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。     

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。     

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。     

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.     

兔椎间失稳软骨终板退变的实验研究

[目的]通过电镜研究软骨终板在椎间失稳环境下的退变过程,为椎间盘退变的治疗提供新的思路和方法.[方法]取48只6个月龄日本大耳白兔,雌雄不限,体重为(2.5±0.2)kg,随机进行分组,分为对照组和实验组,对照组为21只;实验组为27只;先将实验组兔腰背部皮毛剪除,用安定注射液1.25 mg/kg、氯胺酮0.02 g/kg、阿托品0.125 mg/kg顺次耳缘静脉注射麻醉后,俯卧固定于手术台上,用1%碘伏消毒手术区域,以髂嵴平对椎间隙(即L6.7)为中心,从正中取一长约4 cm纵行切口,切开皮肤及皮下组织,锐性分离,暴露棘突、椎板及上下关节突,将附着于棘突、椎板及小关节的肌肉全部分离开,然后依次切除L6.7棘上及棘间韧带,咬除第6腰椎两侧下关节突,造成椎间失稳,用无菌生理盐水冲洗切口,依次缝合各层组织;术后动物在笼中自由活动.实验组分别在术后2个月、4个月、6个月取材,对照组在相同条件下饲养后2个月、4个月、6个月取材;对椎间盘软骨终板用透射电镜观察软骨终板的结构,以综合判断软骨终板的退变过程.[结果]椎间失稳可导致椎问软骨终板胶原纤维结构由整齐有序、排列紧密向杂乱无章、排列松散退变.[结论]椎间失稳能明显导致椎间软骨终板的退变.     

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.     

颈椎间盘退变病因研究进展

目前关于颈椎间盘退变机制的研究报道很多 ,但其确切原因还不清楚 ,现将这方面的研究进展情况综述如下。1　颈椎间盘退变早期的影响因素1 1　软骨终板的改变软骨终板渗透是椎间盘营养供应的主要途径。年龄与应力等因素可引起软骨板内软骨细胞与基质成分的改变。成人软骨终板厚度约为 1mm ,随着年龄的增长而逐渐变薄 ,中年以后软骨终板可出现裂隙与破裂 ,且随年龄增长软骨终板血管数目减少 ,血流减慢淤积 ,蛋白多糖含量减少 ,终板逐渐钙化 ,出现不同程度的退变。这些改变不仅影响椎间盘细胞的营养供应 ,妨碍废物的排出 ,破坏基质代谢平衡 ,还…     

影响椎间盘退变生物化学改变的因素

椎间盘退卞的生物化学改变表现为 :蛋白多糖含量减少 ,硫酸角质素与硫酸软骨素的比例增加 ,Ⅰ型型胶原增多 ,Ⅱ型胶原减少 ,水分减少等 ,这一变化严重影响了椎间盘的生物力学特性 ,由此构成了椎间盘突出的病理基础。近年来 ,随着分子生物学、分子免疫学等医学基础学科的迅速发展 ,椎间盘退变生物化学改变及其影响因素等方面的研究取得了一些进展 ,现在综述如下 :1　应力对椎间盘退变的生物化学影响椎间盘由四周的纤维环、中心的髓核及上下软骨终板组成。正常椎间盘髓核呈流体静压状态 ,椎间盘内压为轴间压载荷的 1.3～ 1.5倍 ,当外载荷达 2 …     

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     

椎间盘退变影响因素研究进展

椎间盘退变是由多种因素影响所致。长期过高和过低的压力负荷均为椎间盘退变的病因之一。近年研究证实软骨终板钙化引起的椎间盘营养供应减少可能是启动椎间盘退变的关键因素。椎间盘老化或营养供应障碍时椎间盘细胞合成一些细胞因子,影响细胞活性和细胞间信息交流,导致细胞凋亡。椎间盘内环境改变后激活潜伏状态的降解酶,使椎间盘基质分解加速,导致椎间盘退变。该文就生物力学、营养、细胞凋亡、细胞因子及降解酶等因素对椎间盘退变的影响及作用机制,作一综述。     

High Endplate Hounsfield Units Value Indicate Intervertebral Disc Degeneration Following Transforaminal Lumbar Interbody Fusion Surgery

Objective

Lumbar disc degeneration (LDD) is a common cause of low back pain and disability, and its prevalence increases with age. The aim of this study is to investigate whether endplate Hounsfield unit (HU) values have an effect on lumbar disc degeneration (LDD) after transforaminal lumbar interbody fusion (TLIF) surgery in patients with degenerative lumbar stenosis.

Methods

This study was a retrospective analysis of patients who underwent TLIF surgery in January 2016 to October 2019. One hundred and fifty-seven patients who underwent TLIF surgery for degenerative lumbar stenosis were enrolled in this study. Demographic data was recorded. VAS and ODI values were compared to assess the surgical outcomes in patients with or without process of LDD after TLIF surgery. Correlation analysis was performed to investigate associations between LDD and endplate HU value. Binary logistic regression analysis was carried out to study relationships between the DDD and the multiple risk factors.

Results

There was a statistically significant correlation between LDD, body mass index (BMI), age, paraspinal muscle atrophy, and total endplate scores (TEPS). Also, a strong and independent association between endplate HU value and LDD was found at every lumbar disc level (p < 0.01). After conditioning on matching factors, multivariate logistic regression analysis showed that higher endplate HU (odds ratio [OR]: 1.003, p = 0.003), higher TEPS (OR: 1.264, p = 0.002), higher BMI (odds ratio [OR]: 1.202, p = 0.002), a smaller cross-sectional area (CSA) of the paraspinal muscle preoperatively (OR: 0.096, p < 0.001) were significant predictors of LDD development after TLIF surgery.

Conclusions

There is a significant association between LDD and endplate HU value after TLIF surgery in patients with degenerative lumbar stenosis. Beyond that, results from this study provide a mechanism by which high endplate HU value predisposes to LDD after TLIF surgery.     

Accumulated Spinal Axial Biomechanical Loading Induces Degeneration in Intervertebral Disc of Mice Lumbar Spine

Objective

To investigate the effect of accumulated spinal axial biomechanical loading on mice lumbar disc and the feasibility of applying this method to establish a mice intervertebral disc degeneration model using a custom‐made hot plate cage. In previous studies, we observed that the motion pattern of mice was greatly similar to that of humans when they were standing and jumping on their lower limbs. There is little data to demonstrate whether or not accumulated spinal axial biomechanical loading could induce intervertebral disc degeneration in vivo.

Methods

Twenty‐four 0‐week‐old mice were randomly divided into model 1‐month and 3‐month groups, and control 1‐month and 3‐month groups (n = 6 per group). The model groups was transferred into the custom‐made hot plate cage three times per day for modeling. The control group was kept in a regular cage. The intervertebral disc samples of the L₃–L₅ were harvested for histologic, molecular, and immunohistochemical studies after modeling for 1 and 3 months.

Results

Accumulated spinal axial biomechanical loading affects the histologic, molecular, and immunohistochemical changes of mice L_3–L₅ intervertebral discs. Decreased height of disc and endplate, fissures of annulus fibrosus, and ossification of cartilage endplate were found in morphological studies. Immunohistochemical studies of the protein level showed a similar expression of type II collagen at 1 month, but a slightly decreased expression at 3 months, and an increased expression level of type X collagen and matrix metalloproteinase 13 (MMP13). Molecular studies showed that ColIIa1 and aggrecan mRNA expression levels were slightly increased at 1 month (P > 0.05), but then decreased slightly (P > 0.05). ColXa1, ADAMTS‐5, and MMP‐13 expression levels werer increased both at 1 and 3 months (P < 0.05). In addition, increased expression of Runx2 was observed.

Conclusion

Accumulated spinal axial loading provided by a custom‐made hot plate accelerated mice lumbar disc and especially endplate degeneration. However, this method requires further development to establish a lumbar disc degeneration model.     

外伤性青少年腰椎间盘突出症

目的：分析外伤性青少年腰椎间盘突出症特点，提高诊治水平。方法：9例13－18岁腰椎间盘症患者，3例因就诊时腰腿痛有神经损害明显，未行保守治疗，其余6例曾经1月－1年保守治疗无效，其中5例神经损害加重。9例全部后路手术治疗。结果：7例经1年－8年，平均4．3年随记，全部神经功能恢复，5例无腰腿痛，1例运动后有少行腰腿痛，1例第1次手术症状消失后7年，腰腿痛症状复发。结论：本病有以下特点：明显腰部外伤后发病；临床症状体症常明显；突出多为破裂游离型；手术治疗是主要方法，疗效满意。     

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。     

伴腰骶部移行椎的腰椎间盘突出症

本文分析讨论了29例经手术治疗的伴腰骶部移行椎的腰椎间盘突出症。认为该症特点是椎间盘突出发生在L_(5～6)或L_5～移行椎椎间最常见,多数发生在移行椎的上椎间。移行椎的腰骶部神经根走行可有变异,也可不对称;它在解剖上的定位与机能有时不相符合,其感觉和肌力可呈分离现象。临床上往往表现为非单根神经根受损害的症状,在诊断和定位时应充分注意。     

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。     

腰椎椎体后缘骨内软骨结节所致腰椎管狭窄症的临床特征

目的　总结腰椎椎体后缘骨内软骨结节 (LPMN)所致腰椎管狭窄症的诊断和治疗特点 ,探讨有关的发病因素。方法　对经手术证实的 16例LPMN所致腰椎管狭窄症的临床表现、影像学特征、手术方式进行回顾性分析总结。结果　 16例均有间歇性跛行 ,10例腰腿痛 ,直腿抬高试验阳性 4例。影像学检查见腰椎椎体后下缘骨缺损及游离骨块突入椎管内。采用单侧椎板扩大开窗 +骨块切除术 4例 ,优 3例 ,良 1例。双侧椎板扩大开窗 +骨块切除术 12例 ,优 9例 ,良 3例 ,随访 1～ 5年。结论　 1、LPMN的形成可能是在软骨板先天性缺陷的基础上 ,由于应力和创伤的作用 ,髓核经缺陷破裂的软骨板突出到椎体和骨突环之间 ,引起骨突环撕脱、后移 ,最终骨化。 2、手术时机愈早愈好 ,单侧椎板扩大开窗 +骨块切除和双侧椎板扩大开窗+骨块切除为有效术式     

Treatment of Intervertebral Disc Degeneration

Intervertebral disc degeneration (IDD) causes a variety of signs and symptoms, such as low back pain (LBP), intervertebral disc herniation, and spinal stenosis, which contribute to high social and economic costs. IDD results from many factors, including genetic factors, aging, mechanical injury, malnutrition, and so on. The pathological changes of IDD are mainly composed of the senescence and apoptosis of nucleus pulposus cells (NPCs), the progressive degeneration of extracellular matrix (ECM), the fibrosis of annulus fibrosus (AF), and the inflammatory response. At present, IDD can be treated by conservative treatment and surgical treatment based on patients'' symptoms. However, all of these can only release the pain but cannot reverse IDD and reconstruct the mechanical function of the spine. The latest research is moving towards the field of biotherapy. Mesenchymal stem cells (MSCs) are regard as the potential therapy of IDD because of their ability to self‐renew and differentiate into a variety of tissues. Moreover, the non‐coding RNAs (ncRNAs) are found to regulate many vital processes in IDD. There have been many successes in the in vitro and animal studies of using biotherapy to treat IDD, but how to transform the experimental data to real therapy which can apply to humans is still a challenge. This article mainly reviews the treatment strategies and research progress of IDD and indicates that there are many problems that need to be solved if the new biotherapy is to be applied to clinical treatment of IDD. This will provide reference and guidance for clinical treatment and research direction of IDD.     

腰椎间盘突出人工髓核置换术的生物力学测试

目的 对腰椎间盘人工髓核置换术进行生物力学评价，为临床应用提供理论依据。方法 取6具新鲜成人尸体腰椎标本（L1～S1），制成三种L4～L5运动节段的试验模型：正常腰椎，椎间盘髓核切除术后，人工髓核植人术后，分别对其进行生物力学测试，记录不同运动状态下脊柱节段运动范围（ROM）的改变情况。结果 与正常脊柱组比较，去髓核组运动节段活动明显增大（P〈0．05），稳定性下降，人工髓核植入组与去髓核组比较运动节段活动明显减小（P〈O．05），与正常脊柱组相比较，运动节段活动差异无显著性（P〉0．05）。结论 腰椎椎间盘人工髓核的植人能较好地恢复腰椎间盘髓核摘除后运动节段的生物力学稳定性。