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轻度(非重度)椎间盘退变与双侧L5椎弓根峡部裂进展为椎体滑脱有关。

Mild (not severe) disc degeneration is implicated in the progression of bilateral L5 spondylolysis to spondylolisthesis.

作者信息

Ramakrishna Vivek A S, Chamoli Uphar, Viglione Luke L, Tsafnat Naomi, Diwan Ashish D

机构信息

Spine Service, Department of Orthopaedic Surgery, St. George & Sutherland Clinical School, University of New South Wales Australia, Kogarah, Sydney, NSW, 2217, Australia.

School of Biomedical Engineering, University of Technology Sydney, Ultimo, NSW, 2007, Australia.

出版信息

BMC Musculoskelet Disord. 2018 Apr 2;19(1):98. doi: 10.1186/s12891-018-2011-0.

DOI:10.1186/s12891-018-2011-0
PMID:29609581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5879802/
Abstract

BACKGROUND

Spondylolytic (or lytic) spondylolisthesis is often associated with disc degeneration at the index-level; however, it is not clear if disc degeneration is the cause or the consequence of lytic spondylolisthesis. The main objective of this computed tomography based finite element modelling study was to examine the role of different grades of disc degeneration in the progression of a bilateral L5-lytic defect to spondylolisthesis.

METHODS

High-resolution computed tomography data of the lumbosacral spine from an anonymised healthy male subject (26 years old) were segmented to build a 3D-computational model of an INTACT L1-S1 spine. The INTACT model was manipulated to generate four more models representing a bilateral L5-lytic defect and the following states of the L5-S1 disc: nil degeneration (NOR LYTIC), mild degeneration (M-DEG LYTIC), mild degeneration with 50% disc height collapse (M-DEG-COL LYTIC), and severe degeneration with 50% disc height collapse(S-COL LYTIC). The models were imported into a finite element modelling software for pre-processing, running nonlinear-static solves, and post-processing of the results.

RESULTS

Compared with the baseline INTACT model, M-DEG LYTIC model experienced the greatest increase in kinematics (Fx range of motion: 73% ↑, Fx intervertebral translation: 53%↑), shear stresses in the annulus (Fx anteroposterior: 163%↑, Fx posteroanterior: 31%↑), and strain in the iliolumbar ligament (Fx: 90%↑). The S-COL LYTIC model experienced a decrease in mobility (Fx range of motion: 48%↓, Fx intervertebral translation: 69%↓) and an increase in normal stresses in the annulus (Fx Tensile: 170%↑; Fx Compressive: 397%↑). No significant difference in results was noted between M-DEG-COL LYTIC and S-COL LYTIC models.

CONCLUSIONS

In the presence of a bilateral L5 spondylolytic defect, a mildly degenerate index-level disc experienced greater intervertebral motions and shear stresses compared with a severely degenerate index-level disc in flexion and extension bending motions. Disc height collapse, with or without degenerative changes in the stiffness properties of the disc, is one of the plausible re-stabilisation mechanisms available to the L5-S1 motion segment to mitigate increased intervertebral motions and shear stresses due to a bilateral L5 lytic defect.

摘要

背景

峡部裂性(或溶解性)腰椎滑脱常与病变节段的椎间盘退变相关;然而,椎间盘退变是峡部裂性腰椎滑脱的原因还是结果尚不清楚。这项基于计算机断层扫描的有限元建模研究的主要目的是探讨不同程度的椎间盘退变在双侧L5峡部裂缺损进展为腰椎滑脱过程中的作用。

方法

对一名匿名健康男性受试者(26岁)的腰骶椎高分辨率计算机断层扫描数据进行分割,以构建一个完整的L1-S1脊柱的三维计算模型。对完整模型进行处理,生成另外四个模型,分别代表双侧L5峡部裂缺损以及L5-S1椎间盘的以下状态:无退变(NOR LYTIC)、轻度退变(M-DEG LYTIC)、伴有50%椎间盘高度塌陷的轻度退变(M-DEG-COL LYTIC)以及伴有50%椎间盘高度塌陷的重度退变(S-COL LYTIC)。将这些模型导入有限元建模软件进行预处理、运行非线性静态求解以及结果后处理。

结果

与基线完整模型相比,M-DEG LYTIC模型在运动学方面增加最多(Fx运动范围:上升73%,Fx椎间平移:上升53%),纤维环中的剪应力(Fx前后向:上升163%,Fx后前向:上升31%),以及髂腰韧带中的应变(Fx:上升90%)。S-COL LYTIC模型的活动度降低(Fx运动范围:下降48%,Fx椎间平移:下降69%),纤维环中的正应力增加(Fx拉伸:上升170%;Fx压缩:上升397%)。M-DEG-COL LYTIC模型和S-COL LYTIC模型的结果未观察到显著差异。

结论

在存在双侧L5峡部裂缺损的情况下,与重度退变的病变节段椎间盘相比,轻度退变的病变节段椎间盘在屈伸弯曲运动中经历了更大的椎间运动和剪应力。椎间盘高度塌陷,无论椎间盘刚度特性是否有退变改变,都是L5-S1运动节段可利用的一种合理的重新稳定机制,以减轻由于双侧L5峡部裂缺损导致的椎间运动和剪应力增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9416/5879802/ec1f18116c53/12891_2018_2011_Fig7_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9416/5879802/ec1f18116c53/12891_2018_2011_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9416/5879802/dcb03554cc3e/12891_2018_2011_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9416/5879802/1ad53c71b127/12891_2018_2011_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9416/5879802/b0c50036ae5a/12891_2018_2011_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9416/5879802/ff21db6f87b2/12891_2018_2011_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9416/5879802/269277ae5439/12891_2018_2011_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9416/5879802/afe9c189b4b4/12891_2018_2011_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9416/5879802/ec1f18116c53/12891_2018_2011_Fig7_HTML.jpg

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