In previous studies of disc degeneration,the structural and mechanical properties of the endplate were often neglected.In this paper,the station legislation was used to construct an animal model of minor trauma disc d...In previous studies of disc degeneration,the structural and mechanical properties of the endplate were often neglected.In this paper,the station legislation was used to construct an animal model of minor trauma disc degeneration,and the mechanism of disc degeneration was further investigated by observing the changes of mesoscopic structure and developing the mechanical properties of endplate bone.Twenty-eight 6-month-old Japanese white rabbits were divided into two groups:control group and experimental group.An animal model of intervertebral disc degeneration was established by upright experiment in the experimental group.The bone mesoscopic structures in different areas of each endplate were observed by histological and imaging methods,and the mechanical properties of the endplates were measured by indentation method.The two groups of data were compared by one-way ANOVA.After the experimental animals stood for 17 weeks,The experimental group showed the characteristics of early disc degeneration.The microstructure of the degenerative group showed that the end plate mineralization degree was higher,the bone mass was larger,and the number and thickness of bone trabeculae were larger.The results of indentation test showed that the mechanical properties of the degeneration group were enhanced,and the lower endplate was obviously enhanced.We successfully established a model of human disc degeneration with non invasive trauma and more consistent with the process of human disc degeneration through the standing experiment.In the experimental group,the internal structure of the endplate was dense and pore distance was reduced.The change of bone mesoscopic structure further affects the endplate,resulting in the enhancement of the mechanical properties of the endplate after intervertebral disc degeneration.The reduction of the pore distance and the narrowing of the internal channel structure of the endplate also hinder the nutrition supply of the intervertebral disc,which may be the key reason affecting the degeneration of the intervertebral disc.A biomechanical method for investigating the mechanism of intervertebral disc degeneration can be provided in this paper.展开更多
Background This study aimed to investigate the effect of pcDNA3.1-vascular endothelial growth factor (VEGF)165 vector on vertebral cartilage endplate vascular buds and intervertebral discs. Methods Rabbits were rand...Background This study aimed to investigate the effect of pcDNA3.1-vascular endothelial growth factor (VEGF)165 vector on vertebral cartilage endplate vascular buds and intervertebral discs. Methods Rabbits were randomly assigned to the control and experimental groups with 10 in each. In the experimental group, we anesthetized the rabbits and exposed the front vertebral body. Using the mark of the longitudinal ossature of the front vertebral body of the lumbar vertebrae, we advanced a needle at the central point of the front fourth and fifth lumbar intervertebral discs and injected 20 pl pcDNA3.1-VEGF165. Similarly, in the control group, we injected 20 IJl pcDNA3.1. At 4 and 8 weeks post-injection, we examined the changes of the vertebral cartilage endplate using X-ray radiograph, histology, and scanning electron microscopy. Results The vertebral cartilage endplate calcification and degeneration in the experimental group were less than those in the control group at 8 weeks post-operation. The average number and diameter of vascular buds obviously increased in the experimental group at 4 and 8 weeks post-operation. The number of vascular buds and the diameter in the region of the inner annulus increased when compared to those in the area near the nucleus pulposus. Conclusions The pcDNA3.1-VEGF165 plasmid can increase the average number and diameter of vascular buds and decelerate intervertebral disc degeneration.展开更多
基金the National Natural Science Foundation of China(11472185,11972243)for fundingFund Program for the Scientific Activities of Selected Returned Overseas Professionals in Shanxi Province(2020040)for funding。
文摘In previous studies of disc degeneration,the structural and mechanical properties of the endplate were often neglected.In this paper,the station legislation was used to construct an animal model of minor trauma disc degeneration,and the mechanism of disc degeneration was further investigated by observing the changes of mesoscopic structure and developing the mechanical properties of endplate bone.Twenty-eight 6-month-old Japanese white rabbits were divided into two groups:control group and experimental group.An animal model of intervertebral disc degeneration was established by upright experiment in the experimental group.The bone mesoscopic structures in different areas of each endplate were observed by histological and imaging methods,and the mechanical properties of the endplates were measured by indentation method.The two groups of data were compared by one-way ANOVA.After the experimental animals stood for 17 weeks,The experimental group showed the characteristics of early disc degeneration.The microstructure of the degenerative group showed that the end plate mineralization degree was higher,the bone mass was larger,and the number and thickness of bone trabeculae were larger.The results of indentation test showed that the mechanical properties of the degeneration group were enhanced,and the lower endplate was obviously enhanced.We successfully established a model of human disc degeneration with non invasive trauma and more consistent with the process of human disc degeneration through the standing experiment.In the experimental group,the internal structure of the endplate was dense and pore distance was reduced.The change of bone mesoscopic structure further affects the endplate,resulting in the enhancement of the mechanical properties of the endplate after intervertebral disc degeneration.The reduction of the pore distance and the narrowing of the internal channel structure of the endplate also hinder the nutrition supply of the intervertebral disc,which may be the key reason affecting the degeneration of the intervertebral disc.A biomechanical method for investigating the mechanism of intervertebral disc degeneration can be provided in this paper.
基金This study was supported by a grant from the National Natural Science Foundation of China,the Anhui Province Education Department Key Fund Project
文摘Background This study aimed to investigate the effect of pcDNA3.1-vascular endothelial growth factor (VEGF)165 vector on vertebral cartilage endplate vascular buds and intervertebral discs. Methods Rabbits were randomly assigned to the control and experimental groups with 10 in each. In the experimental group, we anesthetized the rabbits and exposed the front vertebral body. Using the mark of the longitudinal ossature of the front vertebral body of the lumbar vertebrae, we advanced a needle at the central point of the front fourth and fifth lumbar intervertebral discs and injected 20 pl pcDNA3.1-VEGF165. Similarly, in the control group, we injected 20 IJl pcDNA3.1. At 4 and 8 weeks post-injection, we examined the changes of the vertebral cartilage endplate using X-ray radiograph, histology, and scanning electron microscopy. Results The vertebral cartilage endplate calcification and degeneration in the experimental group were less than those in the control group at 8 weeks post-operation. The average number and diameter of vascular buds obviously increased in the experimental group at 4 and 8 weeks post-operation. The number of vascular buds and the diameter in the region of the inner annulus increased when compared to those in the area near the nucleus pulposus. Conclusions The pcDNA3.1-VEGF165 plasmid can increase the average number and diameter of vascular buds and decelerate intervertebral disc degeneration.