Cervical spinal instability causes vertebral microarchitecture change and vertebral endplate lesion in rats

• Published in: Journal of Orthopaedic Translation
• Main Authors: Qi Liu, Zhou Yang, Yapu Liu, Wei Ji, Zucheng Huang, Junhao Liu, Junyu Lin, Yue Hua, Zhiping Huang, Xiuhua Wu, Qingan Zhu
• Format: Article
• Language: English
• Published: Elsevier 2020-09-01
• Subjects: Biomechanical property; Bone formation; Intervertebral disc degeneration; Spinal instability; Vertebral endplate damage
• Online Access: http://www.sciencedirect.com/science/article/pii/S2214031X19302177

Background: The 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. Methods: Forty-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. Results: CMS 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. Conclusions: Spinal 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 article: Our 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.