兔椎间盘急性损伤模型中椎间盘、面关节和椎体终板之间的机械串扰

IF 3.4 3区 医学 Q1 ORTHOPEDICS JOR Spine Pub Date : 2023-10-24 DOI:10.1002/jsp2.1287
Matthew Fainor, Brianna S. Orozco, Victoria G. Muir, Sonal Mahindroo, Sachin Gupta, Robert L. Mauck, Jason A. Burdick, Harvey E. Smith, Sarah E. Gullbrand
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引用次数: 0

摘要

背景 在动物和人类身上都有椎间盘内板硬化和面骨关节炎的记录。然而,目前还不清楚这些相邻病变是如何与椎间盘发生串扰的。本研究试图通过评估每个区室对急性椎间盘损伤的反应来阐明这种串扰。 方法 11只新西兰白兔接受了使用16G或21G针头进行的椎间盘环形穿刺。在 4 周和 10 周时,对运动节段的各个区段进行分析。用核磁共振成像造影剂钆双胺对椎间盘进行T1弛豫成像,并进行T2成像。椎间盘和椎面分别通过椎体-椎间盘-椎体张力-压缩蠕变测试和压痕测试进行机械测试。通过μCT对终板骨密度进行量化。对椎间盘和切面进行切片和染色,以进行组织学评分。 结果 随着穿刺针直径的增加和穿刺后时间的延长,椎间盘的退变程度加剧。与 21G 和 16G 穿刺椎间盘相邻的终板骨密度也有所增加,导致 10 周后钆二胺转运减少。然而,面关节并没有遵循同样的趋势。在10周时,与21G穿刺椎间盘相邻的面关节退化程度低于与16G穿刺椎间盘相邻的面关节。16G关节面在4周时的退变程度比10周时严重,这表明软骨已经恢复。16G穿刺椎间盘在4周和10周之间形成了严重的椎间盘骨质增生,这很可能减轻了切面软骨的负荷,从而导致了所观察到的恢复。 结论 总体而言,本研究支持椎间盘损伤后整个脊柱运动节段的退变。椎间盘损伤后出现的椎间盘终板增厚限制了小分子物质向椎间盘的扩散。这项研究还表明,椎间盘力学的改变可诱发切面退变,而椎间盘附近极度的骨质重塑可通过关节软骨的卸载促进切面软骨的恢复。
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Mechanical crosstalk between the intervertebral disc, facet joints, and vertebral endplate following acute disc injury in a rabbit model

Background

Vertebral endplate sclerosis and facet osteoarthritis have been documented in animals and humans. However, it is unclear how these adjacent pathologies engage in crosstalk with the intervertebral disc. This study sought to elucidate this crosstalk by assessing each compartment individually in response to acute disc injury.

Methods

Eleven New Zealand White rabbits underwent annular disc puncture using a 16G or 21G needle. At 4 and 10 weeks, individual compartments of the motion segment were analyzed. Discs underwent T1 relaxation mapping with MRI contrast agent gadodiamide as well T2 mapping. Both discs and facets underwent mechanical testing via vertebra—disc—vertebra tension-compression creep testing and indentation testing, respectively. Endplate bone density was quantified via μCT. Discs and facets were sectioned and stained for histology scoring.

Results

Intervertebral discs became more degenerative with increasing needle diameter and time post-puncture. Bone density also increased in endplates adjacent to both 21G and 16G punctured discs leading to reduced gadodiamide transport at 10 weeks. The facet joints, however, did not follow this same trend. Facets adjacent to 16G punctured discs were less degenerative than facets adjacent to 21G punctured discs at 10 weeks. 16G facets were more degenerative at 4 weeks than at 10, suggesting the cartilage had recovered. The formation of severe disc osteophytes in 16G punctured discs between 4 and 10 weeks likely offloaded the facet cartilage, leading to the recovery observed.

Conclusions

Overall, this study supports that degeneration spans the whole spinal motion segment following disc injury. Vertebral endplate thickening occurred in response to disc injury, which limited the diffusion of small molecules into the disc. This work also suggests that altered disc mechanics can induce facet degeneration, and that extreme bony remodeling adjacent to the disc may promote facet cartilage recovery through offloading of the articular cartilage.

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来源期刊
JOR Spine
JOR Spine ORTHOPEDICS-
CiteScore
6.40
自引率
18.90%
发文量
42
审稿时长
10 weeks
期刊最新文献
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