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随着年龄增长,在椎间软骨终板中可以观察到什么?一项关于过度轴向机械负荷的动物模型研究。

What can be observed in intervertebral cartilage endplate with aging? An animal model study of excessive axial mechanical loading.

作者信息

Hu Zhouyang, He Fan, Li Xinhua, Jiang Bei, Yan Shuaifeng, Tan Jun, Li Lijun

机构信息

Huazhong University School of Science and Technology Union Shenzhen Hospital, Shenzhen, China.

Department of Spine Surgery, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.

出版信息

Front Med (Lausanne). 2024 Nov 5;11:1429208. doi: 10.3389/fmed.2024.1429208. eCollection 2024.

DOI:10.3389/fmed.2024.1429208
PMID:39564510
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11573515/
Abstract

INTRODUCTION

The cartilage endplate (CEP) plays a crucial role as both a mechanical barrier and nutrient channel for the intervertebral disc, but it is vulnerable to excessive axial loading. We modified the Ilizarov external fixator and applied it to the CEP of the rat tail to impose diurnal, controllable excess axial loading. The objective was to measure morphological changes in the CEP when subjected to loading during the aging process.

METHODS

Two Kirschner wires were, respectively, inserted into the center of the eighth and ninth coccygeal vertebrae (Co8/9) of rat ( = 54) to apply axial loading to the CEP. A remote control device was used to establish the diurnal loading schedule. At the end of 4, 8, and 12-week periods, the Co8/9 CEPs in each group were analyzed using MRI, histological staining, and immunohistochemical staining techniques.

RESULTS

The novel Ilizarov model that we modified successfully induced degeneration of the rat coccygeal CEP. MRI analysis revealed significant degenerative changes in the loaded Co8/9 CEP, including decreased signal intensity and the formation of Schmorl's nodes at 8 and 12 weeks. Histological examination showed progressive CEP degeneration (CEPD), characterized by decreased microporosity, thinning, and structural irregularities. Immunohistochemical analysis demonstrated a significant reduction in Aggrecan and Collagen II expression in the CEP and nucleus pulposus over time. Control and sham groups maintained normal CEP structure and composition throughout the study period.

CONCLUSION

Excessive axial loading induced CEPD in the rat tail, primarily characterized by the formation of Schmorl's nodes and a reduction in CEP microporosity in this study. Our modified Ilizarov rat tail compression model, featuring stable and controllable axial loading capabilities, provided an alternative experimental paradigm for further investigation into CEPD.

摘要

引言

软骨终板(CEP)作为椎间盘的机械屏障和营养通道发挥着关键作用,但它易受过度轴向负荷的影响。我们对Ilizarov外固定器进行了改良,并将其应用于大鼠尾部的CEP,以施加昼夜可控的过度轴向负荷。目的是测量衰老过程中CEP在承受负荷时的形态变化。

方法

将两根克氏针分别插入大鼠(n = 54)第八和第九尾椎(Co8/9)的中心,对CEP施加轴向负荷。使用遥控装置制定昼夜负荷计划。在4周、8周和12周结束时,使用磁共振成像(MRI)、组织学染色和免疫组织化学染色技术对每组的Co8/9 CEP进行分析。

结果

我们改良的新型Ilizarov模型成功诱导了大鼠尾椎CEP的退变。MRI分析显示,加载的Co8/9 CEP出现明显的退变变化,包括8周和12周时信号强度降低以及Schmorl结节的形成。组织学检查显示CEP进行性退变(CEPD),其特征为微孔减少、变薄和结构不规则。免疫组织化学分析表明,随着时间的推移,CEP和髓核中聚集蛋白聚糖和胶原蛋白II的表达显著降低。在整个研究期间,对照组和假手术组的CEP结构和组成保持正常。

结论

过度轴向负荷在大鼠尾部诱导了CEPD,在本研究中其主要特征为Schmorl结节的形成和CEP微孔减少。我们改良的Ilizarov大鼠尾部压缩模型具有稳定且可控的轴向负荷能力,为进一步研究CEPD提供了一种替代实验范式。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/0eda38416928/fmed-11-1429208-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/465dd67f81b2/fmed-11-1429208-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/a5bb39a3a6dd/fmed-11-1429208-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/5a9a0c1e90c4/fmed-11-1429208-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/339acdbdc4c7/fmed-11-1429208-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/0eda38416928/fmed-11-1429208-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/465dd67f81b2/fmed-11-1429208-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/534bf3649221/fmed-11-1429208-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/a5bb39a3a6dd/fmed-11-1429208-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/5a9a0c1e90c4/fmed-11-1429208-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/339acdbdc4c7/fmed-11-1429208-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6a/11573515/0eda38416928/fmed-11-1429208-g006.jpg

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