载荷频率下承受循环载荷的变质对盘内固液相互作用的影响。使用反向分析结合体外实验来发现完整的和酶诱导的变性猪圆盘的弹性模量和水力渗透率。结果表明,在体外循环测试过程中,平均的峰-峰圆盘变形与有限的有限元模拟以及两个圆盘组的二次响应面回归非常吻合。结果表明,较高的加载频率会提高椎间盘内压力,减少总流体损失,并稍微增加固体基质内的最大轴向应力。酶引起的变性降低了椎间盘内压力和总液体流失,几乎没有改变固体基质内的最大轴向应力。当酶诱导的变性椎间盘的频率升高至0.1 Hz后,椎间盘内压力的增加和总流体损失随加载频率的增加变得不那么敏感。基于该研究,发现酶诱导的变性降低了盘的能量衰减能力,但是较少改变盘的强度。

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