兔椎体软骨终板血管芽增龄性变化

目的 探讨不同年龄段兔椎体软骨终板内血管芽的形态变化与椎间盘退变的关系.方法 15只不同年龄段新西兰兔,2月龄5只,1年龄5只,3年龄5只,雌雄不限.X线观察终板有无钙化及椎体周围有无骨赘形成,组织学观察软骨终板和椎间盘的形态学变化,血管铸型后扫描电镜观察终板各部位血管的形态变化.按Miyamoto等分级标准将椎间盘分为1～5级,分别规定为1～5分.采用t检验,分别对2月龄组和1年龄组髓核区与内层纤维环区,2月龄组及1年龄组兔髓核区、内层纤维环区椎体终板内血管直径进行比较.结果 2月龄组终板无明显钙化、软骨终板结构良好、潮标清晰,髓核及纤维环结构饱满清晰;1年龄组终板轻度钙化,髓核皱缩,纤维环出现裂隙;3年龄组终板钙化明显,密度增高,并可见骨赘形成,髓核消失.随着年龄增加,终板内微血管逐渐减少,最终消失,软骨终板中心部位较周围部血管减少更为明显.组织学显示软骨终板出现钙化,软骨终板退变重于椎间盘;钙化的程度与椎间盘退变程度呈正相关.2月龄组髓核区与内层纤维环区椎体终板内血管直径比较,差异有统计学意义;2月龄组与1年龄组髓核区椎体终板内血管直径比较,差异有统计学意义.结论 随着兔年龄增加终板内血管逐渐减少,终板发生退变,其程度重于椎间盘,提示椎体终板内微血管的变化可能是椎间盘退变的重要促进因素.

Abstract：

Objective To observe the morphologic changes of of vascular buds in vertebral cartilage endplate in age-specific rabbits and also to investigate the correlation between the changes of vascular buds and interverbral disc degeneration. Methods There were 15 New Zealand white rabbits in our study,which include three groups, 2-week-old rabbits, 1-year-old rabbits and 3-year-old rabbits, and each groups had five rabbits. The X-ray radiograph, histology and scanning electron microscope were used to observe the changes of vertebral cartilage endplate. According to Miyamoto standard, the interverbral disc was graded 1-5, and scored 1-5 respectively. Results The changes of micro-vascular structure of vertebral cartilage endplate were observed during aging. Under the scanning electron microscope, the vascular structure degenerated gradually, and disappeared in the end. The blood vessels in the central region of the vertebral cartilage endplate reduced more obviously than those in periphery region. The severe degeneration was found in vertebral endplate, compared with intervertebral disc. The changes of vascular buds in rabbits vertebral cartilage endplate had positive correlation with the vertebral endplate calcification and the interbertebral disc degeneration. Conclusion Changes of vascular buds in vertebral endplate may accelerate intervertebral disc degeneration.     

Localization of cathepsins D, K, and L in degenerated human intervertebral discs.

STUDY DESIGN: Localization of cathepsins D, K, and L in degenerated intervertebral discs was examined by immunohistochemistry. OBJECTIVES: To determine the involvement of cathepsins in the pathomechanism of intervertebral disc degeneration by monitoring the immunolocalization of cathepsins in degenerated intervertebral disc tissue. SUMMARY OF BACKGROUND DATA: Cathepsins D, K, and L are enzymes that contribute to the matrix destruction seen in the articular cartilage affected by osteoarthritis and rheumatoid arthritis. However, little is known about the contribution of these cathepsins to intervertebral disc degeneration. METHODS: Paraffin-embedded sections of degenerated intervertebral disc tissue collected at the time of surgery (13 discs from 12 patients) were immunohistochemically stained with antibodies for cathepsins D, K, and L. For further characterization of the stained cells, immunohistochemical detection of CD68 and TRAP staining were performed. RESULTS: Hematoxylin and eosin staining revealed obvious signs of degeneration in all sections. Cathepsins D and L were immunolocalized in disc fibrochondrocytes at various sites exhibiting degeneration. Cathepsins K were found in tartrate-resistant acid phosphatase-positive multinucleated cells, in particular near the cleft within the cartilaginous endplate. However, few cells were positive for these cathepsins in anulus fibrosus that maintained the lamellar structure of collagen fibers. CONCLUSIONS: Marked expression of cathepsins D and L was observed at the site of degeneration. Cathepsins D and K localized in tartrate-resistant acid phosphatase-positive multinucleated cells existed at the cleft between the cartilaginous endplate and vertebral body. The site-specific localization of these cathepsins suggests the association of these proteinases with endplate separation and disorganization of the anulus fibrosus in degenerative spinal disorders.     

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。     

低温等离子体射频消融术应用于椎间松解的组织学观察

目的评价低温等离子体射频消融术应用在椎间松解及其自然转归的组织学变化。方法将12只2.0~2.5月龄的健康雌性山羊随机分为低温等离子体消融组(消融组,n=6)和传统胸椎椎间盘切除组(传统组,n=6)。每只动物均处理中段6个胸椎椎间盘(T_5/T_6/T_7/T_8/T_9/T_(10)/T_(11)),光镜下分别比较2种术式术后即刻和术后12周自然转归的组织学变化。结果消融组术后即刻椎间盘组织(纤维环,髓核和软骨终板)基本被去除,仅在软骨终板和骨性终板交界处残留一薄层软骨终板,表面光整,厚度均匀,周围组织细胞形态基本正常。传统组术后即刻纤维环、软骨终板有不同程度的剩余,骨性终板无明显破坏,松解面凹凸不平,刀痕周围的组织细胞形态正常。消融组术后12周显微镜下见椎间残留有部分薄层软骨终板已被不同程度的钙化,椎间前后缘融合稍差;椎间中部被大量成纤维细胞连接,软骨细胞增生更加明显,椎体骨小梁和终板下骨小梁之间无明确的界限,潮标前移变薄。传统术后12周显微镜下见软骨终板大部分消失,仅在近椎体后缘残留;终板下骨小梁排列不规则,上下终板下骨小梁之间未呈连续性生长,而是被大量由软骨细胞和成纤维细胞组成的组织连接,其中可见新生的毛细血管,上下潮标不对称并前移。结论采用低温等离子体消融术行椎间准备可以较好地去除软骨终板,处理后的终板面较传统组光整,且对周围健康组织影响小,和传统组都能获得早期的椎间融合倾向。     

Association and histological characteristics of endplate injury and intervertebral disc degeneration in a rat model

IntroductionThe purpose of this study was to construct a rat caudal vertebral body fracture model and to analyze the association and histological characteristics of vertebral body fracture with endplate injury and adjacent intervertebral disc degeneration.Materials and methodsThis study included 144 clean-grade male Sprague-Dawley rats, which were randomly divided into a control, middle vertebral body injury (MI), and endplate injury (EI) groups. A vertebral body fracture with or without endplate injury was developed by either drilling a hole in the middle of a rat caudal vertebral body to create a fracture with an intact endplate or drilling a hole in the vertebral body near the intervertebral disc to create a vertebral body fracture with endplate injury. The histological differences in the adjacent intervertebral discs of vertebral body fractures with or without endplate injury were detected using imaging, non-specific histological staining, immunohistochemistry and TUNEL assay.ResultsImaging results revealed that the EI group showed a significant decrease in intervertebral space height and intervertebral disc T2 signal over time. Non-specific histological staining revealed that in the EI group, the intervertebral disc was degenerative. Immunohistochemistry indicated that Aggrecan and Collagen-II were decreased and inflammatory factors were increased in the EI group. The TUNEL detection found that apoptosis was significantly increased in the EI group as compared with the MI and control groups.ConclusionIn rat caudal vertebral body fractures, a fracture with endplate injury is more likely to induce or accelerate degeneration of adjacent intervertebral discs.     

Analysis of the effect of lumbar spine fusion on the superior adjacent intervertebral disk in the presence of disk degeneration, using the three-dimensional finite element method

The purpose of this study was to analyze the effect of lumbar spine fusion on the superior adjacent intervertebral disk in the context of disk degeneration, using a nonlinear three-dimensional finite element method. Detailed L3-L5 motion segment models of normal and degenerated intervertebral disks were developed. In fusion models, L4-L5 was fixed by either posterolateral fusion or posterior lumbar interbody fusion (PLIF). Various loading conditions such as compression loading, compression loading plus flexion moment loading, or compression loading plus extension moment loading were applied to study the corresponding stress. Tresca stress on the posterolateral part of intervertebral annulus fiber and von Mises stress on the vertebral endplate (the superior and inferior sides of L3 and L4) were reduced in all degenerated disk models compared with the normal disk models. The PLIF model showed an increase in the percentage change of stress on the vertebral endplate and on the intervertebral annulus fibrosus when flexion and extension moment loadings were applied. This finding suggests that surgeons should consider the risk of exacerbating degeneration of intervertebral disks by undertaking lumbar spine fusion, when degeneration is found in intervertebral disks adjacent to vertebrae requiring fusion.     

颈椎终板软骨细胞凋亡的检测及相关意义

目的检测颈椎终板软骨细胞的细胞凋亡指数,探讨其在椎间盘退变中可能的作用机制。方法颈椎间盘终板及髓核取自我院行颈椎前路手术的35例颈椎椎间盘退变患者（退变组）和19例颈椎外伤患者（外伤组）。光镜观察退变组和外伤组终板和髓核的细胞密度,TUNEL法检测两组终板软骨细胞和髓核细胞的细胞凋亡指数,咔唑分光光度法比较两组髓核蛋白多糖含量。结果退变组终板细胞密度较外伤组减少（P〈0.05）,TUNEL染色显示退变组终板细胞凋亡指数为（34.6±16.1）%,外伤组为（20.1±9.3）%,两组间比较差异有统计学意义（P〈0.05）。Pearson相关分析显示,颈椎终板TUNEL染色阳性细胞率与终板细胞密度、髓核蛋白多糖含量之间呈负相关（r=—0.805,P=0.001;r=—0.677,P=0.023）,与髓核TUNEL阳性细胞率之间呈正相关（r=0.758,P=0.003）。结论颈椎退变终板软骨细胞凋亡率较高,推测在椎间盘退变过程中可能发挥重要作用;软骨细胞凋亡可能与髓核细胞凋亡增加、终板细胞密度与髓核蛋白多糖含量降低密切相关。     

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。     

An immunohistochemical evaluation of extracellular matrix components in the spinal posterior longitudinal ligament and intervertebral disc of the tiptoe walking mouse

Ossification of the posterior longitudinal ligament (OPLL) in the spine is caused by systemic and/or regional factors affecting the regulation of osteocartilaginous formation and maintenance. The aims of this study were to elucidate the relationship between the degeneration of the intervertebral discs and changes in the posterior longitudinal ligament (PLL) in the tiptoe walking (ttw) mouse, an animal model of OPLL, and to analyze the sequential changes of the cells producing extracellular matrix components using immunohistochemical methods. At 6 weeks of age, the discs degenerated and the chondrocytes in the nucleus pulposus were positive for chondroitin-6-sulfate in the ttw mice. The fibroblasts in the PLL at the disc level were positively stained with type II and XI collagens. At 14 weeks, the discs herniated into the thickened PLL, and chondrocyte-like cells appeared in the PLL at vertebral endplate level. At 18 and 22 weeks, the number of chondrocyte-like cells increased in the PLL and expressed type I collagen. A potent regional factor causing OPLL in the ttw mice appears to be the initial degeneration and subsequent herniation of the nucleus pulposus. These sequential changes in the ttw mice were accelerated by administration of etidronate. It was suggested that etidronate stimulated the cartilaginous hyperplasia in the PLL of the ttw mice. It appeared as if the PLL transformed itself into cartilaginous tissue to repair the degeneration of the intervertebral disc.     

The relationship of degeneration of the intervertebral disc to mechanical loading conditions on lumbar vertebrae

Degeneration of lumbar intervertebral discs is typical for the aging process and contributes to common low-back problems. It is likely to influence vertebrae by changing the mechanical interaction within each motion segment. This study focuses on the influence of disc degeneration on the mechanism of load transmission through the lumbar vertebral body. Effective stresses, ways of load transmission and failure modes of vertebral body were examined in cases of healthy and degenerated discs. The stress analysis was performed using the Finite Element Method. For healthy discs, the highest effective stresses were found in the center of bony end-plates. For degenerated discs, they were found in the lateral aspects of the end-plates, in the cortical wall, and also in the vertebral body rims. However, regardless of the disc condition, the highest effective stresses do not occupy the whole thickness of the endplate and/or the cortical wall, but are concentrated near the spongy core. Ways of load transmission through the lumbar vertebral body and modes of eventual damage to it are also strongly influenced by the disc condition.     

退变椎体周边关节软骨产生碱性磷酸酶与骨赘形成的关系

目的：研究椎体骨赘形成的机理。方法：通过切除免颈棘上韧带及棘间和分离颈椎后旁两侧肌肉引起动物颈椎力学上的失衡,经３个月的时间的发展而造成免颈椎间盘退变模型。用生物化学方法分别测定每个动物颈椎间盘纤维环和髓核、椎体关系软骨、周边关节软碱性磷酸酶性结果：颈椎间盘退变动物椎体周边关节软骨中碱性磷酸酶活性明显升高。结论：研究结果在生物化学上支持椎体骨赘来自于周边关节软骨增殖、化生、钙化和骨化的组织学观察。     

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.     

椎体终板损伤对兔椎问盘髓核Ⅰ、Ⅱ型胶原的影响

目的 观察椎体终板损伤对兔椎间盘髓核Ⅰ、Ⅱ型胶原的影响并探讨其机制.方法 4个月龄清洁级日本大白兔12只,完整取出40个包含终板的完整椎间盘(L2-L5),随机分为实验组和对照组,每组20个.实验组参考Daniel Haschtmann的方法建立终板损伤模型.椎间盘整体培养2周后,免疫组织化学方法观察椎间盘髓核中Ⅰ、Ⅱ型胶原的表达情况,并用HMIAS-2000图像分析系统进行半定量分析.结果 免疫组织化学染色显示:实验组椎间盘髓核Ⅰ型胶原的表达比对照组高;而Ⅱ型胶原的表达则比对照组低,差异均有统计学意义(P<0.05).结论 外伤致椎体终板损伤后会导致椎间盘髓核Ⅰ、Ⅱ型胶原的变化,继而加速椎间盘退行性变.     

Effect of endplate reduction on endplate healing morphology and intervertebral disc degeneration in patients with thoracolumbar vertebral fracture

Objective

To determine the effect of endplate reduction on the final healing morphology and degenerative changes in intervertebral discs.

Methods

Forty-eight patients with single-level thoracolumbar fractures with endplate injury were included. All patients underwent posterior reduction and pedicle screw fixation, and postoperative imaging was used to determine whether endplate reduction was successful. The healing morphology of the endplate was divided into three types: increased endplate curvature, irregular healing and traumatic Schmorl node. MRI was performed at baseline and at the last follow-up evaluation to observe changes in disc degeneration (disc height and nucleus pulposus signal) and Modic changes.

Results

The reduction rate in the central area was significantly lower than that in the peripheral area (P = 0.017). In patients with successful reduction, 90.9% (20/22) of the endplates healed with increased curvature. In patients with an unsuccessful endplate reduction, 63.4% (26/41) of the endplates healed irregularly, and 34.1% (14/41) of the endplates formed traumatic Schmorl nodes. Endplate reduction was closely related to the final healing morphology of the endplate (P < 0.001), which had a significant protective effect on the degeneration of the intervertebral disc. At the last follow-up evaluation, there was no statistically significant correlation between different endplate healing morphologies and new Modic changes.

Conclusions

The reduction rate in the central area is significantly lower than that in the peripheral area. Although all of the intervertebral discs corresponding to fractured endplates had degenerated to different degrees, successful endplate fracture reduction can obviously delay the degeneration of intervertebral discs.

     

Development of a rat model with lumbar vertebral endplate lesion

Purpose

Vertebral endplate lesion (EPL) caused by severe disc degeneration is associated with low back pain. However, there is no suitable animal model to elucidate the pathophysiology of EPL. This study aimed to develop a rat model of EPL and evaluate rat behavior and imaging and histological findings.

Methods

The L4-5 intervertebral discs of Sprague–Dawley rats were transperitoneally removed, except for the outer annulus fibrosus and cartilage endplate, in the EPL group. The L4-5 discs were not removed and simply exposed in the sham group. Changes around the vertebral endplate on magnetic resonance imaging (MRI) and computed tomography (CT) were evaluated. Additionally, pain-related behavioral and histological assessments were performed.

Results

In the EPL group, a low-signal area around the vertebral endplate was observed on T1-weighted and T2-weighted fat-saturated MRI at 8 weeks or later after surgery. In the same group, CT showed osteosclerosis around the vertebral endplate at 12 weeks after surgery. The sham group did not show abnormal imaging features on the MRI and CT. Behavioral evaluation showed that the EPL group had a significantly longer grooming time than the sham group. Conversely, the 12-week postoperative locomotion time and the 1- and 12-week postoperative standing times were significantly shorter in the EPL group than in the sham group. Histological evaluation showed a high degree of vertebral endplate degeneration and an increased number of osteoclasts and proportion of nerve fibers expressing calcitonin gene-related peptide in the EPL group compared to those in the sham group.

Conclusion

Our rat EPL model showed pain-related behavioral patterns and an increased expression of pain-related neuropeptide. This model could contribute to the study of the pathophysiology of EPL and will help in the treatment of low back pain in the future.

     

大鼠不同部位软骨细胞的形态及表型特征比较研究

目的:比较研究大鼠椎间盘软骨终板和膝关节软骨的细胞表型特征的相关性.方法:大鼠的软骨终板和关节软骨细胞分别予以消化培养.进行光镜、电镜观察其形态.使用免疫组化技术分别检测不同部位细胞的Ⅱ型胶原表达.结果:大鼠椎间盘软骨终板和关节软骨细胞形状相似,并且均表达Ⅱ型胶原.结论:本研究提示软骨终板表达软骨细胞的特征性胶原,与关节软骨细胞相似.     

Regional variations in the compressive properties of lumbar vertebral trabeculae. Effects of disc degeneration

The compressive mechanical properties of human lumbar vertebral trabeculae were examined on the basis of anatomic origin, bone density, and intervertebral disc properties. Trabecular bone compressive strength and stiffness increased with increasing bone density, the latter proportional to strength and stiffness to the one-half power. Regional variations within each segment were found, the most prevalent differences occurring in regions of bone overlying the disc nucleus in comparison with bone overlying the disc anulus. For normal discs, the ratio of strength of bone overlying the disc nucleus to bone overlying the disc anulus was 1.25, decreasing to 1.0 for moderately degenerated discs. These results suggest that an interdependency of trabecular bone properties and intervertebral disc properties may exist.     

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”。     

Age changes in lumbar vertebrae and intervertebral discs

Reduction of stature in old age has been attributed to loss of disc height. A measurement study of 204 cadaveric lumbar spines from subjects ranging in age from one day to 97 years confirmed data on loss of "spinal stature" but could not confirm a loss of disc height. With aging, there is a progressive increase in vertebral end-plate concavity, associated with decreased bone density. These changes are more evident and take place earlier in females than in males. In the cancellous bone of vertebral bodies, a decrease in the number of horizontal trabecular "cross braces" leads to fracture of the vertical weight-bearing "beams" supporting the vertebral endplate. The intervertebral discs expand centrally and become increasingly convex. Measurements of average disc height demonstrate that loss of disc height is unusual in a normal, aging population. Only a minority of lower lumbar discs from elderly subjects show "thinning" and degeneration (beyond Rolander's Grade 2). Thus, loss of stature in the elderly is attributable to loss in vertebral height rather than loss in disc height. Dessication and thinning of discs, or discs that "bulge like underinflated automobile tires" are not typical of elderly spines.     

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