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椎间盘退变会影响相邻松质骨内的应变大小和应力分布。

Disc degeneration influences the strain magnitude and stress distribution within the adjacent trabecular bone.

作者信息

Raftery Kay A, Kargarzadeh Alireza, Tavana Saman, Newell Nicolas

机构信息

Department of Bioengineering, Imperial College London, London, United Kingdom.

出版信息

Front Bioeng Biotechnol. 2024 Dec 17;12:1511685. doi: 10.3389/fbioe.2024.1511685. eCollection 2024.

DOI:10.3389/fbioe.2024.1511685
PMID:39741500
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11685154/
Abstract

INTRODUCTION

Up to one in five will suffer from osteoporotic vertebral fracture within their lifetime. Accurate fracture prediction poses challenges using bone mineral density (BMD) measures. Trabecular bone strains may be influenced by the underlying intervertebral disc (IVD). Understanding how disc degeneration alters load distribution to the vertebra may demonstrate that supplementing fracture risk tools with IVD metrics could improve predictions. The aim of this study was to assess the influence of IVD degeneration on the stress and strain magnitude and distribution in the trabecular bone of adjacent vertebrae.

METHODS

Ten human cadaveric lumbar bi-segment specimens (20 IVDs, 9 degenerated, 11 non-degenerated) were µCT-imaged under 1000N. Digital volume correlation was used to quantify axial, principal, maximum shear, and von Mises strain in the superior and inferior regions of the vertebra. Volumetric BMD from quantitative-CT was used to calculate Young's modulus, which was then registered with the von Mises strain field to calculate internal von Mises stress.

RESULTS

Two bi-segments fractured during mechanical testing, resulting in N = 8 endplate regions per group. Trabecular bone adjacent to degenerated IVDs presented higher maximum principal and shear strains in the anterior region, relative to non-degenerated (peak ε: 6,020 ± 1,633 µε 3,737 ± 1,548 µε, < 0.01; peak γ: 6,202 ± 1948 µε 3,938 ± 2086 µε, < 0.01). Von Mises stress distribution was significantly skewed towards the anterior region in the degenerated group only (28.3% ± 10.4%, < 0.05). Reduced disc height correlated with increased central-region axial compressive strain, decreased central-region BMD, and increased anterior region von Mises stress (all < 0.05).

DISCUSSION

Disc degeneration may encourage high strains to be experienced within the anterior region of the adjacent bone, owing to changes in load distribution. This study demonstrates the potential of utilising IVD metrics in fracture risk assessment, to inform clinical decision making and preventative treatment.

摘要

引言

高达五分之一的人在其一生中会遭受骨质疏松性椎体骨折。使用骨密度(BMD)测量进行准确的骨折预测具有挑战性。小梁骨应变可能受其下方椎间盘(IVD)的影响。了解椎间盘退变如何改变椎体的负荷分布可能表明,用IVD指标补充骨折风险评估工具可改善预测。本研究的目的是评估IVD退变对相邻椎体小梁骨应力和应变大小及分布的影响。

方法

对10个尸体腰椎双节段标本(20个IVD,9个退变,11个未退变)在1000N负荷下进行µCT成像。采用数字体积相关技术量化椎体上下区域的轴向、主应变、最大剪应变和冯·米塞斯应变。定量CT的体积骨密度用于计算杨氏模量,然后将其与冯·米塞斯应变场配准以计算内部冯·米塞斯应力。

结果

两个双节段在力学测试中发生骨折,每组最终有8个终板区域。与未退变的IVD相邻的小梁骨在前部区域表现出更高的最大主应变和剪应变(峰值ε:6,020±1,633με对3,737±1,548με,P<0.01;峰值γ:6,202±1948με对3,938±2086με,P<0.01)。仅退变组的冯·米塞斯应力分布明显偏向于前部区域(28.3%±10.4%,P<0.05)。椎间盘高度降低与中央区域轴向压缩应变增加、中央区域骨密度降低以及前部区域冯·米塞斯应力增加相关(均P<0.05)。

讨论

由于负荷分布的变化,椎间盘退变可能促使相邻骨的前部区域承受高应变。本研究证明了在骨折风险评估中利用IVD指标的潜力,为临床决策和预防性治疗提供依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/2330625dc033/fbioe-12-1511685-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/bb1b1a798eca/fbioe-12-1511685-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/544c1c7aec6f/fbioe-12-1511685-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/47629d488afb/fbioe-12-1511685-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/03bf123dce56/fbioe-12-1511685-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/f92ccf75092d/fbioe-12-1511685-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/45e748ecb265/fbioe-12-1511685-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/2330625dc033/fbioe-12-1511685-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/bb1b1a798eca/fbioe-12-1511685-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/544c1c7aec6f/fbioe-12-1511685-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/47629d488afb/fbioe-12-1511685-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/5b5f988ddf98/fbioe-12-1511685-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/03bf123dce56/fbioe-12-1511685-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/f92ccf75092d/fbioe-12-1511685-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/45e748ecb265/fbioe-12-1511685-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d32/11685154/2330625dc033/fbioe-12-1511685-g008.jpg

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