颈椎终板生物力学与终板形态学及椎间盘退变的关系

颈椎终板解剖学及生物力学特点在脊柱外科融合治疗中扮演极其重要角色.终板几何形态、大小以及厚度、骨密度均与终板受力情况密切相关,特别是后两者在一定程度上与终板力学分布呈正相关.随着终板受力情况改变,终板形态也随之发生适应性改变.解剖形态异常和受力异常可导致终板及椎间盘退变,退变反过来导致终板解剖形态及力学特性进一步改变.临床上对退变性颈椎病进行手术治疗时需要妥善处理终板,平衡好力学支持与血管长入椎间融合器之间的关系.植入物设计的理想状态应该是与终板表面契合,避免点状受力,以降低术后融合器沉降,最终达到骨性愈合.     

颈椎椎间盘退变对终板结构生物力学特性的影响

目的研究颈椎椎间盘对终板结构生物力学特性的影响。方法50节颈椎标本,采用Nachemson椎间盘分级标准将标本分为4组,正常组(n=22)、Ⅰ度退变组(n=10)、Ⅱ度退变组(n=9)、Ⅲ度退变组(n=9),对每一终板平面上20个特定的测试点进行压缩实验,直径2mm的半球形压头以003mm/s的速度垂直于终板平面下压2mm,由所得的力─位移曲线计算出最大压缩力及刚度,采用单因素方差分析、析因分析、SNK检验及相关分析对实验数据进行统计学分析。结果颈椎椎间盘退变可导致颈椎终板最大压缩力及刚度的显著性减小(P<001),且存在负相关关系(分别为rs=-0429,P<0001;rs=-0244,P<0001);上终板随着椎间盘退变的加重终板平面中央承力逐渐变弱,外周承力逐渐增强,下终板的力学分布无明显改变。结论颈椎椎间盘退变是影响终板结构生物力学特性的重要因素,在进行颈椎前路融合术时应警惕由于椎间盘退变引起的“植入物沉陷”。     

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。     

椎间盘软骨终板退变的研究进展

椎间盘的退变与多种因素相关,其中软骨终板作为椎间盘的组成部分,通过其渗透作用为椎间盘提供大部分营养,在维持椎间盘正常功能方面发挥重要作用。软骨终板退变作为椎间盘退变的始动因素近来受到广泛关注。软骨终板退变的具体机制尚不明确,但现有研究表明其退变与年龄、异常应力、局部炎症因子、软骨细胞凋亡、软骨基质退变等因素相关,深入研究各因素在终板退变过程中的具体作用机制将为治疗椎间盘退变性疾病提供新的方法,现对软骨终板退变的主要因素做如下综述。     

颈椎前融合对颈椎退变的影响

本文探讨颈椎等合术退变加重的根本原因,以提高颈椎病患者的手相治疗效果。     

椎体终板与椎间盘退变

椎间盘退变是导致下腰痛的常见原因,与之密切相关的椎体终板退变也逐渐受到重视.MRI的T1和T2加权像上,退变的椎体终板表现为终板与终板下骨相对于正常终板的信号改变,且与对应的椎间盘退变有较高的相关性.经椎体终板的弥散是椎间盘获得营养的主要途径,同时椎体终板又是脊柱运动单位中最容易受损伤的部位,轴向负荷可导致软骨终板、骨性终板及终板下骨小梁弯曲变形,软骨终板与骨性终板分离.这一系列的终板损伤和软骨终板钙化和骨化会妨碍椎间盘营养供应,导致椎间盘组织学退变.新近研究进一步表明椎体终板与椎间盘退变不仅在组织学上密切相关,而且在力学上也密不可分,椎板形状如曲率也与椎间盘退变和突出存在一定的关联.     

颈椎前融合对颈椎退变的影响

本文探讨颈椎融合术导致颈椎退变加重的根本原因,以提高颈椎病患者的手术治疗效果。对实施颈椎融合术的76例颈椎间盘突出症患者和64例颈椎骨折脱位患者进行回顾性对比分析,归纳出影响颈椎融合术治疗效果的根本原因。结果显示:76例颈椎间盘突出症患者术后有33例发生颈椎退变明显加重,其中4例再次发生颈椎间盘突出症;64例颈椎骨折脱位患者术后有8例出现颈椎退变加重。作者认为:融合术前,融合节段上下端颈椎已有的退变是导致术后退变加重的根本原因,手术治疗时应给予特别的关注。     

尼莫地平对退变腰椎间盘软骨终板血供的影响

目的 探讨尼莫地平对退变腰椎间盘动物模型软骨终板血供的影响.方法 选用中国白兔24只.随机分为对照组和尼莫地平组.每组12只.两组均采取前路手术损伤纤维环,尼莫地平组于术后10天给予尼莫地平针剂(1.0mg/kg·d)腹腔注射,持续2周.术后4、8、12周,每组随机抽取4只实验兔行MRI及病理学检查.结果 MRI检查显示,与对照组相比,尼莫地平组术后4周、8周、12周腰椎生理前凸曲度轻微变直.椎间隙高度略微下降,脑脊液白线在椎间盘部位出现轻度压迹,硬膜囊轻度受压;病理学检查显示,尼莫地平组髓核无变性及纤维化,血管数明显增多,软骨终板出现点状钙化灶,且以术后12周最为明显.结论 尼莫地平可改善软骨终板血供,从而延缓椎间盘退变.     

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只兔腰椎棘间、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。     

Disc degeneration in the cervical spine

One hundred and twenty-eight cervical discs obtained from 30 autopsied subjects were examined morphologically. The cervical degenerative process was divided into five stages: (i) The initial stage—characterized by the disappearance and calcification of cells of the cartilagenous plate; (ii) the early stage—characterized by vessel invasion and formation of a calcification front; (iii) the progressive stage—characterized by progressive degenerative changes in all disc components; (iv) the late stage—characterized by destruction of the cartilagenous plates; and (v) the terminal stage—c characterized by eburnation of the bony end-plate. The cervical spine has three main differences from other regions of the spine: a large range of motion, the capacity for frequent and rapid movements, and the presence of Luschka's joint. Each of these three features is related to cervical disc degeneration. A preliminary report of this paper was presented at the 2nd Annual Orthopaedic Research Meeting of the Japanese Orthopaedic Association (Kyoto, Japan, September, 1987) and at the 22nd Annual Meeting of the Japan Spine Research Society (Toyama, Japan, June, 1993).     

颈椎间盘退变对颈椎生物力学影响的有限元研究

目的建立人体颈椎C4-C5-C6节段颈椎间盘退变三维有限元模型,分析椎间盘退变对颈椎运动节段生物力学的影响。方法通过改变椎间盘材料特性和高度等参数,建立椎间盘轻度退变模型(LD)、中度退变模型(MD)和重度退变模型(SD)。在45 N垂直载荷下,分别对正常、轻、中、重度4种有限元模型进行生物力学测试,比较4种模型之间各项生物力学参数的差异。结果建立了C4-C5-C6节段颈椎间盘逐级退变三维有限元模型。45 N垂直载荷条件下,正常模型(ND)、MD、SD椎间盘轴向位移及向外膨出位移逐渐变小,LD椎间盘轴向位移及膨出位移比ND增大,四组模型纤维环轴向压缩应力逐渐增大,髓核内压力逐渐减小。ND、MD、SD关节突关节接触力逐渐减小,LD关节突关节接触力较ND轻度增大。结论椎间盘轻度退变时,颈椎稳定性下降。中、重度退变时,颈椎稳定性重新获得。从生物力学方面证明退变的椎间盘对维持颈椎的稳定性有一定的代偿作用。     

Anterior cervical interbody constructs: effect of a repetitive compressive force on the endplate

Graft subsidence following anterior cervical reconstruction can result in the loss of sagittal balance and recurring foraminal stenosis. This study examined the implant–endplate interface using a cyclic fatigue loading protocol in an attempt to model the subsidence seen in vivo. The superior endplate from 30 cervical vertebrae (C3 to T1) were harvested and biomechanically tested in axial compression with one of three implants: Fibular allograft; titanium mesh cage packed with cancellous chips; and trabecular metal. Each construct was cyclically loaded from 50 to 250 N for 10,000 cycles. Nondestructive cyclic loading of the cervical endplate–implant construct resulted in a stiffer construct independent of the type of the interbody implant tested. The trabecular metal construct demonstrated significantly more axial stability and significantly less subsidence in comparison to the titanium mesh construct. Although the allograft construct resulted in more subsidence than the trabecular metal construct, the difference was not significant and no difference was found when comparing axial stability. For all constructs, the majority of the subsidence during the cyclic testing occurred during the first 500 cycles and was followed by a more gradual settling in the remaining 9,500 cycles. © 2011 Orthopaedic Research Society. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 30:587–592, 2012     

Influence of biochemical composition on endplate cartilage tensile properties in the human lumbar spine

Endplate cartilage integrity is critical to spine health and is presumably impaired by deterioration in biochemical composition. Yet, quantitative relationships between endplate biochemical composition and biomechanical properties are unavailable. Using endplate cartilage harvested from human lumbar spines (six donors, ages 51–67 years) we showed that endplate biochemical composition has a significant influence on its equilibrium tensile properties and that the presence of endplate damage associates with a diminished composition–function relationship. We found that the equilibrium tensile modulus (5.9 ± 5.7 MPa) correlated significantly with collagen content (559 ± 147 µg/mg dry weight, r² = 0.35) and with the collagen/GAG ratio (6.0 ± 2.1, r² = 0.58). Accounting for the damage status of the adjacent cartilage improved the latter correlation (r² = 0.77) and indicated that samples with adjacent damage such as fissures and avulsions had a diminished modulus–collagen/GAG relationship (p = 0.02). Quasi‐linear viscoelastic relaxation properties (C, τ₁, and τ₂) did not correlate with biochemical composition. We conclude that reduced matrix quantity decreases the equilibrium tensile modulus of human endplate cartilage and that characteristics of biochemical composition that are independent of matrix quantity, that is, characteristics related to matrix quality, may also be important. © 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:245–252, 2014.     

颈椎终板抗压强度分布规律的生物力学研究

[目的]研究颈椎终板不同位点抗压强度及其分布规律。[方法]选用5具成年男性新鲜颈椎标本(C3～7),共25个椎体50个终板。对终板平面49个测试点用直径1.5 mm的平底压头以12 mm/min的速度进行连续压缩加载试验,获得最大压缩力,进行统计分析。[结果](1)抗压强度自C3～7逐渐减小(P﹤0.05);(2)下终板抗压强度大于上终板(P=0.000);(3)椎间隙相邻面上一椎体下终板的抗压强度大于下一椎体上终板抗压强度(P<0.05);(4)随着压力点逐渐外移,抗压强度逐渐增大(P﹤0.05);(5)处于不同角度的压力点,其抗压强度存在差异(P=0.029);(6)终板后部强于前部(P=0.003)。上终板后部抗压强度大于前部(P=0.000)。[结论]颈椎终板抗压强度自C3～7逐渐减小,下终板强于上终板,外周大于中央,后部强于前部。椎间隙相邻面上一椎体下终板的抗压强度大于下一椎体上终板抗压强度。     

腰椎终板、椎间盘退变及椎间盘造影疼痛激发试验的相关性研究

目的探讨下腰痛患者腰椎终板Modic退变、椎间盘退变及CT引导下腰椎间盘造影疼痛激发试验的相关性.方法对45例下腰痛患者常规行腰椎X线和MR检查,分别按Modic终板退变标准（0～3级）与Pearce椎间盘退变标准（Ⅰ～Ⅴ级）对终板和椎间盘进行评估.在CT引导下对45例患者中的40例（120个椎间盘）进行造影和疼痛激发试验,并按Dallas椎间盘造影分级系统（DDD）测评椎间盘退变程度.采用SPSS 11.5统计学软件分析腰椎终板Modic退变、椎间盘退变与腰椎间盘造影疼痛激发试验之间的相关性.结果40例下腰痛患者的腰椎终板Modic分级与椎间盘退变Pearce分级存在较强的相关性（Pearson x^2=43.326,P=0.000）,与椎间盘造影疼痛激发试验有显著相关性（Pearson x^2=27.858,P=0.000）;椎间盘退变Pearce分级与CT椎间盘造影椎间盘退变Dallas分级也呈较强的相关性.结论腰椎终板Modic退变分级与椎间盘退变Pearce分级密切相关,而与椎间盘疼痛激发试验有显著相关性,提示终板Modic退变可能是下腰痛的原因之一.     

Morphology of the human vertebral endplate

It is presumed that poor intervertebral disc cell nutrition is a contributing factor in degeneration, and is exacerbated by vertebral endplate sclerosis. Yet, quantitative relationships between endplate morphology and degeneration are unavailable. We investigated how endplate bone microstructure relates to indices of disc degeneration, such as morphologic grade, proteoglycan content, and cell density. Intervertebral core samples [n = 96, 14 subjects, L1–L5 level, ages 35–85 (64 ± 16 years), degeneration grade 1 (n = 4), grade 2 (n = 32), grade 3 (n = 44), grade 4 (n = 10), grade 5 (n = 6)] that included subchondral bone, cartilage endplate, and adjacent nucleus were harvested from human cadaveric lumbar spines. The morphology of the vertebral endplate was analyzed using µCT and the adjacent nucleus tissue was collected for biochemical and cellular analyses. Relationships between vertebral endplate morphology and adjacent disc degeneration were analyzed. Contrary to the prevailing notion, vertebral endplate porosity increased between 50% and 130% and trabecular thickness decreased by between 20% and 50% with advancing disc degeneration (p < 0.05). We also observed that nucleus cell density increased (R² = 0.33, p < 0.05) and proteoglycan content decreased (R² = 0.47, p < 0.05) as the endplate became more porous. Our data suggest that endplate sclerosis is not a fundamental factor contributing to disc degeneration. Rather, the opposite was observed in our samples, as the endplate became progressively more porous with age and degeneration. Since ischemic disc cell behavior is commonly associated with degenerative change, this may be related to other factors such as the quality of vertebral capillaries, as opposed to decreased permeability of intervening tissues. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 30:280–287, 2012     

IL-1β、IL-6、TNF-α在兔腰椎软骨终板退变中的变化及作用

[目的]研究IL-1β、IL-6、TNF—α在软骨终板退变中的作用。[方法]新西兰白兔24只随机分为实验组与对照组。实验组通过腰椎失稳而诱导了腰椎软骨终板退变动物模型。分别于术后12、24、36周摄腰椎X线片及扫描电镜观察，检测不同时段软骨终板中IL-1β、IL-6、TNF—α含量。[结果]X线片示实验组较对照组钙化明显；Brad-ner指数示椎间隙高度随时间延长而逐渐降低；扫描电镜示实验组软骨终板随时间延长胶原纤维逐渐变细、排列紊乱、出现裂隙，蛋白多糖丢失加剧，上述变化较对照组显著；实验组IL-1β、IL-6、TNF-α含量较对照组增多（P〈0．05）。[结论]IL-1β、IL-6、TNF-α在软骨终板退变过程中含量相应增加，提示炎性细胞因子可能在软骨终板退变的形成和发展中起重要作用。     

Negative effects of ADAMTS‐7 and ADAMTS‐12 on endplate cartilage differentiation

The roles of ADAMTS‐7 and ADAMTS‐12 in disc degeneration have not been previously examined. The purpose of this study was to examine the expression of ADAMTS‐7 and ADAMTS‐12 in the endplate cells isolated from patients with degenerative disc disease and to see whether they are associated with the pathological change of endplate. Sixty‐four degenerated lumbar endplate specimens were obtained from the patients with degenerative disc disease categorized as type Modic I or II in magnetic resonance imaging (MRI) and 12 nondegenerative specimens as control (vertebra burst fracture patients without degenerative change in MRI) during surgical procedures. The expression of ADAMTS‐7 and ADAMTS‐12 was examined by real‐time PCR and Western blotting. A statistically significant increase in mRNA expression of ADAMTS‐7 and ADAMTS‐12 was observed in the endplate cells in degenerative discs compared with nondegenerative discs. The corresponding protein levels of ADAMTS‐7 and ADAMTS‐12 had the same expression patterns. Moreover, ADAMTS‐7 and ADAMTS‐12 down‐regulated the expression of Col II, Sox9, and Col X the marker genes for chondrogenesis. Our results indicate that ADAMTS‐7 and ADAMTS‐12 appear to be potent negative regulators of endplate cartilage development. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1238–1243, 2012