Objective:To investigate the effect of osteoporosis and intervertebral disc degeneration on the endplate cartilage injury in rats.Methods:A total of 48 female Sprague Dawley rats(3 months)were randomly divided into Gr...Objective:To investigate the effect of osteoporosis and intervertebral disc degeneration on the endplate cartilage injury in rats.Methods:A total of 48 female Sprague Dawley rats(3 months)were randomly divided into Groups A,B,C and D with 12 rats in each group.Osteoporosis and intervertebral disc degeneration composite model,simple degeneration model and simple osteoporosis model were prepared in Groups A,B and C respectively.After modeling,four rats of each group at 12th.18th and 24th week were sacrificed,Intervertebral height of cervical vertebra C6/C7 was measured.Micro-CT was used to image the endplate of cephalic and caudal cartilage at C6/C7 intervertebral disc.Abraded area rate of C6 caudal and C7 cephalic cartilage endplate was calculated,and then C6/C7 intervertebral disc was routinely embedded and sectioned.stained with safranin O to observe histological changes microscopically.Results:At 12,18 and24 weeks,intervertebral disc height of C6/C7 were(0.58±0.09)mm,(0.53±0.04)mm and(0.04±0.06)mm in Group A rats,(0.55±0.05)mm,(0.52±0.07)mm and(0.07±0.05)mm in Group B rats.At 24th week.intervertebral disc height of Group A rats was significantly lower than that of Group B rats(P<0.05);intervertebral disc height of Groups A and B rats at each time point were significantly lower than that of Groups C and D(P<0.05).There was no significantly statistical difference of intervertebral disc height between Groups C and D(P>0.05).At 12 and 18 weeks,the abraded rate of C6 caudal and C7 cephalic cartilage endplate in Group A rats were significantly higher than that in Groups B.C and D rats(P<0.05);the abraded rate in Group B was significantly higher than that in Groups C and D(P>0.05).Microscopic observation of CT showed that ventral defects in C6caudal or C7 cephalic cartilage endplate in Groups A and B appeared after 12 weeks of modeling;obvious cracks were found in front of the C6 and C7 vertebral body,and cartilage defect shown the trend of"repairing"at 18 and 24 weeks after modeling.Conclusions:Intervertebral disc degeneration and osteoporosis can cause damage to the cartilage endplate.Co-existence of these two factors can induce more serious damage to the endplate.which has possitive correlation with intervertebral disc degeneration.Osteoporosis plays a certain role in intervertebral disc degeneration process,and accelerates the degeneration of intervertebral disc in a specific time window.展开更多
The degenerative disease of the intervertebral disc is nowadays an important health problem,which has still not been understood and solved adequately.The vertebral endplate is regarded as one of the vital elements in ...The degenerative disease of the intervertebral disc is nowadays an important health problem,which has still not been understood and solved adequately.The vertebral endplate is regarded as one of the vital elements in the structure of the intervertebral disc.Its constituent cells,the chondrocytes in the endplate,may also be involved in the process of the intervertebral disc degeneration and their role is central both under physiological and pathological conditions.They main functions include a role in homeostasis of the extracellular environment of the intervertebral disc,metabolic support and nutrition of the discal nucleus and annulus beneath and the preservation of the extracellular matrix.Therefore,it is understandable that the cells in the endplate have been in the centre of research from several viewpoints,such as development,degeneration and growth,reparation and remodelling,as well as treatment strategies.In this article,we briefly review the importance of vertebral endplate,which are often overlooked,in the intervertebral disc degeneration.展开更多
Discogenic low back pain is a serious medical and social problem, and accounts for 26%-42% of the patients with chronic low back pain. Recent studies found that the pathologic features of discs obtained from the patie...Discogenic low back pain is a serious medical and social problem, and accounts for 26%-42% of the patients with chronic low back pain. Recent studies found that the pathologic features of discs obtained from the patients with discogenic low back pain were the formation of the zones of vascularized granulation tissue, with extensive innervation in fissures extending from the outer part of the annulus into the nucleus pulposus. Studies suggested that the degeneration of the painful disc might originate from the injury and subsequent repair of annulus fibrosus. Growth factors such as basic fibroblast growth factor, transforming growth factor β1, and connective tissue growth factor, macrophages and mast cells might play a key role in the repair of the injured annulus fibrosus and subsequent disc degeneration. Although there exist controversies about the role of discography as a diagnostic test, provocation discography still is the only available means by which to identify a painful disc. A recent study has classified discogenic low back pain into two types that were annular disruption-induced low back pain and internal endplate disruption-induced low back pain, which have been fully supported by clinical and theoretical bases. Current treatment options for discogenic back pain range from medicinal anti-inflammation strategy to invasive procedures including spine fusion and recently spinal arthroplasty. However, these treatments are limited to relieving symptoms, with no attempt to restore the disc's structure. Recently, there has been a growing interest in developing strategies that aim to repair or regenerate the degenerated disc biologically.展开更多
目的观察不同浓度的苦杏仁苷对IL-1β诱导的大鼠椎间盘软骨终板细胞的影响,并进一步探讨其作用的可能机制。方法从1月龄SD大鼠椎间盘中分离软骨终板并培养,经鉴定后,随机分组为正常组、诱导组、苦杏仁苷10-2、10-3、10-4、10-5mol·...目的观察不同浓度的苦杏仁苷对IL-1β诱导的大鼠椎间盘软骨终板细胞的影响,并进一步探讨其作用的可能机制。方法从1月龄SD大鼠椎间盘中分离软骨终板并培养,经鉴定后,随机分组为正常组、诱导组、苦杏仁苷10-2、10-3、10-4、10-5mol·L-1给药组,CCK-8法检测各组对大鼠椎间盘软骨终板细胞增殖的影响。Real-time PCR(RTPCR)检测聚集蛋白聚糖(aggrecan-1)、Ⅱ型胶原(type II collagen,Col2a1)、Ⅹ型胶原(type X collagen,Col10al)、基质金属蛋白酶-13(matrix metalloproteinase 13,MMP-13)基因的表达情况。细胞免疫荧光检测分析Col2a1、Col10al的表达,流式细胞仪检测其对软骨终板细胞凋亡的影响。结果苦杏仁苷10-2mol·L-1给药组能够抑制椎间盘软骨终板细胞的增殖,与正常组比较差异有统计学意义(P<0.05)。流式分析,其细胞凋亡比例较诱导组及正常组均较高。RT-PCR检测结果显示一定浓度的苦杏仁苷能够上调Aggrecan、Col2a1mRNA的表达,下调Col10al、MMP-13 mRNA的表达,与诱导组比较,差异有统计学意义(P<0.05)。一定浓度的苦杏仁苷能够上调Col2a1蛋白的表达,下调Col10al蛋白的表达。结论一定浓度的苦杏仁苷能够抑制IL-1β诱导大鼠椎间盘软骨终板细胞发生退变,起到延缓椎间盘退变的作用。展开更多
基金supported by National Science Foundation.Grant No.81171764
文摘Objective:To investigate the effect of osteoporosis and intervertebral disc degeneration on the endplate cartilage injury in rats.Methods:A total of 48 female Sprague Dawley rats(3 months)were randomly divided into Groups A,B,C and D with 12 rats in each group.Osteoporosis and intervertebral disc degeneration composite model,simple degeneration model and simple osteoporosis model were prepared in Groups A,B and C respectively.After modeling,four rats of each group at 12th.18th and 24th week were sacrificed,Intervertebral height of cervical vertebra C6/C7 was measured.Micro-CT was used to image the endplate of cephalic and caudal cartilage at C6/C7 intervertebral disc.Abraded area rate of C6 caudal and C7 cephalic cartilage endplate was calculated,and then C6/C7 intervertebral disc was routinely embedded and sectioned.stained with safranin O to observe histological changes microscopically.Results:At 12,18 and24 weeks,intervertebral disc height of C6/C7 were(0.58±0.09)mm,(0.53±0.04)mm and(0.04±0.06)mm in Group A rats,(0.55±0.05)mm,(0.52±0.07)mm and(0.07±0.05)mm in Group B rats.At 24th week.intervertebral disc height of Group A rats was significantly lower than that of Group B rats(P<0.05);intervertebral disc height of Groups A and B rats at each time point were significantly lower than that of Groups C and D(P<0.05).There was no significantly statistical difference of intervertebral disc height between Groups C and D(P>0.05).At 12 and 18 weeks,the abraded rate of C6 caudal and C7 cephalic cartilage endplate in Group A rats were significantly higher than that in Groups B.C and D rats(P<0.05);the abraded rate in Group B was significantly higher than that in Groups C and D(P>0.05).Microscopic observation of CT showed that ventral defects in C6caudal or C7 cephalic cartilage endplate in Groups A and B appeared after 12 weeks of modeling;obvious cracks were found in front of the C6 and C7 vertebral body,and cartilage defect shown the trend of"repairing"at 18 and 24 weeks after modeling.Conclusions:Intervertebral disc degeneration and osteoporosis can cause damage to the cartilage endplate.Co-existence of these two factors can induce more serious damage to the endplate.which has possitive correlation with intervertebral disc degeneration.Osteoporosis plays a certain role in intervertebral disc degeneration process,and accelerates the degeneration of intervertebral disc in a specific time window.
文摘The degenerative disease of the intervertebral disc is nowadays an important health problem,which has still not been understood and solved adequately.The vertebral endplate is regarded as one of the vital elements in the structure of the intervertebral disc.Its constituent cells,the chondrocytes in the endplate,may also be involved in the process of the intervertebral disc degeneration and their role is central both under physiological and pathological conditions.They main functions include a role in homeostasis of the extracellular environment of the intervertebral disc,metabolic support and nutrition of the discal nucleus and annulus beneath and the preservation of the extracellular matrix.Therefore,it is understandable that the cells in the endplate have been in the centre of research from several viewpoints,such as development,degeneration and growth,reparation and remodelling,as well as treatment strategies.In this article,we briefly review the importance of vertebral endplate,which are often overlooked,in the intervertebral disc degeneration.
文摘Discogenic low back pain is a serious medical and social problem, and accounts for 26%-42% of the patients with chronic low back pain. Recent studies found that the pathologic features of discs obtained from the patients with discogenic low back pain were the formation of the zones of vascularized granulation tissue, with extensive innervation in fissures extending from the outer part of the annulus into the nucleus pulposus. Studies suggested that the degeneration of the painful disc might originate from the injury and subsequent repair of annulus fibrosus. Growth factors such as basic fibroblast growth factor, transforming growth factor β1, and connective tissue growth factor, macrophages and mast cells might play a key role in the repair of the injured annulus fibrosus and subsequent disc degeneration. Although there exist controversies about the role of discography as a diagnostic test, provocation discography still is the only available means by which to identify a painful disc. A recent study has classified discogenic low back pain into two types that were annular disruption-induced low back pain and internal endplate disruption-induced low back pain, which have been fully supported by clinical and theoretical bases. Current treatment options for discogenic back pain range from medicinal anti-inflammation strategy to invasive procedures including spine fusion and recently spinal arthroplasty. However, these treatments are limited to relieving symptoms, with no attempt to restore the disc's structure. Recently, there has been a growing interest in developing strategies that aim to repair or regenerate the degenerated disc biologically.
文摘目的观察不同浓度的苦杏仁苷对IL-1β诱导的大鼠椎间盘软骨终板细胞的影响,并进一步探讨其作用的可能机制。方法从1月龄SD大鼠椎间盘中分离软骨终板并培养,经鉴定后,随机分组为正常组、诱导组、苦杏仁苷10-2、10-3、10-4、10-5mol·L-1给药组,CCK-8法检测各组对大鼠椎间盘软骨终板细胞增殖的影响。Real-time PCR(RTPCR)检测聚集蛋白聚糖(aggrecan-1)、Ⅱ型胶原(type II collagen,Col2a1)、Ⅹ型胶原(type X collagen,Col10al)、基质金属蛋白酶-13(matrix metalloproteinase 13,MMP-13)基因的表达情况。细胞免疫荧光检测分析Col2a1、Col10al的表达,流式细胞仪检测其对软骨终板细胞凋亡的影响。结果苦杏仁苷10-2mol·L-1给药组能够抑制椎间盘软骨终板细胞的增殖,与正常组比较差异有统计学意义(P<0.05)。流式分析,其细胞凋亡比例较诱导组及正常组均较高。RT-PCR检测结果显示一定浓度的苦杏仁苷能够上调Aggrecan、Col2a1mRNA的表达,下调Col10al、MMP-13 mRNA的表达,与诱导组比较,差异有统计学意义(P<0.05)。一定浓度的苦杏仁苷能够上调Col2a1蛋白的表达,下调Col10al蛋白的表达。结论一定浓度的苦杏仁苷能够抑制IL-1β诱导大鼠椎间盘软骨终板细胞发生退变,起到延缓椎间盘退变的作用。
