软骨终板的形态与椎间盘退变的关系

软骨终板位于椎体上、下表面与椎间盘的纤维环和髓核之间 ,刘润田〔1〕等认为是椎间盘的一个组成部分 ,另一些学者〔2〕认为椎体上、下表面的皮质外层。软骨终板和纤维环一起将胶状的髓核密封 ,使椎间盘形成一个自行限制的密闭容器 ,起缓冲外力的作用。若软骨终板破裂 ,髓核会通过其破裂处突入椎体骨质内形成许莫结节 ( Schmorl) ;或向后突入椎管内形成椎间盘突出。本文就软骨终板的形态和功能作一综述 ,旨在为椎间盘退变的进一步研究和人工椎间盘置换术等临床应用提供解剖学依据。椎间盘是人体最大的无血运组织 ,其营养途径主要有 :( 1 )…     

兔软骨终板退变过程超微结构的观察

目的：研究兔软骨终板退变过程中的超微结构变化。方法：将18只新西兰白兔随机均分为实验组和对照组，实验组通过切除兔腰椎棘上、棘间韧带，咬除部分关节突关节，分离椎旁肌造成腰椎软骨终板退变模型，分别于术后12、24、36周对腰椎摄X线片，并行扫描电镜观察软骨终板超微结构的变化。结果：X线片示软骨终板随时间的延长而逐渐钙化，且实验组较对照组钙化明显；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，且上述变化较对照组显著。结论：椎间失稳可造成软骨终板退变，导致软骨终板基质的破坏。     

PINK1/Parkin介导的线粒体自噬在力学失衡诱导终板软骨退变中的作用

目的 检测脊柱失稳诱导终板软骨退变模型大鼠中线粒体自噬水平的变化,探讨PINK1/Parkin介导的线粒体自噬在终板软骨以及椎间盘退变中的作用。方法 通过手术切除大鼠L2～L5棘上、棘间韧带,咬除L2～L5两侧关节突,构建大鼠脊柱失稳模型。18只SD大鼠分为正常组、退变组及羰基氰化物3-氯苯腙（CCCP）组,每组6只。正常组大鼠无特殊处理,退变组大鼠构建大鼠脊柱失稳模型,CCCP组大鼠在构建大鼠脊柱失稳模型后于椎间盘注射5μL CCCP (10μmol/L)。利用HE染色观察终板软骨及椎间盘形态变化,番红-固绿染色观察终板软骨细胞外基质变化。RT-PCR检测各组大鼠终板软骨组织中Ⅱ型胶原（COL-2A）、蛋白聚糖（ACAN）、PINK1、Parkin mRNA表达水平;Western blot检测COL-2A、ACAN、PINK1、Parkin及线粒体膜蛋白Tomm20、Timm23蛋白表达水平变化。结果 与正常组比较,退变组大鼠椎间盘髓核破坏明显,终板软骨细胞外基质分泌减少;CCCP组大鼠椎间盘结构较完整,终板软骨细胞外基质分泌较退变组明显增多。与正常组比较,退变组大鼠终板软骨组织C...     

腰椎间盘退变对软骨终板生物力学特性影响的有限元分析

目的　研究腰椎终板不同位点的压应力分布规律,分析腰椎间盘退变对软骨终板压应力的影响。 方法　选取一青壮年男性新鲜尸体的腰椎运动节段标本,螺旋CT机对腰椎运动节段进行连续CT扫描,利用有限元分析方法,建立L4/5运动节段有限元分析模型,在此基础上建立椎间盘退变模型。模拟椎间盘正常状态和椎间盘退变状态,在L4、L5椎体终板上选择具有代表性的结点,分别代表椎体终板正中部、左右侧边缘、后中部和前中部,对上下软骨终板压应力分布进行有限元分析。 结果　椎间盘退变组较正常组的终板压应力均显著增大,上下终板在轴向加载、前屈、后伸、左旋和右旋加载时椎间盘退变组较正常状态时应力分布均显著增大,具有统计学意义（P<0.05）。 结论　腰椎椎间盘退变因素对终板的应力分布有明显影响, 随着椎间盘退变,椎间盘软骨终板应力显著增大。     

椎间失稳致兔腰椎软骨终板退变的形态学研究

目的:研究兔腰椎软骨终板退变中的形态学变化.方法:将24只新西兰白兔随机均分为实验组和对照组,实验组通过切除兔腰椎棘上、棘间韧带,咬除部分关节突关节,分离椎旁肌造成腰椎软骨终板退变模型,分别于术后12、24、36周对腰椎摄X线片,行HE及甲苯胺蓝染色观察软骨终板形态学的变化;并行软骨终板蛋白多糖及胶原检测.结果:X线片示软骨终板随时间的延长而逐渐钙化,且实验组较对照组钙化明显;随软骨终板退变进程,HE染色示实验组软骨终板较对照组明显变薄,潮标明显前移,血管芽周嗣钙化;甲苯胺蓝染色示实验组软骨终板染色逐渐变淡,细胞层数明显变少;蛋白多糖含量及胶原释放量逐渐降低,不同时间段实验组明显较对照组低(P<0.01).结论:椎间失稳可导致软骨终板形态学及细胞外基质变化,造成软骨终板退变,为进一步研究其退变机理提供理论依据.     

IL-1β诱导小鼠椎间盘软骨终板细胞炎性退变的细胞模型研究

目的通过IL-1β体外诱导小鼠椎间盘软骨终板细胞建立退变细胞模型,并研究其作用机制。方法 10 ng/ml IL-1β诱导小鼠椎间盘软骨终板细胞24 h后,用cck-8法检测不同时间点IL-1β对软骨终板细胞增殖作用的影响,透射电镜观察细胞退变情况,细胞免疫荧光和Western blot检测细胞退变相关蛋白表达。结果诱导组细胞较正常组细胞增殖减慢,细胞肥大化比例增加,出现线粒体肿胀、核扭曲、染色质边集,染色质及胞质松散等细胞坏死及凋亡表现,且colⅡ、Aggrecan表达下降,colⅩ、MMP-1、MMP-3、MMP-13、TIMP-1表达增加。结论 IL-1β可诱导软骨终板细胞发生退变。     

力学刺激与软骨细胞培养

为保持体外培养的软骨细胞的正常形态，从而保证其正常代谢和表型，许多作者进行了压力刺激与软骨细胞代谢方面的研究。初步表明机械压力对培养软骨的作用在有效范围内与压力值无关，而与压缩程度（静压力）和频率（循环压力）有关，持续的静压抑制软骨的合成功能，一定频率的循环压力促进软骨细胞的合成功能。     

抑制半乳糖凝集素3促进椎间盘软骨终板细胞凋亡诱导椎间盘退变

背景:椎间盘软骨终板的退变破坏了椎间盘完整性,影响了营养和代谢物交换及细胞外基质代谢平衡,是导致椎间盘退变的主要因素.半乳糖凝集素3(Galectin-3)是半乳糖凝集素家族的一员,参与调控细胞增殖、凋亡、细胞黏附等多种生理和病理过程,但是Galectin-3在椎间盘软骨终板中的调控作用尚不明确.目的:通过抑制剂GB1...     

针刺损伤兔椎间盘退变模型组织病理变化及软骨样细胞的迁移规律**☆

背景：兔椎间盘退变模型间盘退变表现为随时间进展脊索细胞将被软骨样细胞逐渐替代,但兔针刺纤维环间盘退变模型中软骨样细胞的来源和移行规律尚不明确。 目的：观察针刺兔纤维环间盘退变模型椎间盘病理变化过程,并初步探讨软骨样细胞来源及移行规律。 方法：将24只新西兰大白兔随机分为手术组与假手术组。手术组使用16 G穿刺针针刺L2/L3、L3/L4、L4/L5及L5/L6椎间盘纤维环,假手术组暴露至相同椎间盘前方后冲洗闭合伤口。 结果与结论：针刺损伤椎间盘退变过程中的软骨样细胞来源于终板。在髓核与上下终板交界处,软骨细胞脱离终板成串向髓核中心迁移;在髓核与内层纤维环交界处,软骨细胞沿纤维走行迁移并随之向皱缩的髓核边缘迁移。椎间盘退变过程中非钙化层逐渐变薄,非钙化层/钙化层比值逐渐降低。 关键词：椎间盘退变;软骨细胞;软骨终板;纤维环穿刺;新西兰大白兔  doi:10.3969/j.issn.1673-8225.2012.09.018     

力学刺激与软骨细胞培养

为保持体外培养的软骨细胞的正常形态，从而保证其正常代谢和表型，许多作者进行了压力刺激与软骨细胞代谢方面的研究。初步表明机械压力对培养软骨的作用在有效范围内与压力值无关，而与压缩程度（静压力）和频率（循环压力）有关，持续的静压抑制软骨的合成功能，一定频率的循环压力促进软骨细胞的合成功能。     

力学刺激在破骨细胞分化中的作用

骨组织细胞主要有成骨细胞、破骨细胞、骨细胞3种类型,与细胞外基质共同维持骨的结构完整性和功能性。破骨细胞专门负责骨吸收,通过释放酸性物质和蛋白水解酶降解骨基质,发挥骨吸收作用;通过与成骨细胞相互协调,共同维持骨稳态。破骨细胞增多,导致骨吸收增加,从而引起骨质疏松症等骨骼疾病;破骨细胞生成过少,将导致骨吸收减弱等相关疾病,例如骨硬化症。因此,对于破骨细胞功能的精确调控,在维持骨稳态的平衡中发挥极为关键的作用。既往研究多从生物化学角度解释和阐述各种生物因素对破骨细胞的调控。然而越来越多的研究证实,力学刺激在破骨细胞分化过程中发挥着重要的作用。本文着眼于力学刺激对破骨细胞分化的影响,讨论力学刺激在其中可能发挥的作用,并对该领域的新发现以及未来的发展进行探讨。     

Geometry of the Intervertebral Volume and Vertebral Endplates of the Human Spine

Replacement of a degenerated vertebral disc with an artificial intervertebral disc (AID) is currently possible, but poses problems, mainly in the force distribution through the vertebral column. Data on the intervertebral disc space geometry will provide a better fit of the prosthesis to the vertebrae, but current literature on vertebral disc geometry is very scarce or not suitable. In this study, existing CT-scans of 77 patients were analyzed to measure the intervertebral disc and vertebral endplate geometry of the lumbar spine. Ten adjacent points on both sides of the vertebrae (S1-superior to T12-inferior) and sagittal and transverse diameters were measured to describe the shape of the caudal and cranial vertebral planes of the vertebrae. It was found that the largest endplate depth is located in the middle or posterior regions of the vertebra, that there is a linear relationship between all inferior endplate depths and the endplate location (p < 0.0001) within the spinal column, and that the superior endplate depth increases with age by about 0.01 mm per year (p < 0.02). The wedge angle increases from T12-L1 to L5-S1. The results allow for improvement of the fit of intervertebral disc-prostheses to the vertebrae and optimized force transmission through the vertebral column.     

The Collagenous Nature of Amianthoid Degeneration of Human Costal Cartilage

Amianthoid (asbestoid) fibers in aging human costal cartilage are shown to be collagenous both by their electron microscopic appearance and solubilization by clostridial collagenase. The fibers differ morphologically from collagen of dermis, synovium, tendon, fibrocartilage and hyaline articular cartilage in dimension, contour and arrangement. They measure up to 1 μ in width, and their period length is 560 to 620 Å. Their thickness, straightness and parallel organization suggest that amianthoid fibers are rigid. Their stability in the face of the preparative technics suggests that cohesive forces rather than spatial apposition through depletion of ground substance operate to hold the component fibrils together. These forces may or may not arise from covalent cross-links.     

The Role of Macrophages in Wallerian Degeneration

The present review focuses on macrophage properties in Wallerian degeneration. The identification of hematogenous phagocytes, the involvement of cell surface receptors and soluble factors, the state of activation during myelin removal and the signals and factors leading to macrophage recruitment into degenerating peripheral nerves after nerve transection are reviewed. The main effector cells in Wallerian degeneration are hematogenous phagocytes. Resident macrophages and Schwann cells play a minor role in myelin removal. The macrophage complement receptor type 3 is the main surface receptor involved in myelin recognition and uptake. The signals leading to macrophage recruitment are heterogenous and not yet defined in detail. Degenerating myelin and axons are suggested to participate. The relevance of these findings for immune-mediated demyelination are discussed since the definition of the role of macrophages might lead to a better understanding of the pathogenesis of demyelination.     

Investigating the Mechanisms of Massage Efficacy: The Role of Mechanical Immunomodulation

Massage has the potential to attenuate the inflammatory process, facilitate early recovery, and provide pain relief from muscular injuries. In this hypothesis-driven paper, we integrate the concept of mechanotransduction with the application of massage to explore beneficial mechanisms. By altering signaling pathways involved with the inflammatory process, massage may decrease secondary injury, nerve sensitization, and collateral sprouting, resulting in increased recovery from damage and reduction or prevention of pain. Our goal is to provide a framework that describes our current understanding of the mechanisms whereby massage therapy activates potentially beneficial immunomodulatory pathways.Key Words: inflammation, mechanotransduction, neutrophils, macrophages, apoptotic signaling, sensitization, nociception, afferent nervesComplementary and alternative medicine (CAM), sometimes referred to as complementary integrative medicine (CIM), is steadily gaining popularity. It covers a vast range of treatments from dietary supplementation to practitioner-based chiropractic and massage therapies.^1–3 Individuals seeking CAM/CIM treatments generally pay out-of-pocket costs that are comparable to family medical practitioner costs in a given year.^1,3 In 2007, the estimated costs were reported to be $33.9 billion for CAM/CIM treatment in the United States alone, a third ($11.9 billion) of which stemmed from costs for practitioners, such as massage therapists.³ Researchers² have shown that the most commonly cited reason for seeking CAM/CIM therapy, such as massage, is the treatment or prevention of musculoskeletal conditions or conditions associated with chronic pain. Most individuals use CAM/CIM modalities in conjunction with traditional treatment, with “relief of symptoms” as one of the most common reasons cited.¹Previous investigations regarding the efficacy of massage have been highly variable and inconclusive, most likely due to a lack of randomized control trials⁴ and inherent challenges associated with investigating the effects of massage, such as inconsistent modes of massage application (ie, effleurage versus petrissage, or a combination of the two), applied forces, and duration of reported massage application. In a systematic review, Best et al⁵ concluded that although researchers have attempted to mimic the clinical setting, the variability that exists between and within these investigations makes them difficult to interpret. Additionally, many of the studies reviewed relied exclusively on subjective participant outcomes⁵; therefore, conclusions about cellular and molecular responses were absent.Considering the large number of individuals receiving CAM/CIM therapies and the purported positive health benefits these modalities provide, the purpose of this communication is to explore how massage affects inflammatory responses and their modulation of pain. Beginning with an overview of the inflammatory response, readers will gain an in-depth understanding of immune-cell function and how endogenous chemicals released in this process affect pain transmission through the sensitization of afferent nerve fibers. We also introduce the concept of mechanotransduction and its importance in stimulating cell-signaling pathways. Finally, we present the immunomodulatory effects of massage, which combine all of these elements, to discuss the physiologic benefits of massage application following injury. A better understanding of the physiologic consequences that massage induces on cellular mechanisms underlying inflammatory pathways and pain modulation will allow clinicians to make informed decisions about treatments associated with musculoskeletal injuries.     

Regeneration of Achilles' Tendon: The Role of Dynamic Stimulation for Enhanced Cell Proliferation and Mechanical Properties

The tissue engineering of tendon was studied using highly elastic poly(L-lactide-co-ε-caprolactone) (PLCL) scaffolds and focusing on the effect of dynamic tensile stimulation. Tenocytes from rabbit Achilles tendon were seeded (1.0 × 10⁶ cells/scaffold) onto porous PLCL scaffolds and cultured for periods of 2 weeks and 4 weeks. This was performed in a static system and also in a bioreactor equipped with tensile modulation which mimicked the environmental surroundings of tendons with respect to tensile extension. The degradation of the polymeric scaffolds during the culture was relatively slow. However, there was an indication that cells accelerated the degradation of PLCL scaffolds. The scaffold/cell adducts from the static culture exhibited inferior strength (at 2 weeks 350 kPa, 4 weeks 300 kPa) compared to the control without cells (at 2 weeks 460 kPa, 4 weeks 340 kPa), indicating that the cells contributed to the enhanced degradation. On the contrary, the corresponding values of the adducts from the dynamic culture (at 2 weeks 430 kPa, 4 weeks 370 kPa) were similar to, or higher than, those from the control. This could be explained by the increased quantity of cells and neo-tissues in the case of dynamic culture compensating for the loss in tensile strength. Compared with static and dynamic culture conditions, mechanical stimulation played a crucial role in the regeneration of tendon tissue. In the case of the dynamic culture system, cell proliferation was enhanced and secretion of collagen type I was increased, as evidenced by DNA assay and histological and immunofluorescence analysis. Thus, tendon regeneration, indicated by improved mechanical and biological properties, was demonstrated, confirming the effect of mechanical stimulation. It could be concluded that the dynamic tensile stimulation appeared to be an essential factor in tendon/ligament tissue engineering, and that elastic PLCL co-polymers could be very beneficial in this process.     

下肢力线与膝关节软骨下骨板杆结构和软骨退变的关系

目的利用骨小梁分割技术(individual trabecula segmentation,ITS)和组织学方法分析膝关节骨关节炎(osteoarthritis,OA)的胫骨平台骨软骨标本,研究下肢力线与软骨下小梁骨显微结构以及软骨退变的关系。方法接受全膝关节置换术病人术前进行下肢全长X线平片拍摄,进行髋-膝-踝(hip-knee-ankle,HKA)角测量。收集术中切除的胫骨平台标本进行显微CT扫描,利用ITS分析软骨下骨小梁结构。通过组织学方法评价软骨退变。对下肢力线与软骨下骨显微结构参数改变和软骨退变进行相关性分析。结果胫骨平台软骨下骨小梁体积分数(BV/TV)、骨小板(pBV/TV)体积分数、骨小杆体积分数(rBV/TV)及轴向骨小梁体积分数(aBV/TV)、骨小板及骨小杆体积比值(P/R)、骨小板数量(pTb. N)、骨小板厚度(pTb. Th)、骨小板表面积(pTb. S)、骨小杆长度(rTb. L)、骨小板-骨小板连接密度(P-P Junc. D)、骨小板-骨小杆连接密度(P-R Junc. D)与软骨退变程度和下肢力线角度显著相关。HKA角度绝对值越大,受累侧胫骨平台软骨下骨小板增厚,骨小板数量增加,骨小板-骨小板以及骨小板-骨小杆的连接性越强,同时软骨退变OARSI评分也越高。结论下肢力线异常可能通过改变膝关节正常的应力分布而导致胫骨平台软骨下骨小梁显微结构异常,尤其是骨小板和轴向骨小梁的显著增多和增厚可能是进一步加重被覆软骨退变、导致OA进展的危险因素。因此,通过改变力线和调节软骨下骨代谢有望成为早期干预骨关节炎发生和发展的切入点。     

Stimulation of Regeneration of Hyaline Cartilage in Experimental Osteochondral Injury

A model of osteochondral intra-articular defect in rats is presented. During spontaneous healing, the stage of formation of granulation tissue is followed by its replacement with bone and fibrous tissue. Chondroinductive properties of collagen 1 sponge used for defect filling manifested in the formation of fibrous cartilage with fields of hyaline cartilage. Filling of the defect with collagen 1 sponge containing bone powder stimulated regeneration of the bone tissue and hyaline cartilage. Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 146, No. 11, pp. 597–600, November, 2008