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首页> 外文期刊>Journal of Orthopaedic Translation >Cervical spinal instability causes vertebral microarchitecture change and vertebral endplate lesion in rats
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Cervical spinal instability causes vertebral microarchitecture change and vertebral endplate lesion in rats

机译:颈椎不稳定性导致椎体微体系结构改变和椎体底板病变在大鼠中

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BackgroundThe vertebral endplate (VEP) was damaged after spinal instability induced by cervical muscle section (CMS). Whether CMS induces bone formation and mechanical loading change in the vertebra is still obscure. This study was aimed to explore mechanical loading change and endplate damage after CMS.MethodsForty-eight rats were randomly divided into the CMS group and the sham group. The C6/7 segments were harvested at 4, 8, and 12 weeks after surgery. The microarchitectures of the C6 vertebra??and the vertebral endplate lesions and intervertebral disc height of C6/7 were measured by micro–computed tomography. Micro–finite element analysis was used to evaluate biomechanical properties of the C6 vertebra. Bone remodelling of the C6 vertebra??and the endplate??sclerosis and intervertebral disc degeneration of C6/7 were evaluated by histological and immunohistochemical analyses.ResultsCMS significantly induced bone formation of the C6 ventral vertebra??and increased the biomechanical properties of mainly the ventral side at 4 weeks, which was gradually rebalanced throughout the rest of the study. CMS also significantly increased protein expression of transforming growth factor-β1 (TGF-β1) and phosphorylated small mothers against decapentaplegic (pSmad)2/3??at 4 weeks. Moreover, tartrate-resistant acid phosphatase staining showed that osteoclast-positive cells were slightly in number decreased at 4 weeks, but were obviously increased at 8 weeks. The VEP of the ventral side was abraded earlier followed by calcification in situ later after CMS, consistent with the biomechanical enhancements observed. The degree of endplate degeneration was aggravated with time. Finally, CMS decreased intervertebral disc height and increased disc degeneration scores with time.ConclusionsSpinal instability induced by CMS increases bone mass and biomechanical loading of the ventral side of vertebra in the early stage, which might initiate VEP damage and cause intervertebral disc degeneration.The translational potential of this articleOur study indicates that vertebral trabecular changes may involve in intervertebral disc degeneration induced by spinal instability. This may help to elucidate the mechanisms by which disc degeneration occur.
机译:背景技术在宫颈肌部分(CMS)诱导的脊柱不稳定性后椎体端板(VEP)受损。 CMS是否诱导骨质形成和椎骨的机械加载变化仍然模糊。本研究旨在探讨CMS.Methodsforty-8大鼠随机分为CMS组和假组后机械加载变化和端口损伤。在手术后4,8和12周收获C6 / 7区段。通过微计算断层扫描测量C6椎骨的微体系结构和C6 / 7的椎体端板病变和椎间盘高度。微型元素分析用于评估C6椎骨的生物力学性质。 C6椎骨的骨质重塑和端板的硬化和椎间盘和椎间盘突出的C6 / 7的退化是通过组织学和免疫组织化学分析评估的。方法显着诱导C6腹椎骨的骨形成并增加了主要的生物力学特性腹侧4周,在整个研究中逐渐重新平衡。 CMS在4周时,CMS还显着增加转化生长因子-β1(TGF-β1)和磷酸化的小母亲的蛋白质表达,并在4周内对甲板(PSMAD)2/3进行磷酸化的小母亲。此外,耐酒型耐酸性磷酸酶染色表明,在4周内略微下降,骨质细胞阳性细胞略微下降,但在8周内明显增加。腹侧的VEP早先磨损,然后在CMS后以后原位钙化,与观察到的生物力学增强一致。终板变性的程度随时间加剧。最后,CMS减少了椎间盘高度和随时间的增加的椎间盘退化分数。CMS诱导的结合性缺乏性增加了早期椎体腹侧的骨质和生物力学载荷,这可能引发VEP损伤并引起椎间盘变性。翻译该物质研究的潜力表明椎骨细胞分枝变化可能涉及脊柱不稳定性诱导的椎间盘退化。这可能有助于阐明发生椎间盘变性的机制。

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