颈椎软骨终板钙化与颈椎间盘退变和椎体骨赘形成的关系

目的：研究颈椎软骨终板钙化与颈椎间盘退变和颈椎椎体骨赘形成的关系。方法：应用组织学方法观察颈前路环锯手术切下的18例脊髓型颈椎病和4例颈椎过伸性损伤致颈椎间盘突出患者的颈椎间盘及相邻的上下椎体标本,研究不同退变程度颈椎间盘软骨终板和椎间盘的形态学变化及椎体骨赘形成过程。结果：退变程度较轻或基本正常的颈椎间盘软骨终板结构良好,潮标清晰,退变程度较重的颈椎间盘软骨终板发生明显纤维化,潮标前移,钙化软骨和软骨下骨板增厚,退变颈椎间盘周边软骨终板潮标明显前移,钙化和骨化层增厚,形成突向外侧的椎体边缘的骨赘。结论：颈椎软骨终板的不断钙化和骨化导致颈椎间盘营养发生障碍可能是启动颈椎间盘退变的关键因素,退变椎体周边软骨终板的不断钙化和骨化是椎体骨赘形成的根本原因。     

软骨终板钙化在椎间盘退变过程中的作用机理

目的：研究椎体软骨终板钙化在椎间盘退变过程中的作用。人新西兰兔随机分为造模与对照组２组,每组发３个月和８个月２个观察亚组。切作造模组动物颈棘上、棘间韧带及分离颈椎后旁两侧肌肉,造成颈椎力学上的失衡而诱导兔颈椎间盘退行性改变。在术后３个月和８个地分别处死,取颈椎间盘组织,行病理学检查在形态学上评定颈椎间盘退变程度,测定不同退变程度椎间盘软骨终板钙化层厚度。结果：退变程度较轻或基本正常的颈椎间盘,软骨     

软骨终板钙化与椎间盘退变关系的实验研究

目的　研究椎体软骨终板钙化与椎间盘退变的关系。　方法　通过切除２０ 只兔颈椎棘上、棘间韧带及分离颈椎后旁两侧肌肉造成颈椎力学上的失稳而诱导了颈椎间盘退变动物模型。在形态学上评定颈椎间盘退变程度,测定不同退变程度椎间盘软骨终板钙化层与非钙化层厚度。　结果　软骨终板钙化层厚度与椎间盘退变程度呈高度正相关性（ｒ＝ ０－９２） 。　结论　软骨终板的钙化可能是椎间盘退变的启动和促进因素     

退变颈椎间盘中丝氨酸蛋白酶活性变化

目的：研究退变颈椎间盘中的丝氨酸蛋白酶的活性变化。方法：通过切除实验动物颈棘上、棘间韧带及分离颈椎旁两侧肌肉,造成颈椎力学上的失衡而诱导了兔的颈椎间盘退行性变化。在术后３月和８月时分别处死３月组动物和８月组动物,取动物颈椎间盘组织,用生物化学方法测定其中丝氨酸蛋白酶活性。结果：研究表明：（１）３月组实验组动物颈椎间盘中丝氨酸蛋白酶活性明显高于３月对照组动物。（２）８月实验组动物颈椎间盘中丝氨酸蛋白酶活性明显高于８月对照组动物。（３）３月组实验组动物颈椎间盘中酶活性高于８月实验组动物。结论：退变颈椎间盘中丝氨酸蛋白酶活性明显升高,但酶活性升高程度并不与椎间盘退变程度成正比     

退变颈椎间盘中胶原酶活性变化

目的 研究退变颈椎间盘中的胶原酶的活性变化。方法 通过切除实验动物颈棘上、棘间韧带及分离颈椎旁两侧肌肉,造成颈椎力学上的失衡而诱导了兔的颈椎间盘退行性变化。在术后３月和８月时分别处死３月组动物和８月组动物,取动物颈椎间盘组织,用生物化学方法测定其中胶原酶活性。结果 研究表明：（１）３月组实验组动物颈椎间盘中胶原酶活性明显高于３月对照组动物。（２）８月实验组动物颈椎间盘中胶原酶活性明显高于８月对照组     

退变颈椎椎间盘纤维环成纤维细胞成骨分化与颈椎病

颈椎病是一种缓慢进展的退行性病变。现有研究认为该病是以颈椎椎间盘退变为基础病理进而造成椎间隙变窄、关节囊松弛以及进行性骨赘形成,进而分别刺激、压迫相邻的颈脊神经根、颈脊髓,椎动脉、椎旁交感神经等神经血管组织所致。前人对于颈椎椎间盘的退变研究主要集中在髓核,对于颈椎椎间盘纤维环退变后的转归及加速退     

腰椎侧凸软骨终板退变的X线表现及临床意义

目的探讨腰椎侧凸软骨终板退变的X线表现及其临床意义。方法收治的退变性腰椎侧凸43例,均行X线平片检查,观察其影像学特点。分别测定凹侧和凸侧每个椎体头、尾侧关节软骨的钙化层厚度,均数行t检验。结果 X线片显示椎间隙楔形样变、椎间隙狭窄、终板钙化和骨赘形成。退变的软骨终板潮标明显前移,钙化和骨化层增厚,形成突向外侧的椎体边缘的骨赘。凹侧和凸侧椎间盘关节软骨钙化层厚度分别为(35±8)μm和(72±12)μm,差异有统计学意义(P0.01)。结论软骨终板退变较其他椎间盘退变的X线征象出现早,详细研究其X线特点,对于诊断退变性腰椎侧凸和设计合理的手术方式具有重要的指导作用。     

实验性椎间盘退变的放射影像学与病理学观察

目的　研究椎间盘退变过程中 ,椎间盘退变的放射影像学与病理学改变。方法　选用 4 0只新西兰大白兔随机分为 2组 ,实验组切除兔腰椎间棘间、棘上韧带及棘突、关节突 ,造成力学失稳状态诱导形成椎间盘退变模型。术后一周、 3个月、 8个月时摄腰椎正、侧位X线片 ,观察腰椎影像学变化。第 3个月、 8个月时取腰椎间盘 ,进行组织检查 ,评定椎间盘退变的病理改变情况。结果　模型建立后 ,3个月、 8个月的X线片显现对照组无明显改变 ,实验组腰椎后突畸形 ,椎间隙狭窄 ,随着时间延长椎体软骨终板钙化更加明显。组织学观察发现 ,实验组随术后时间延长 ,髓核由椎间盘内脱出 ,并伴有椎间盘两侧软骨终板的纤维化即软骨终板发生退变。结论　椎体软骨终板的退变是椎间退变早期的主要表现方式。     

实验性椎间盘退变的放射影像学与病理学观察

目的 研究椎间盘退变过程中，椎间盘退变的放射影像学与病理学改变。方法 选用40只新西兰大白兔随机分为2组，实验组切除兔腰椎间棘间、棘上韧带及棘突、关节突，造成力学失稳状态诱导形成椎间盘退变模型。术后一周、3个月、8个月时摄腰椎正、侧位X线片，观察腰椎影像学变化。第3个月、8个月时取腰椎间盘，进行组织检查，评定椎间盘退变的病理改变情况。结果 模型建立后，3个月、8个月的X线片显现对照组无明显改变，实验组腰椎后突畸形，椎间隙狭窄，随着时间延长椎体软骨终板钙化更加明显。组织学观察发现，实验组随术后时间延长，髓核由椎间盘内脱出，并伴有椎间盘两侧软骨终板的纤维化即软骨终板发生退变。结论 椎体软骨终板的退变是椎间退变早期的主要表现方式。     

椎间盘及部分椎体切除加钛网植骨钛板内固定术治疗单节段颈椎椎间盘突出伴椎体后缘骨赘

目的 评价颈椎椎间盘及相邻椎体部分切除加钛网植骨钛板内固定术治疗单节段颈椎椎间盘退变突出伴相邻椎体后缘骨赘的疗效. 方法 应用颈椎椎间盘及相邻椎体部分切除加钛网植骨钛板内固定术治疗单节段颈椎椎间盘退变突出伴相邻椎体后缘骨赘22例.取颈椎前路手术切口,术中仅切除突出的椎间盘及相邻椎体的1/3～ 1/2,使脊髓得到彻底的减压.再用填满碎骨的钛网植于骨缺损处加用钛板螺丝钉内固定,固定范围仅限于相邻椎体.术前和术后通过神经功能JOA评分、颈部轴性症状、颈椎动态侧位片和颈椎MRI比较临床疗效. 结果 均获随访,平均15(6 ～24)个月,术后JOA评分优良率86.4％,颈部轴性症状减轻,脊髓功能明显得到恢复.颈椎活动度良好.X线检查见钛网植骨及钛板内固定良好,未见不稳现象.MRI示颈髓压迫解除. 结论 颈椎椎间盘及相邻椎体部分切除加钛网植骨钛板内固定术治疗单节段颈椎椎间盘突出伴相邻椎体骨赘效果显著,可最大限度地保留颈椎节段的活动度.     

Experimental study on mechanism of vertebral osteophyte formation

Objective:The purpose of this experimental study was to explore the mechanism of the vertebral osteophyte formation.Methods:An experimental model of cervical spondylosis in rabbits was established by resection of the cervical supraspinous and interspinous ligaments and detachment of the posterior paravertebral muscles from cervical vertebrae.Because of individual difference,The natural development procedure of the vertebral osteophyte formation could be seen with a microscope by dynamic observation.Results:The cartilage end-plate was divided into a growth cartilage layer and an articular cartilage layer.Vertebrae and discs from the 3-month control group rabbits showed normal structure.The changes of cartilage plates from the 3-monthe experimental group and the 8-month control group animals showed proliferation in peripheral articular cartilage.The osteophytes from the 8-monthe experimental group animals could be seen.The osteophyte obviously arised from proliferation,calcification and ossification of the peripheral articular cartilage.Conclusions: The vertebral osteophyte arises from proliferation of peripheral articular cartilage which undergoes cartilaginous osteophyte,and then changes into bony osteophyte through an endochondrqal calcification and ossification.     

MRI evaluation of spontaneous intervertebral disc degeneration in the alpaca cervical spine

Animal models have historically provided an appropriate benchmark for understanding human pathology, treatment, and healing, but few animals are known to naturally develop intervertebral disc degeneration. The study of degenerative disc disease and its treatment would greatly benefit from a more comprehensive, and comparable animal model. Alpacas have recently been presented as a potential large animal model of intervertebral disc degeneration due to similarities in spinal posture, disc size, biomechanical flexibility, and natural disc pathology. This research further investigated alpacas by determining the prevalence of intervertebral disc degeneration among an aging alpaca population. Twenty healthy female alpacas comprised two age subgroups (5 young: 2–6 years; and 15 older: 10+ years) and were rated according to the Pfirrmann‐grade for degeneration of the cervical intervertebral discs. Incidence rates of degeneration showed strong correlations with age and spinal level: younger alpacas were nearly immune to developing disc degeneration, and in older animals, disc degeneration had an increased incidence rate and severity at lower cervical levels. Advanced disc degeneration was present in at least one of the cervical intervertebral discs of 47% of the older alpacas, and it was most common at the two lowest cervical intervertebral discs. The prevalence of intervertebral disc degeneration encourages further investigation and application of the lower cervical spine of alpacas and similar camelids as a large animal model of intervertebral disc degeneration. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:1776–1783, 2015.     

椎间盘退变与终板内微血管形态改变的相关性研究

目的:通过观测大白兔椎间盘退变过程中椎间盘终板内的血管形态以及血流量的改变,探讨终板内微血管的改变与椎间盘退变之间的相关性。方法:选用40只新西兰大白兔随机分为2组,通过切除造模组20只免腰椎棘间、棘上韧带及棘突、关节突,造成力学失稳状态诱导形成椎间盘退变模型。分别在术后4、8个月通过扫描电镜、血流激光多普勒仪测定椎体终板内的血管形态以及血流量。结果:在椎间盘退变过程中,椎间盘终板内的血管芽形态逐渐被破坏,微血管数量相应减少,终板内的血流量也明显减少,同时终板内血流量中心部位(靠近髓核区域)血流量多于终板内周围区域的血流量。结论:椎体终板内微血管的改变可能是椎间盘退变的促进因素。     

终板下椎体缺血诱导兔椎间盘退行性变模型的建立及终板中内皮素1的表达

目的通过终板下注射无水乙醇阻碍椎体-终板营养,建立一种新型兔腰椎椎间盘退行性变模型,并观察终板退行性变过程中内皮素1(ET-1)的表达情况。方法健康4月龄新西兰兔32只,随机分成4组,每组8只,选取L5,6椎体(对应L4/L5及L5/L6椎间盘)注射300μL无水乙醇,选取L4椎体(对应L3/L4椎间盘)注射磷酸盐缓冲液(PBS)作为实验对照,L7椎体(对应L6/L7椎间盘)未注入任何物质作为正常对照。其中1组造模后1个月提取软骨终板细胞,行免疫细胞化学染色检测ET-1表达;余3组分别于造模后1、3和5个月进行椎间盘X线和MRI检查,取椎间盘组织行HE染色观察形态学改变,免疫组织化学染色观察ET-1表达。结果注射无水乙醇后,随着时间进展,X线片显示椎间隙高度显著下降、椎间隙变窄、边缘骨赘增生,MRI T2WI显示椎间盘低信号;苏木精-伊红染色(HE)显示终板的生长板厚度变薄,终板结构破损,同时软骨终板细胞退化、直至消失,髓核中细胞发生转化(由空泡细胞转变为软骨样细胞,进而形成纤维软骨样细胞)造成髓核纤维化,纤维环结构排列紊乱、纤维化程度逐步加重;免疫组织化学染色显示,发生退行性变的终板组织内有ET-1表达,但随着退行性变加剧,ET-1表达强度下降;提取的退行性变软骨终板细胞(造模后1个月)也显示细胞质内ET-1强表达。结论通过注射无水乙醇阻碍椎体-终板营养途径可成功建立兔椎间盘退行性变模型,终板退行性变过程中伴随ET-1的表达。     

腰椎经皮内镜双侧椎间孔一次成形的有限元分析

目的采用有限元分析法分析腰椎经皮内镜双侧椎间孔一次成形对腰椎生物力学的影响。方法选取1例健康成年男性志愿者,通过腰椎CT三维重建检查获取腰椎CT数据,通过Solidworks 15.0软件建立椎间盘及关节软骨模型,建立正常L4,5椎体三维有限元模型(A模型)。模拟双侧椎间孔入路经皮内镜腰椎间盘切除术过程,在A模型的基础上通过软件上圆柱体切割工具模拟环锯作用,切除上关节突部分骨质行椎间孔扩大成形术,建立双侧椎间孔一次成形模型(B模型)。比较两种模型在左旋、右旋、左屈、右屈、前屈、后伸等运动状态下的最大位移变化和椎间盘受力情况。结果与A模型相比,在前屈、后伸、左屈、右屈、左旋、右旋运动状态下,B模型的最大位移和椎间盘受力均增大。侧屈、旋转取左侧和右侧平均值时,B模型最大位移变化为前屈>侧屈>旋转>后伸;椎间盘受力变化为侧屈>前屈>旋转>后伸。结论通过建立有效的腰椎经皮内镜双侧椎间孔一次成形的有限元模型,发现在6种运动过程下,L4,5节段的运动幅度均增大,椎间盘的应力均增加,推测双侧关节突损伤可造成脊柱的活动范围增大,加重脊柱不稳的趋势,增加腰椎椎间盘退变的风险。     

Contribution of disc degeneration to osteophyte formation in the cervical spine: a biomechanical investigation.

Cervical spine disorders such as spondylotic radiculopathy and myelopathy are often related to osteophyte formation. Bone remodeling experimental-analytical studies have correlated biomechanical responses such as stress and strain energy density to the formation of bony outgrowth. Using these responses of the spinal components, the present study was conducted to investigate the basis for the occurrence of disc-related pathological conditions. An anatomically accurate and validated intact finite element model of the C4-C5-C6 cervical spine was used to simulate progressive disc degeneration at the C5-C6 level. Slight degeneration included an alteration of material properties of the nucleus pulposus representing the dehydration process. Moderate degeneration included an alteration of fiber content and material properties of the anulus fibrosus representing the disintegrated nature of the anulus in addition to dehydrated nucleus. Severe degeneration included decrease in the intervertebral disc height with dehydrated nucleus and disintegrated anulus. The intact and three degenerated models were exercised under compression, and the overall force-displacement response, local segmental stiffness, anulus fiber strain, disc bulge, anulus stress, load shared by the disc and facet joints, pressure in the disc, facet and uncovertebral joints, and strain energy density and stress in the vertebral cortex were determined. The overall stiffness (C4-C6) increased with the severity of degeneration. The segmental stiffness at the degenerated level (C5-C6) increased with the severity of degeneration. Intervertebral disc bulge and anulus stress and strain decreased at the degenerated level. The strain energy density and stress in vertebral cortex increased adjacent to the degenerated disc. Specifically, the anterior region of the cortex responded with a higher increase in these responses. The increased strain energy density and stress in the vertebral cortex over time may induce the remodeling process according to Wolff's law, leading to the formation of osteophytes.