山羊腰椎间盘损伤后蛋白基因产物9．5免疫组化染色阳性神经纤维的分布

目的：观察山羊腰椎间盘损伤后不同时间点蛋白基因产物9．5（protein gene product 9．5，PGP9．5）免疫组化染色阳性神经纤维在损伤椎间盘内的分布，探讨山羊椎间盘损伤后是否出现神经内生长。方法：15只6月龄山羊，用直径1．2mm的穿刺针刀刺伤L5/6椎间盘前纤维环全层和L6／7椎间盘后部纤维环内层，L4/5椎间盘作为对照椎间盘。在造模后3周、3个月、6个月各取5只动物处死，取目标椎间盘光镜下观察椎间盘后部纤维环的组织学改变，检测PGP9．5免疫阳性神经纤维的分布并用半定量方法进行评分。结果：在观察期间L6／7椎间盘后部损伤纤维环未愈合，L4/5椎间盘在各个时间点均未出现裂隙，L5/6椎间盘仅在6个月时有1个椎间盘出现多个裂隙。损伤后3、6个月，在L6/7椎间盘右后1／4区很容易检测到PGP9．5免疫阳性神经纤维，神经纤维沿穿刺道及周围组织向内生长。L4／5和L5/6椎间盘相同区域未检测到相关免疫阳性反应神经纤维。在髓核中没发现PGP9．5免疫染色阳性神经纤维。结论：山羊经椎间盘前方损伤后部纤维环内层后，纤维环内层很难愈合，并出现PGP9．5免疫阳性神经纤维分布，说明椎间盘后部纤维环内层损伤可发生神经内生长。     

腰椎间盘损伤后MRI表现及组织学改变的实验研究

目的：探讨山羊腰椎间盘损伤后不同时间点MRI表现和组织学改变。方法：15只山羊．人为刺伤L5／6椎间盘前纤维环全层和L6／7后部纤维环内层，在伤后3周、3个月、6个月进行腰椎MRI检查观察髓核和纤维环的信号改变，光镜下观察实验椎间盘后部纤维环组织学改变。结果：L6H椎间盘损伤后部纤维环内层后．在实验期间未发生愈合，通过MRI定性、定量分析发现，椎间盘出现退变，并随时间进行性加重（3周，3、6个月）．且退变过程较L5／6加速。他像上未发现一例出现HIZ。结论：经山羊椎间盘前方损伤后部纤维环内层后．纤维环内层很难愈合，早期出现椎间盘退变。     

新型山羊腰椎间盘突出模型的建立

目的建立新型的山羊腰椎间盘退变合并突出的动物模型。方法9只6月龄山羊，随机分成3组，每组18个腰椎间盘，再将每只山羊的6个腰椎间盘随机等分成正常组和模型组。模型组椎间盘左前外侧纤维环用直径2．5mm的微型环锯限深5mm造成柱状纤维环缺损。术后2、4、6个月时对正常及模型椎间盘摄X线片和MR扫描，观察X线片上的椎间盘高度指数、MRI T2加权像上的椎间盘高信号区的面积和平均R弛豫时间、椎间盘纤维环损伤区的形态学变化，进行组织病理学切片观察（HE染色、Masson三色胶原染色和番红O-固绿染色），对椎间盘组织形态学变化、生物化学变化和组织学评分等指标进行评估。结果正常成年山羊椎间盘组织学结构特点与人类相似；模型椎间盘在损伤后2个月即出现明显退变（P〈0．01），包括椎间盘高度指数降低、椎间盘T2加权像高信号区面积和平均R弛豫时间减低、组织学退变评分增高；MRI和组织学均发现损伤纤维环外侧1／3修复，内2／3出现髓核组织突出充填。损伤后4、6个月模型椎间盘退变加重，但与损伤后2个月的指标差异无统计学意义（P〉0．05）；椎间盘突出形态稳定。结论以成年山羊为对象，应用微型环锯对椎间盘前外侧纤维环定量损伤可以获得快速、有效、重复性好的腰椎间盘突出动物模型。     

椎体前路钢板加压诱导羊椎间盘退变的实验研究

目的 建立新型的山羊腰椎间盘退变动物模型.方法 8只6月龄山羊,取腰椎右侧腹膜后入路,L3～4、L4～5椎间盘为目标椎间盘,于L3、L5椎体前外侧给予重建钢板加压固定.术后6个月对正常及目标椎间盘行MRI检查和组织学检查,观察MRI T2加权像上的椎间盘信号区的变化和HE染色下椎间盘组织形态学变化.结果 7只山羊存活,1只山羊因麻醉原因死亡.6个月时MRI检查显示目标椎间盘T2加权像信号明显降低,组织学观察发现目标椎间盘出现髓核纤维化和纤维环退化破裂的退变表现.结论 山羊椎间盘组织学结构特点与人类相似,通过椎体前路钢板加压的方法可以建立羊的椎间盘退变模型.     

白介素-1受体拮抗剂对椎间盘纤维环胶原纤维代谢的影响

目的 探讨白介素-1受体拮抗剂(IL-1Ra)对双后肢大鼠椎间盘纤维环胶原代谢的影响.方法 建立双后肢大鼠模型36只,随机分为试验组和对照组,每组18只.试验组从造模当天即予腹腔注射IL-1Ra(50ng/kg体重),隔天重复注射至处死;对照组18只不予任何处理.于造模后1、3、6个月每组分别处死6只,完整取出L3～4椎间盘固定、切片,予SABC法进行免疫组化,使用图像分析系统对髓核中Ⅰ、Ⅱ型胶原染色进行面积扫描,并使用扫描电镜观察纤维环胶原纤维超微结构.结果 术后第1个月试验组与对照组椎间盘纤维环中Ⅰ、Ⅱ型胶原面积差异无显著性(P＞0.05),第3个月及第6个月试验组与对照组Ⅰ、Ⅱ型胶原面积相比差异有显著性(P＜0.01).结论 IL-1Ra对双后肢大鼠椎间盘纤维环中Ⅰ、Ⅱ型胶原的代谢有重要的作用.     

纤维环穿刺诱导椎间盘退变动物模型的实验研究

目的：探讨纤维环穿刺诱导椎间盘退变建立动物模型的可行性。方法：新西兰大白兔24只，用持针器夹持18G皮肤穿刺针从左前外侧刺人L3/4、L4/5、L5/6椎间盘的纤维环，深度控制在5mm。术前及术后3、6、10周对造模后的椎间盘及对照的椎间盘（L2／3）行MRI检查，并行免疫组化及组织学观察。结果：术后第3周到第10周，造模后的椎间盘MRI T2WI信号呈现持续减弱趋势，免疫组化及组织学观察发现髓核细胞的数量及Ⅱ型胶原含量较对照间盘进行性减少（P〈0．01）。结论：纤维环穿刺法可以诱导兔椎间盘的缓慢退变，为研究椎间盘的退行性变提供有效的动物模型。     

人工生物膜修复椎间盘纤维环的研究

目的 用不同方法处理椎间盘纤维环,观察人工生物膜对椎间盘纤维环缺损的修复作用.方法 成年山羊8只,雌雄各4只,对每只羊的腰椎(腰2/3、腰3/4、腰4/5)椎间盘纤维环进行随机处理,处理方法包括:(1)暴露出椎间盘纤维环,不作任何处理;(2)暴露出椎间盘纤维环后,将其切开,用人下生物膜填充缺口;(3)暴露出椎间盘纤维环,尖刀将其切开,作为对照组.12周后,通过生物力学测试、核磁共振(MRI)及脱钙病理切片染色观察椎间盘纤维环的修复效果.结果 12周后,测试纤维环承受最大压力,单纯暴露组为(4.92±0.17)MPa,纤维环单纯切开组为(2.48±0.39)MPa,人工生物膜修复组为(3.76±1.56)MPa.人工生物膜修复组与单纯切开组,椎间盘纤维环完整性及生物强度均不如单纯暴露组,人工生物膜修复组优于单纯切开组,两组间的差异有统计学意义(P＜0.05),人工生物膜可与椎间盘纤维环的胶原纤维良好融合.结论 人工生物膜可对椎间盘纤维环缺口起到修复作用,能使其生物力学强度平均恢复76.4%,人工生物膜可以促进椎间盘结构完整性的恢复.     

大鼠腰椎间盘针刺退变模型的建立

[目的]建立大鼠腰椎间盘针刺退变模型并进行MRI和组织学观察。[方法]Sprague-Dawley大鼠32只,20只进行腰椎间盘纤维环厚度测量,确定针刺深度;12只经腹膜手术,L3、4、L4、5、L5、6椎间盘使用21G针分别行纤维环部分针刺或全层针刺,L6S1椎间盘作为对照,术前及术后4、8周行MRI检查,然后处死,椎间盘行HE染色。[结果]测量大鼠腰椎间盘纤维环厚度后,确定适用于L3、4、L4、5、L5、6、L6S1椎间盘纤维环部分针刺深度为1.5mm,纤维环全层针刺深度为2.3mm。MRI检查在纤维环全层针刺4周,部分针刺8周后的椎间盘信号强度显著降低。组织学检查发现纤维环全层针刺和部分针刺椎间盘4周时都发生退变,而纤维环全层针刺退变较严重。[结果]纤维环部分针刺或全层针刺方法可以成功建立大鼠腰椎间盘退变模型,方法可靠、有效、重复性好。     

腰椎间盘退变动物模型的建立及影像学改变

目的建立腰椎间盘退变的动物模型。方法取新西兰大白兔6只,采用腹膜后入路进行腰椎手术,L3/L4椎间盘作为对照椎间盘;L4/L5椎间盘作为假手术椎间盘,只进行暴露;L5/L6椎间盘作为处理椎间盘,手术暴露后用24 G针头从椎间盘的前外侧针刺3次。4周后通过X线片观察针刺损伤对椎间盘高度的影响,通过MRI观察椎间盘在针刺损伤后退变的程度。结果腹膜后入路可以很好的显露新西兰大白兔腰椎间盘,所有动物均成活至术后4周,统计学分析说明针刺、手术暴露以及对照对术后4周椎间盘高度、MRI的T2加权信号强度的影响不同。用Newman-Keuls法对3样本均数两两比较结果显示：L3/L4与L4/L5之间的均数比较P〉0.05;L3/L4和L5/L6之间的均数比较P〈0.01;L4/L5和L5/L6之间的均数比较P〈0.01。结论术后4周针刺损伤实验动物椎间盘可以造成椎间盘高度、MRI的T2加权信号强度的降低,具有统计学意义。椎间盘损伤是造成椎间盘退变的原因之一。     

纤维环穿刺抽吸法和纤维环切开法建立兔椎间盘退变模型的比较

[目的]通过纤维环穿刺抽吸法和纤维环切开法建立兔椎间盘退变模型,分析此两种方法的可行性及特点.[方法]取10个月龄健康日本大耳白兔24只,随机分为2组,其中A组为纤维环穿刺抽吸组,利用18G穿刺针分别在兔L3、4、L4、5、L5、6椎间盘刺入并抽吸髓核8～ 12 mg;B组为纤维环切开组,利用手术刀分别在兔L3、4、L4、5、L5、6椎间盘纤维环上做水平位切口;造模完毕,两组兔分别于术后4、8、12、16周进行MRI检查,病理组织学观察和免疫组化染色观察.[结果]A、B两组退变椎间盘MRI T2加权像信号随时间延长呈现持续减弱趋势,术后4、8周纤维环穿刺组T2加权像信号强度评分较纤维环切开组低(P＜0.05),组织学观察发现造模组髓核细胞逐渐减少;免疫组化染色观察Ⅱ型胶原和蛋白聚糖表达含量随时间延长逐渐降低,且B组含量明显低于A组.[结论]两种方法均能建立兔椎间盘退变模型,但纤维环切开法椎间盘的退变程度较纤维环穿刺法出现较早且较为剧烈.     

短节段椎弓根钉固定术对相邻椎间盘影响的生物力学研究

目的 比较跨节段3椎体4枚、经骨折伤椎3椎体5枚及3椎体6枚椎弓根钉固定治疗胸腰椎爆裂性骨折对相邻椎间盘应变的影响,为临床术式选择提供力学依据. 方法采用6具国人新鲜脊柱尸体标本(T11～L3),模拟失去前柱支持的完全不稳定L4椎体爆裂性骨折.实验分三组:跨节段固定组(4枚钉组)、5枚钉组和6枚钉组.每个标本依次进行完整状态、跨节段3椎体4枚椎弓根钉固定状态(4枚钉组)、3椎体5枚椎弓根钉固定状态(5枚钉组)、3椎体6枚椎弓根钉固定状态(6枚钉组)的试验测试.应用混合力-位移控制加载的六自由度机器人实验装置对标本施加前屈,后伸,左、右侧弯及左、右轴向旋转6种运动方式,测试上、下相邻椎间盘的应变,比较三组间差异. 结果随着螺钉数的增加,固定节段相邻椎间盘(T11-12、L2-3)应变逐渐增大.上位相邻椎间盘(T11-12)仅在轴向旋转状态下,6枚钉组和5枚钉组与4枚钉组比较差异均有统计学意义(P<0.05),6枚钉组与5枚钉组间差异无统计学意义(P>0.05);其他状态下三组差异均无统计学意义(P>0.05).固定节段F位相邻椎间盘(L2-3)任何状态下两两比较差异均无统计学意义(P>0.05). 结论跨节段3椎体4枚椎弓根钉、经骨折椎3椎体5枚椎弓根钉、经骨折椎3椎体6枚椎弓根钉固定治疗胸腰椎爆裂性骨折,随着螺钉数的增加,邻近椎间盘应变增加,且上位相邻椎间盘应变增加更为明显,其退变的可能性大于下位相邻椎间盘.     

退变性腰椎侧凸形成和发展的相关因素分析

目的 探讨退变性腰椎侧凸患者椎问盘的不对称指数、腰椎间盘退变程度以及骨密度降低对侧凸角度的影响.方法 采用回顾性研究的方法,选取2002年1月至2010年8月,共96例退变性腰椎侧凸患者为研究对象(侧凸组);2002年1月至2010年8月确诊为腰椎管狭窄症并且资料齐全的患者96例为对照组;两组间性别、年龄、体质量指数匹配.侧凸组:在腰椎正位X线片上测量凸凹侧顶椎间盘及其上下椎间盘的高度和顶椎及其上下椎体的高度,利用Adobe Photoshop 6.0软件,测量MRI图像T2WI顶椎及其上下椎间盘内髓核与脑脊液的相对信号强度.对照组:取2～3、L3-4、L4-5这3个椎间盘为研究对象测定上述指标.应用双能X线吸收法测定两组患者腰椎(L2-4)及股骨颈、股骨粗隆和Ward's三角的T值.结果 侧凸组凸侧椎间盘高度和为(40±7)mm高于凹侧的(28±7)mm(P<0.01),凸侧椎体高度和为(76±12)mm高于凹侧的(72±10)mm(P=0.016):两组之间的椎间盘退变程度差异有统计学差异(P=0.003);两组之间骨密度T值的平均值和骨质疏松的发生率差异有统计学意义(均P<0.01).通过多元线性回归分析结果 显示患者椎间盘的不对称指数、椎间盘的退变程度、骨密度T值影响退变性腰椎侧凸角度.结论 退变性腰椎侧凸常伴有凸凹两侧椎间盘高度以及椎体高度不对称.侧凸角度与椎间盘的不对称指数、椎间盘的退变程度呈正相关,与骨密度值T值呈负相关.

Abstract：

Objectives To investigate the correlation between scoliosis angle and the asymmetric index of degenerative lumbar scoliosis, the degree of intervertebral disc degeneration, decreased bone density. Methods As a retrospectively study, a total of 96 patients with degenerative lumbar scoliosis were retrospectively enrolled from January 2002 to August 2010 as scoliosis group, meanwhile % patients with lumbar spinal stenosis matched in gender, age and body mass index (BMI) were selected as control group.All patients were studied with plain radiographs, MRI and dual energy X-ray absorptiometry at presentation. Radiographic measurements include Cobb angle, the height of the convex and concave side of the apical disc and the contiguous disc superiorly and inferiorly, the height of the convex and concave side of the apical and the contiguous vertebral body superiorly and inferiorly in scoliosis group, the height of L2-3, L3-4, L4-5 discs and the height of L2-4 vertebral body in control group. The average relative signal intensity of lumbar intervertebral disc and cerebrospinal fluid in T2WI sagittal image was measured in apex intervertebral disc and adjacent discs by Adobe Photoshop 6.0 in scoliosis group, which was measured in L2-3, L3-4, L4-5 disc in control group. The bone density of lumbar, femoral neck, trochanter, and Ward's triangle regions were measured with dual-energy X-ray absorptiometry. Results The intervertebral disc height in convex side was greater than the height in the concave side [(40 ± 7) mm vs. (28 ± 7) mm, P < 0. 01] , the vertebral body height in convex side was greater than the height in the concave side [(76 ± 12) mm vs. (72 ± 10) mm, P =0.016] in scoliosis group. There was significant statistically difference in the degenerative degree of intervertebral discs between two groups (P = 0. 003). There was significant statistically difference of the average T-value and the rate of osteoporosis between two groups (P < 0. 01). Multiple linear regression analysis showed that the asymmetric disc index, the degenerative degree of intervertebral disc and osteoporosis were the predominant correlative factors, which affected the development of degenerative lumbar scoliosis. Conclusions Degenerative lumbar scoliosis is always accompanied by the height asymmetry of intervertebral discs and vertebral body from convex and concavity sides. There is positive correlation between the angle of scoliosis and the asymmetric disc index, the degeneration of intervertebral disc, and negative correlation between the angle of scoliosis and the bone density (T-value).     

Effects of basic fibroblast growth factor on spontaneous resorption of herniated intervertebral discs. An experimental study in the rabbit.

STUDY DESIGN: Histologic examination was performed on the autologous intervertebral disc material that was removed from the intervertebral space at L1-L2 and then relocated to the L4 posterior epidural space after the addition of basic fibroblast growth factor (bFGF) in a rabbit. OBJECTIVES: To evaluate whether basic fibroblast growth factor influences the resorption process of the herniated intervertebral disc through the promotion of angiogenesis and chemotaxis. SUMMARY OF BACKGROUND DATA: It has been reported that newly formed vessels, inflammatory cells, and their products may play an important role in the spontaneous resorption process of herniated intervertebral discs. In a rabbit model that mimics the sequestration type of intervertebral disc herniation, it has been reported that the autologous intervertebral disc material that relocated into the epidural space was penetrated by newly formed vessels originating from the epidural fat tissue. Therefore, it is possible that promotion of angiogenesis may influence the resorption of herniated intervertebral discs. Basic fibroblast growth factor is well known as an angiogenesis stimulation factor in vivo. METHODS: Thirty-six adult rabbits were divided into three groups. The L1-L2 intervertebral disc was partially incised through a retroperitoneal approach in each rabbit. The harvested disc material, which contained nucleus pulposus and anulus fibrosus, was immersed in one of three kinds of solution before relocation into the posterior epidural space at L4. In the control group, the harvested intervertebral disc was immersed in physiologic saline for 2 hours before relocation. In the group receiving 5 micrograms bFGF, the disc was immersed in 5 micrograms/mL bFGF for 2 hours before the relocation. In the group receiving 20 micrograms bFGF, the disc was immersed in 20 micrograms/mL bFGF for 2 hours before the relocation. Rabbits of each group were killed for histologic examination 1, 2, 4, and 8 weeks after surgery. RESULTS: In the bFGF-treated groups, newly formed vessels were observed to be in more numerous than those in the control group, 1 and 2 weeks after surgery. The number of inflammatory cells, including macrophages, lymphocytes, and fibroblasts, also increased in the bFGF-treated groups. The period from the surgery to the degradation of the intervertebral disc in the bFGF-treated groups was shorter than that in the control group, although the resorption process of the relocated discs was also observed in the control group. The size of relocated intervertebral discs in the bFGF-treated groups decreased at a higher rate than in the control group as time progressed. The rate of decrease in the size of discs in the group treated with 20 micrograms bFGF was more than that in the group treated with 5 micrograms. CONCLUSIONS: Epidural injection of bFGF facilitated the resorption of the intervertebral disc relocated to the epidural space.     

冷冻保存异体椎间盘移植的实验研究

目的 观察猴冷冻保存异体椎间盘移植后的Ｘ线、组织形态学、分子生物学、生物化学少生物力学的变化,探讨移植椎间盘的长期归宿及临床应用的可能性。方法 １７只猴中的１２只随机分为０．５、１、１．５、２、６和２４个月组。移植椎间盘梯度降温至－１９６℃保存,术前复温后手术植入。结果 Ｘ线显示无脱位,２４个月极能维持正常高度的６４．９％。术后２周权在移植椎间盘终板下骨与宿主椎体骨界面区有轻度免疫排斥反应,４周时     

经皮激光腰椎间盘减压术后腰椎关节突关节和椎间高度的变化

目的：观察经皮激光椎间盘减压术（percutaneous laser disc decompression，PLDD）治疗腰椎间盘突出症术后腰椎关节突关节和椎间高度的变化。方法：应用半导体激光系统对32例腰椎间盘突出症患者进行PLDD治疗。29例患者为单节段突出，其中L3/4 3例，L4／5 18例，L5/S1 8例；3例患者同时合并IA／5和L5/S1节段突出。利用Macnab标准评价随访患者的疗效，并观察术前、术后椎间盘突出节段关节突关节角的形态，测量L3，4、L4/5和L5／S1椎间高度指数和椎间盘突出节段关节突关节角的角度。结果：所有患者无术中和术后并发症。随访14～22个月，平均17个月，按Macnab标准评价：优14例（43．75％），良13例（40．63％）；可3例（9．37％），差2例（6．25％），优良率84．38％。术后L5/S1椎间高度指数与术前相比显著性下降（P〈0．05），但L3/4和L4／5椎间高度指数无显著性改变；关节突关节无明显退变；L4／5和L5／S1椎间盘突出侧的关节突关节角角度显著性下降（P〈0．05），但L3/4椎间盘突出侧的关节突关节角度无显著性改变。结论：经皮激光腰椎间盘减压术后患者的L5／S1椎间高度和腰椎间盘突出侧关节突关节角角度下降．有可能增加腰椎滑脱的风险。     

Does long-term compressive loading on the intervertebral disc cause degeneration?

STUDY DESIGN: Coil springs were stretched and attached to produce a compressive force across the lumbar intervertebral discs of dogs for up to 53 weeks. OBJECTIVE: To test the hypothesis that compressive forces applied to the intervertebral disc for a long period of time cause disc degeneration in vivo in a dog model. SUMMARY OF BACKGROUND DATA: It is a commonly held belief that high forces applied to the intervertebral disc, and to joints in general, play a role in causing degeneration. METHODS: Coil springs were stretched and attached to produce a compressive force across the lumbar intervertebral discs (L3/L4) of 12 dogs. After up to a year, the dogs were killed, and their lumbar spines were removed and radiographed. The L3/L4 disc and the controls (T13/L1 and L4/L5) were excised and examined for visible signs of degeneration. The discs then were assessed using immunohistochemical analysis and enzyme-linked immunosorbent assay. Disc chondrocytes also were assayed for apoptosis. RESULTS: No obvious signs of degeneration in the discs (L3/L4) that had been under compression for up to a year could be observed. There was no disc bulging, anular fissures, or disc space narrowing. Some changes were observed at the microscopic level, although no thickening of the endplate was apparent. The enzyme-linked immunosorbent assay analysis provided significant data for all three regions of the disc (nucleus, inner anulus, and outer anulus). When comparing the compressed disc (L3/L4) with either of the control discs (T13/L1 and L4/L5), in the compressed disc: 1) the nucleus contained less proteoglycan and more collagen I and II; 2) the inner anulus contained less proteoglycan and collagen I; and 3) the outer anulus contained more proteoglycan and less collagen I. The collagen II differences for the inner and outer anulus were not significant. CONCLUSION: Compression applied to the lumbar intervertebral discs of dogs for up to a year does not produce degeneration in any visible form. It does produce microscopic changes and numerical changes, however, in the amounts of proteoglycan and collagen in the nucleus, inner anulus, and outer anulus. The present results add no credence to the commonly held belief that high compressive forces play a causative role in disc degeneration.     

阻断双侧终板营养途径构建山羊椎间盘退变模型

目的通过建立山羊腰椎双侧终板营养途径阻断的动物模型,观察椎间盘退变(IDD)的情况,研究椎间盘营养途径与IDD的相关性。方法选取8只24月龄雌性关中山羊,每只山羊L2~3、L3~4作为实验椎间盘,麻醉后在平行于终板2 mm的椎体骨质处造成骨缺损,并使用骨水泥填塞,阻断椎体和终板之间的营养通路,L1~2、L4~5作为对照椎间盘。分别于术后4、12、24、48周行X线、MRI检查,各时间点随机处死2只山羊,采集椎间盘标本,计算骨水泥有效阻断面积、椎间高度指数(DHI)和Pfirrmann分级,并行HE、Masson三色、蛋白多糖、番红O染色组织学检查。结果术后骨水泥有效阻断面积达49.6%~69.6%(60.7%±5.3%)。术后48周时实验椎间盘DHI百分比为60.5%~81.7%(72.7%±5.6%),椎间高度丢失较对照差异有统计学意义(P<0.01);术后48周时实验椎间盘Pfirrmann分级为3~5(4.0±0.7)分,较对照差异有统计学意义(P<0.01)。组织学检查证实,实验椎间盘术后12周即发生退变,并随时间(24、48周)逐步加重。结论骨水泥填塞阻断双侧终板营养途径可以构建山羊IDD的动物模型,阻断终板营养途径可以导致IDD发生。     

Changes in posterior disc bulging and intervertebral foraminal size associated with flexion-extension movement: a comparison between L4-5 and L5-S1 levels in normal subjects.

BACKGROUND CONTEXT: No previous study has used magnetic resonance imaging (MRI) to evaluate changes of posterior disc bulging and intervertebral foraminal size in the normal spine with flexion-extension movement, comparing L4-5 versus L5-S1 intervertebral levels. PURPOSE: To determine changes in posterior disc bulging and intervertebral foraminal size with flexion-extension movement, comparing L4-5 versus L5-S1 intervertebral levels. STUDY DESIGN: An in vivo study of magnetic resonance kinematics with spine flexion extension. METHODS: Spines of three volunteers with no history of low back pain were scanned in neutral, flexion, and extension positions in a vertically open MRI system. MRI was repeated after 6 hours of normal activity and an additional 4 hours of heavy activity with a weighted vest. Posterior bulging of the intervertebral disc and the size of intervertebral foramen were measured at the L4-5 and L5-S1 levels. RESULTS: With spine flexion, posterior bulging of the discs increased at L4-5 in eight of nine measurements (three different spine-loading states for each of three subjects) and L5-S1 discs in six of nine measurements. In most cases, posterior bulging decreased with extension. No significant difference was noted in the degree of disc bulge between levels. Foraminal size at L4-5 increased with flexion and decreased with extension, and the extent of these changes was greater at the L4-5 level than at L5-S1. CONCLUSIONS: This pilot study demonstrates two distinct behavior characteristics of the normal spine with flexion-extension movement.