椎间盘退变时水通道蛋白1表达变化研究

目的阐明水通道蛋白1在椎间盘退变时表达变化特点。方法采用腰椎失稳的方法建立大鼠腰椎间盘退变的动物模型,影像学观察模型建立的可靠性,收集大鼠椎间盘组织,部分用于提取RNA,采用RT-PCR的方法检测水通道蛋白1mRNA表达的变化,部分标本用western blot进行AQP1蛋白的检测。结果腰椎失稳可以建立大鼠腰椎间盘退变模型,AQP1mRNA的表达随椎间盘退变的进程进行性下降,其蛋白表达也呈现进行性下降的趋势,术后3月时同术前相比相差显著(P<0.05),术后6月和9月则下降更为明显(P<0.01);而在手术对照组而言,于术后6月时也出现AQP1基因和蛋白表达水平的下降(P<0.05)。结论腰椎间盘退变时,AQP1在基因和蛋白的表达水平下降,且与退变的时间长短相关,提示AQP1参予了椎间盘退变的发生发展,AQP1表达的下降可能是引起椎间盘退变的原因之一。     

细胞凋亡与软骨终板钙化的关系

软骨终板钙化是一自然退变过程,异常应力、营养通道障碍、炎性细胞因子和细胞凋亡等因素均可加速其钙化,其中细胞凋亡起着主要作用。近年研究证实,细胞凋亡过程实际上是半胱氨酸天冬氨酸特异性蛋白酶(caspase)不可逆性有限水解底物的级联放大反应过程,软骨终板细胞主要经一氧化氮途径和Fas途径诱导细胞凋亡,导致软骨终板营养通道障碍、细胞外基质合成减少和细胞密度降低,并形成恶性循环,加重软骨终板钙化。导致软骨终板细胞凋亡的具体信号转导通路和相关基因,尚待进一步研究。该文就细胞凋亡与软骨终板钙化关系研究进展作一综述。     

骨性关节炎水通道蛋白1的表达与软骨细胞凋亡相关性研究

目的水通道蛋白1(aquaporins 1,AQP-1)表达变化可能与细胞凋亡相关。通过观察软骨组织中AQP-1和半胱天冬氨酸蛋白酶3(Caspase-3)的表达,探讨AQP-1表达与软骨细胞凋亡的相关性,为进一步研究骨性关节炎(os teoarthritis,OA)的发病机制提供实验依据。方法取8周龄清洁级雄性SD大鼠72只,体重286～320 g,平均300 g;随机分为手术组、假手术组和对照组,每组24只。手术组采用切断前交叉韧带及内侧副韧带、部分切除内侧半月板方法制备大鼠双膝OA模型;假手术组仅暴露关节腔;对照组不作处理。造模后观察大鼠一般情况,于1、2、4、8周处死大鼠取膝关节标本行大体、组织学观察;采用实时荧光定量PCR检测AQP-1和Caspase-3 mRNA的表达情况;使用酶标仪检测Caspase-3蛋白酶活性;并对AQP-1 mRNA表达与Caspase-3 mRNA的表达及蛋白酶活性的相关性进行分析。结果术后共6只大鼠死亡,均给予补充;其余大鼠均存活至实验完成。各时间点对照组及假手术组膝关节软骨外观及结构均正常;随时间延长手术组关节软骨表面粗糙且有裂隙,可见大量赘生物,软骨表层纤维化,细胞排列紊乱。参照Mankin评分标准,造模后1周各组组织学评分比较,差异均无统计学意义(P>0.05);2、4、8周时手术组与对照组、假手术组间比较,差异有统计学意义(P<0.05)。造模后1周,手术组AQP-1、Caspase-3 mRNA表达和Caspase-3蛋白酶活性与假手术组及对照组比较,差异均无统计学意义(P>0.05);而2、4、8周时手术组以上指标均明显高于对照组和假手术组(P<0.05),且随时间延长呈增高趋势。AQP-1 mRNA和Caspase-3 mRNA表达成正相关(r=0.817,P=0.000),回归方程为y=0.426 7x2+0.051 5x;AQP-1 mRNA表达和Caspase-3蛋白酶活性亦成正相关(r=0.945,P=0.000),回归方程为y=15.423 0x+4.392 8。结论 AQP-1的表达上调可能与软骨细胞凋亡相关,在OA发病过程中AQP-1表达的变化可能参与了OA的发生、发展。     

大鼠椎间盘软骨终板细胞凋亡体外模型的建立

[目的]建立大鼠椎间盘软骨终板细胞凋亡体外模型.[方法]为了模拟椎间盘内部低营养低代谢环境,采用低胎牛血清培养法培养椎间盘软骨终板细胞分别含0％,1％,3％,5％,8％,10％胎牛血清,设置不同浓度梯度筛选最佳浓度,检测凋亡率、凋亡蛋白表达及caspase酶活性.[结果]低胎牛血清培养组细胞发生形态改变,DAPI染色阳性细胞增多;流式细胞仪检测凋亡率随着FBS浓度降低而升高,1％为最有效诱导凋亡浓度;Western blot示FAS、caspase-3、PARP、细胞色素C表达在1％ FBS组明显高于10％时,同时caspase-3/8/9酶活性增高.[结论]低胎牛血清培养法能诱导体外培养的软骨终板细胞发生凋亡,最终会引起细胞功能丧失和椎间盘退变,caspase家族可能参与了这一过程.     

水通道蛋白在正常大鼠椎间盘组织中的表达与分布

目的：阐明水通道蛋白在椎间盘中的表达类型及分布情况。方法：收集正常大鼠椎间盘组织，部分用于提取RNA，采用RT-PCR的方法检测水通道蛋白表达的类型；部分标本固定后行组织切片，进行AQPs(aquaporin)的免疫组织化学染色，观察其表达与分布。结果：在正常大鼠的椎间盘组织中软骨细胞、纤维环细胞和髓核细胞皆有AQP1、3的表达，软骨终板中心地带的表达强于周边区域，内层纤维环表达强于外层纤维环；其余几种水通道蛋白未见表达。结论：AQPl、3在正常大鼠椎间盘中的表达及其空间分布提示其可能与椎间盘内水、甘油的代谢有关，对维持椎间盘组织的正常功能可能有重要的作用?     

探讨抑制水通道蛋白-1在人前列腺癌细胞中的表达对癌细胞凋亡的影响

目的:通过抑制水通道蛋白-1在前列腺癌PC-3细胞的表达,了解前列腺癌细胞的凋亡情况。方法:设计合成针对前列腺癌PC-3细胞AQP1基因的小干扰RNA并构建高效表达载体,脂质体法转染PC-3细胞,Western Blot检测AQP1蛋白表达的变化。结果:AQP1在前列腺癌PC-3细胞表达,针对AQP1基因siRNA高效表达载体能够抑制AQP1蛋白在PC-3细胞的表达,AQP1蛋白相对表达量为:转染组0.54±0.04,正常对照组0.82±0.08,差异有显著性(P<0.01);成瘤实验中转染组caspase-3的含量明显高于对照组,差异显著(P<0.05),AQP1的表达量与癌细胞的凋亡呈负相关。结论:通过抑制AQP1基因的表达,有效抑制了前列腺癌PC-3细胞AQP1蛋白表达,近而使癌细胞的凋亡增加。     

水通道蛋白3在人正常椎间盘中的表达

目的 观察水通道蛋白-3(aquaporin-3)在人正常椎间盘中的表达及分布.方法 收集10例青年人因腰椎骨折行椎间融合手术摘除的正常椎间盘样本,运用免疫组织化学、逆转录-聚合酶链反应(RT-PCR)、 Western blot检测AQP3在椎间盘中的表达及分布.结果 免疫组织化学显示AQP3表达于椎体软骨终板类软骨细胞,髓核和纤维环未见表达;RT-PCR显示AQP3 mRNA在椎体软骨终板及髓核组织有表达;Western blot检测显示椎间盘组织在29×103左右有一特异性条带.结论 AQP3在人正常椎间盘中的表达及分布提示其可能参与椎间盘内液体平衡,对维持椎间盘组织的正常生理功能、在椎间盘退变的发病机制中可能有重要作用.     

RNAi对前列腺癌细胞水通道蛋白-1的影响

目的探讨RNA干扰技术沉默AQP1基因对前列腺癌PC-3细胞AQP1蛋白表达影响。方法设计合成针对前列腺癌PC-3细胞AQP1基因的小干扰RNA并构建高效表达载体,脂质体法转染PC-3细胞,Western Blot检测AQP1蛋白表达的变化。结果 AQP1在前列腺癌PC-3细胞表达,针对AQP1基因siRNA高效表达载体能够抑制AQP1蛋白在PC-3细胞的表达,AQP1蛋白相对表达量为：转染组0.54±0.04,正常对照组0.82±0.08,差异有显著性（P〈0.01）。结论通过抑制AQP1基因的表达,有效抑制了前列腺癌PC-3细胞AQP1蛋白表达。     

颈椎间盘压缩力学性能改变与终板蛋白多糖变化关系的实验研究

目的:探讨颈椎间盘退变时基质各成分的变化及其对椎间盘力学性能的影响。方法:将24只家兔随机分为对照组和模型组(n=12),模型组保持45°低屈曲位5h/次/d,最长持续3个月。分别于造模后1、2、3个月时各处死4只动物,取C5/6椎间盘测定终板糖胺多糖(glycosaminoglycan,GAG)总量、硫酸软骨素(chongdroitinsulphate,CS)与硫酸角质素(keratansulphate,KS)比值和透明质酸(hyaluronicacid,HA)含量;同时作力学测定。结果:模型组终板抗压强度、断裂时的最大形变、终板基质GAG总含量、CS/KS比值、HA含量都低于对照组(P<0.05),并随造模时间的延长两组差异越显著。结论:长时间的应力不均可造成椎间盘终板材料力学特性改变;终板蛋白多糖含量和成分改变可能是颈椎间盘生物力学性能减退的主要原因之一。     

软骨终板细胞凋亡及其相关研究进展

软骨终板是椎间盘的重要组成部分，它在髓核的营养交换和椎间盘的应力缓冲保护以及维持椎体的正常形态等方面起着重要作用。近年来，越来越多的研究发现细胞凋亡在椎间盘的衰老和退变中起着重要作用。软骨终板不仅是椎间盘的组成结构，并且在椎间盘的生理和退变过程中扮演着重要的角色。同样，软骨终板细胞凋亡在椎间盘的退变中起着重要的作用。     

The relationship between apoptosis of endplate chondrocytes and aging and degeneration of the intervertebral disc.

STUDY DESIGN: Apoptosis in cervical intervertebral disc cells and cartilaginous endplate cells was examined by the nick end labeling (TUNEL) technique during the process of natural aging and in a mouse experimental spondylosis model. OBJECTIVES: To determine the role of apoptosis in aging and degeneration of intervertebral discs by monitoring chronologic changes in the quantity and localization of apoptotic cells. SUMMARY OF BACKGROUND DATA: Apoptosis occurs within human intervertebral discs, but little is known about the pathologic significance of this process. On the other hand, the cartilaginous endplate is known to decrease in thickness and to disappear with aging and degeneration. The cause of this age-related change remains unclear. METHODS: A mouse spondylosis model was prepared via surgical resection of the posterior spinal element in 12 mice to examine the experimentally induced spondylosis process. Eighteen naturally aged mice were also used to examine the influence of aging. Paraffin-embedded midsagittal sections of the cervical spine were obtained 2, 3, 6, and 12 months after surgery in the spondylosis model and in the age-matched naturally aged mice, as well as in 4-week-old and 18-month-old naturally aged mice. Sections were stained with hematoxylin and eosin, safranin-O, and the TUNEL procedure. The number of apoptotic cells and vital cells were counted in the cartilaginous endplate of the intervertebral disc excluding the growth cartilage, and the degree of disappearance of the cartilaginous endplate was evaluated. RESULTS: Apoptosis, particularly noticeable in the cartilaginous endplate, increased with age and resulted in a marked decrease in cell density. Subsequently, the structure of the cartilaginous endplate began to disappear. Apoptosis was more evident and the structure of the cartilaginous endplate began to disappear more rapidly in the surgically treated group than in the naturally aged group. CONCLUSIONS: TUNEL-positive cells in the cartilaginous endplate increased with age, with destruction of the cartilaginous endplate after apoptosis (TUNEL-positive cell death). The application of the spondylosis model increased the incidence of apoptosis preceding the development of spondylosis. This suggests that apoptosis plays a role in the age-related changes seen in the cartilaginous endplate of the intervertebral disc and in the experimentally induced spondylosis process.     

Evaluation of intervertebral disc cartilaginous endplate structure using magnetic resonance imaging

Purpose

The cartilaginous endplate (CEP) is a thin layer of hyaline cartilage positioned between the vertebral endplate and nucleus pulposus (NP) that functions both as a mechanical barrier and as a gateway for nutrient transport into the disc. Despite its critical role in disc nutrition and degeneration, the morphology of the CEP has not been well characterized. The objective of this study was to visualize and report observations of the CEP three-dimensional morphology, and quantify CEP thickness using an MRI FLASH (fast low-angle shot) pulse sequence.

Methods

MR imaging of ex vivo human cadaveric lumbar spine segments (N = 17) was performed in a 7T MRI scanner with sequence parameters that were selected by utilizing high-resolution T1 mapping, and an analytical MRI signal model to optimize image contrast between CEP and NP. The CEP thickness at five locations along the mid-sagittal AP direction (center, 5 mm, 10 mm off-center towards anterior and posterior) was measured, and analyzed using two-way ANOVA and a post hoc Bonferonni test. For further investigation, six in vivo volunteers were imaged with a similar sequence in a 3T MRI scanner. In addition, decalcified and undecalcified histology was performed, which confirmed that the FLASH sequence successfully detected the CEP.

Results

CEP thickness determined by MRI in the mid-sagittal plane across all lumbar disc levels and locations was 0.77 ± 0.24 mm ex vivo. The CEP thickness was not different across disc levels, but was thinner toward the center of the disc.

Conclusions

This study demonstrates the potential of MRI FLASH imaging for structural quantification of the CEP geometry, which may be developed as a technique to evaluate changes in the CEP with disc degeneration in future applications.     

白介素-1受体拮抗剂对双后肢大鼠椎间盘细胞凋亡的影响

目的：探讨白介素-1受体拮抗剂（IL-1Ra）对双后肢大鼠椎间盘细胞凋亡的影响。方法：建立双后肢大鼠模型54只，随机分为试验组、空白对照组和阴性对照组，每组18只．试验组从造模当天即予腹腔注射IL-1Ra（50ng／kg体重），隔天1次重复注射至处死，空白对照组不予任何处理，阴性对照组隔天1次予腹腔注射等量生理盐水。于造模后1、3、6个月每组分别处死6只大鼠，完整取出L4／5椎间盘后进行固定、切片，使用末端脱氧核件酸转移酶介导的dUTP缺口末端标记法（TUNEL法）检测各组大鼠椎间盘细胞的凋亡情况，并使用透射电镜观察凋亡细胞的超微结构。取L5/6椎间盘使用流式细胞仪检测各组大鼠椎间盘细胞的凋亡情况。结果：术后1个月试验组、空白对照组及阴性对照组椎间盘细胞的凋亡无显著性差异（P〉0．05）：术后3个月试验组与空白对照组及阴性对照组相比细胞凋亡明显减少，有显著性差异（P〈0．05）；术后6个月试验组与空白对照组及阴性对照组相比细胞凋亡率有非常显著性差异（P〈0．01）。结论：IL-1Ra对双后肢大鼠椎间盘细胞凋亡有明显的抑制作用。     

腰椎间盘退变性疾患下腰椎终板形态的MRI观察

【摘要】　目的：在MRI片上观察腰椎间盘退变患者下腰椎终板形态的分布规律,分析终板形态和椎间盘退变的关系。方法：回顾分析两组腰椎间盘退变性疾病患者的术前腰椎MRI,A组110例为单节段腰椎间盘突出症患者,B组35例为椎间盘源性腰痛患者。根据正中矢状面MRI T1像,将终板形态分为凹面、平坦、不规则三型;根据Pfirrmann法评定椎间盘退变程度并将Ⅰ～Ⅴ级分别计为1～5分;按Modic改变分级标准判定各节段终板有无Modic改变。分析下腰椎终板的形态特点及三种分型与椎间盘退变程度、Modic改变等的关系。结果：①435个下腰椎节段中,凹面型终板最多（215/435）,A组中占50.6％（167/330）,B组中占45.7％（48/105）,且主要分布于L3/4（108/215）、L4/5（83/215）节段;平坦型终板占29.0％（126/435）,并主要位于L5/S1节段（76/126）;不规则型终板最少（94/435）,A组中占23.0％（76/330）,B组中占17.1％（18/105）,也主要位于L5/S1节段（45/94）。②A组患者中,凹面型终板退变程度平均为3.31±0.81分,平坦型为3.66±0.64分,不规则型为4.16±0.67分,两两比较有显著差异（P＜0.05）;椎间盘突出节段以平坦型（37/110）和不规则型（43/110）终板占多数,无突出节段则以凹面型（137/220）终板占多数,差异有显著性（P＜0.05）;不规则型终板比凹面型和平坦型更容易伴发Modic改变,差异有显著性（P＜0.05）,凹面型和平坦型间无显著性差异（P＞0.05）。③B组患者中,凹面型终板的椎间盘退变程度平均为3.23±0.86分,平坦型为3.54±0.85分,不规则型为3.94±0.54分,仅凹面型和不规则型间差异有显著性（P＜0.05）。④相同终板形态时A组和B组椎间盘退变程度相比均无显著性差异（P＞0.05）。结论：终板形态与椎间盘退变、Modic改变之间有相关性。终板形态由凹面型到平坦型再到不规则型,腰椎间盘退变程度逐渐加重。影像学上终板形态改变在一定程度上反映了椎间盘退变的程度。     

阿伦磷酸钠联合肾骨安对去势小鼠终板结构和椎间盘退变的影响

目的 :观察阿伦磷酸钠(alendronate,ALN)联合补肾中药———肾骨安(herbs,HB)对去势小鼠椎体终板、椎间盘退变(intervertebral disc degeneration,IVDD)的影响,初步探讨ALN+HB干预IVDD的作用机制。方法:32只12周龄健康雌性C57BL/6J小鼠,随机分为正常对照组(对照组,n=8)、去卵巢组(OVX组,n=8)、ALN组(n=8)及ALN+HB组(n=8)。对照组行假手术,其余各组行双侧卵巢摘除。术后3d开始给药,连续给药2个月后取材,HE及番红O-固绿染色观察椎间盘组织形态学改变并进行病理评分,显微计算机断层扫描(u-CT)检测终板表面孔隙变化及附近骨赘增生情况,免疫组织化学法检测椎间盘中Ⅱ型胶原(Collagen-typeⅡ,Col2)的表达。结果:实验过程中无小鼠死亡。HE及番红O-固绿染色对照组椎间盘结构和形态基本正常;OVX组椎间盘终板发生严重骨化重塑,以下位终板更为明显,同时出现终板与髓核的边界结构紊乱,椎间盘基质的丢失及裂隙形成;ALN组终板骨化重塑较OVX组轻,髓核结构形态改善,软骨终板内仍可见一些小的骨化区;ALN+HB组终板骨化重塑不明显,番红O固绿染色染色可见软骨终板着色加深。IVDD病理评分、终板表面孔隙率(%)和Col2积分光密度(IOD)值分别为1.20±0.84、28.60±4.04和27764.7±1958.2,OVX组为4.00±1.58、56.80±9.39和17213.6±1021.3,ALN组为2.40±0.89、36.20±3.42和18921.4±888.1,ALN+HB组为2.00±0.71、29.60±6.19和23420.1±2439.6。OVX组与对照组比较IVDD病理评分、终板孔隙率均显著性升高(P0.05);ALN组、ALN+HB组与OVX组比较二者均显著性降低(P0.05);ALN组、ALN+HB组与对照组比较,及ALN+HB组与ALN组比较二者均无统计学差异(P0.05)。OVX组、ALN组和ALN+HB组与对照组比较Col2 IOD值均显著性降低(P0.05),ALN组与OVX组比较无统计学差异(P0.05),ALN+HB组与OVX组、ALN组比较均显著性升高(P0.05)。结论 :OVX小鼠雌激素缺乏可引起椎体终板的骨化重塑及孔隙率增加,导致IVDD。ALN及ALN+HB均可以抑制椎体终板的重塑,降低终板孔隙率,保证终板结构和功能完整,从而能延缓雌激素缺乏相关IVDD,ALN+HB效果更为明显。     

腰椎间盘突出症患者下腰椎终板矢状面形态特征

目的:观察腰椎间盘突出症(lumbar disc herniation,LDH)患者下腰椎(L3～S1)终板矢状面形态特征。方法:回顾性分析2016年6月～2017年7月就诊我院的腰椎间盘突出症患者和无明确腰椎疾病的志愿者。共纳入LDH患者141例,其中男61例,女80例,年龄61.6±10.1岁(41～79岁),身体质量指数(BMI)为26.3±3.4(18.3～33.2)。对照组纳入志愿者109例,其中男47名,女62名,年龄55.4±12.2岁(40～87岁), BMI为25.3±3.6 (17.6～32.5)。在腰椎CT正中矢状面重建图像上测量LDH患者椎间盘突出节段的终板形态和志愿者腰椎L3下终板至S1上终板的终板形态学参数,包括终板屈曲深度(ECD)、矢状面屈曲角(SCA)和终板屈曲顶点位置(ECA);相应节段椎间盘退变程度在MRI上通过Pfirrmann分级进行评估。应用t检验比较LDH组与对照组终板矢状面形态学参数;选择L4/5和L5/S1两节段中相同退变程度(PfirrmannⅢ级,PfirrmannⅣ级)的椎间盘,比较LDH组患者和对照组志愿者的终板矢状面形态。将LDH组患者和对照组志愿者终板数据合并后按照椎间盘退变程度分组(PfirrmannⅡ级～PfirrmannⅤ级),应用Kruskal-Wallis检验比较不同退变程度椎间盘终板形态参数的组间差异。结果:LDH组各节段终板ECD均显著低于对照组(L4上终板P=0.016,其余终板P0.01),SCA均显著大于对照组(P0.01);除L3下终板外(P=0.014),所有节段终板ECA的组间差异无统计学意义(P0.05)。L4/5和L5/S1节段中PfirrmannⅢ级和Ⅳ级椎间盘终板,相同节段和退变分级的组间比较结果显示,LDH组终板ECD显著小于对照组(P0.05),SCA显著大于对照组(P0.05),ECA未出现组间显著性差异(P0.05)。不同退变程度椎间盘终板形态参数组间比较显示,随着椎间盘退变进展,各节段ECD降低(P0.01),SCA增大(P0.01),ECA未出现一致的组间变化趋势。结论:LDH患者相比对照组志愿者,其下腰椎终板矢状面屈曲程度较低,退变程度较高的椎间盘其终板屈曲程度较小。     

不同年龄大鼠终板软骨细胞抗氧化能力研究

目的 :通过研究不同年龄大鼠的终板软骨细胞氧化应激的差异,探讨衰老对终板软骨细胞抗氧化能力的影响。方法:原代培养获取SD大鼠2个月、18个月来源的终板软骨细胞鉴定后,使用第三代细胞进行实验。实验分为两组,A组为2个月大鼠来源的终板软骨细胞,B组为18个月大鼠来源的终板软骨细胞。待A、B两组细胞贴壁后,通过β-半乳糖脱氢酶染色和RT-PCR对端粒酶长度进行检测,比较两组细胞衰老的差异;通过总抗氧化能力试剂盒检测两组细胞总抗氧化能力的不同。以浓度为200umol/L过氧化氢对细胞进行2.5h的处理,RT-PCR法检测处理前后两组细胞Ⅱ型胶原、蛋白聚糖、caspase-3及B淋巴细胞瘤-2(B-cell lymphoma-2,bcl-2)的m RNA表达情况,使用流式细胞仪检测两组细胞的凋亡情况。对Ⅱ型胶原、蛋白聚糖、caspase-3及bcl-2的相对表达量进行组间t检验,P0.05为差异有统计学意义。结果 :未使用过氧化氢处理时,A、B两组终板软骨细胞的在β-半乳糖脱氢酶染色、Ⅱ型胶原、蛋白聚糖表达及凋亡率无明显差异(P0.05),而B组在端粒酶的相对长度(T/S=10±2)及总抗氧化能力(0.72±0.18)较A组(T/S=135±5,1)显著降低(P0.05)。在相同条件的过氧化氢刺激后,B组终板软骨细胞的Ⅱ型胶原(0.60±0.16)、蛋白聚糖(0.75±0.22)表达明显低于A组细胞(P0.05),而凋亡率显著高于A组细胞(P0.05)。结论 :不同年龄大鼠终板软骨细胞衰老及抗氧化能力存在差异,衰老越明显的终板软骨细胞,总抗氧化能力越低,抵抗过氧化损伤的能力越差。     

Interference in the endplate nutritional pathway causes intervertebral disc degeneration in an immature porcine model

Purpose

Previous studies have shown that blocking the endplate nutritional pathway with bone cement did not result in obvious intervertebral disc degeneration (IDD) in mature animal models. However, there are very few comparable studies in immature animal models. As vertebroplasty currently is beginning to be applied in young, even biologically immature patients, it is important to investigate the effect of cement blocking at the endplate in an immature animal model.

Methods

Two lumbar intervertebral discs in eight immature pigs were either blocked by cement in both endplate pathways or stabbed with a scalpel in the annulus fibrosus (AF) as a positive control, and with a third disc remaining intact as a normal control. Magnetic resonance imaging (MRI) and histology study were performed.

Results

After three months, the cement-blocked discs exhibited severe IDD, with the percentage of disc-height index (DHI), nucleus pulposus (NP) area, and NP T2 value significantly lower than the normal control. These IDD changes were histologically confirmed. Post-contrast MRI showed diseased nutritional diffusion patterns in the cement-blocked discs. Moreover, the degenerative changes of the cement-blocked discs exceeded those of the injured AF positive controls.

Conclusions

The endplate nutritional pathway was interfered with and diseased after three months of bone cement intervention in an immature porcine model. Severe interference in the endplate nutritional pathway in an immature porcine model caused IDD. These findings also draw attention to the fact that interference in endplate nutritional pathways in immature or young patients may affect the vitality of adjacent discs.