关节软骨缺损修复研究进展

关节软骨缺损是临床常见疑难病症之一。滑膜关节表面缺损后难以修复。现就关节软骨缺损的自发修复、自体或异体移植修复、软骨膜或骨膜移植修复、软骨细胞移植修复，以及三维立体细胞培养及组织工程技术修复等五个方面，综述了滑膜关节软骨缺损修复重建的方法学进展     

软骨下骨钻孔修复关节软骨缺损的研究进展

本文阐述了关节软骨损伤的机制和软骨缺损的类型，软骨下骨钻地缺损修复的诱导作用及再生软骨的机制，影响软骨再生的因素等。     

关节软骨缺损修复的研究进展（综述）

本文阐述了关节软骨的理化和生物组织特性，关节软骨损伤的机制和软骨的类型及修复方法。骨膜游离移植和软骨下骨钻孔对缺损修复和诱导作用，两种再生软骨有不同的组织起源。关节运动及负重方式、生物、物理、化学因素对修复关节软骨缺损有较大影响，尤其是近来ＩＧＦ－Ｉ等生长因子对软骨修复的作用正在深入研究。     

关节软骨缺损修复的实验与临床

关节软骨的修复一直是骨科领域尚未完全解决的一大难题。现就关节软骨损伤后促进自身修复、组织或细胞移植修复、组织工程修复等方面对关节软骨修复方法作一综述。     

关节软骨缺损的修复

关节软骨损伤后仅有有限的自我修复能力。既住行钻孔术使骨髓内的未分化细胞聚集于缺损处进行分化产生软骨，然而所形成的纤维软骨无论在生物学上，还是在生物力学上均与原来的软骨不同，且极易退变。近年来尝试骨膜瓣下植入培养的自体软骨细胞修复缺损，使修复组织在质和量方面均有提高。最近，又发展到用骨形态发生蛋白治疗软骨缺损，该方法更优于软骨细胞值入法，修复进一步深入研究以利临床应用。     

关节软骨缺损修复方法及疗效

关节软骨缺损后自我修复能力很差,治疗方法如关节灌洗清理术、Pridie钻孔术、微骨折术、骨膜和软骨膜移植、骨软骨移植、细胞移植和组织工程化软骨修复等的疗效不一.骨软骨移植和细胞移植技术相对成熟且临床效果较好.组织工程化软骨修复是目前研究的热点且已逐步试用于临床,多重复合的仿生支架和携带细胞因子仍是研究重点,临床实际应用还有待观察.     

细胞移植修复关节软骨缺损的研究进展

关节软骨具有耐用性和维持自身的能力,但成熟软骨对抗外伤和各种疾病的能力是脆弱的,极易引起损伤,加之软骨组织自身修复能力很差,这些损伤往往不能修复,而引起疼痛、运动障碍影响人们的生活和健康。要使修复或再生的软骨能满意的执行功能,恢复滑膜关节正常的无痛运动,新形成的组织在结构、组成、机械性能和持久耐用方面必须和正常关节软骨相似。目前恢复损伤关节软骨的方法有两类:刺激关节软骨自身修复和组织细胞移植。前者包括,清创术和灌洗法、软骨下骨钻孔术、微骨折、截骨术等,这些方法可以减轻疼痛、肿胀等临床症状,但刺激产生的是纤…     

关节软骨缺损修复的研究现状

关节软骨缺损修复的研究现状刘景堂葛宝丰作者单位：７３００５０兰州，兰州军区总医院骨研所滑膜关节的软骨病损后，软骨的自我修复能力有限，将直接影响关节功能。假关节置换适合于老年患者，对年轻患者，由于假关节存在许多近、远期并发症，被列为禁忌证［１］。设法在...     

软骨生长因子对兔关节软骨缺损修复作用的实验研究

软骨生长因子(cartilage-derived growth factor，CDGF)是能促进软骨细胞生长，加速骨基质合成的类似于碱性成纤维细胞因子(bFGF)的碱性蛋白^[1]。在体外培养兔软骨细胞中，CDGF能以剂量依赖性的方式促进软骨细胞增殖和胶原的合成^[2]。然而生长因子若没有载体的保护，易被稀释或水解，最终失去生物学活性。我们以新西兰大白兔为实     

The chondrogenic repair response of undifferentiated mesenchymal cells in rat full-thickness articular cartilage defects

OBJECTIVE: The aim of this study is to develop a rat model of full-thickness articular cartilage defects that is suitable for detailed molecular analyses of the regenerative repair of cartilage. MATERIALS AND METHODS: The V-shaped full-thickness defects (width: 0.7 mm; depth: 0.8 mm; and length: 4mm) were created in the femoral patellar groove of 6 weeks old male rats using a custom-built twin-blade device. Prior to starting the repair experiments, our device was examined for its accuracy and reliability in generating defects. Then, the time course of the repair response in these cartilage defects was examined using a semi-quantitative histological grading scale. The expression of chondrogenic differentiation markers in the reparative regions was examined with immunohistochemistry and in situ hybridization. RESULTS: Our device creates full-thickness articular cartilage defects uniformly. In these defects, undifferentiated mesenchymal cells filled the defect cavities (4 days) and initiated chondrogenic differentiation at the center of the defect (7 days). Cartilage formation was observed in the same region (2 weeks). Finally, hyaline-like articular cartilage and subchondral bone layers were reconstituted in their appropriate locations (4 weeks). CONCLUSIONS: We have successfully developed a rat model containing identically sized full-thickness defects of articular cartilage that can undergo chondrogenic repair in a reproducible fashion.     

Analyses of early events during chondrogenic repair in rat full-thickness articular cartilage defects

In this study we investigated the cellular events that occur during the onset of chondrogenic differentiation during the repair of full-thickness defects of articular cartilage. The V-shaped full-thickness cartilage defects (width 0.7 or 1.5 mm; depth 0.8 mm; length 4 mm) were created in the femoral patellar groove of rats using a custom-built twin-blade device. The time course of the repair response in these cartilage defects was examined using a semi-quantitative histological grading scale. Cartilaginous repair responses failed to occur in the larger 1.5 mm defects, which was covered only by fibrous scar tissue. In contrast, hyaline-like articular cartilage was regenerated concomitantly with the repair of the subchondral bone by 4 weeks in smaller 0.7 mm width defects. Cells in the reparative regions were then characterized by immunohistochemistry and in situ hybridization. Undifferentiated mesenchymal cells migrate into the defects and fill the cavities within 4 days of their creation. The expression of PCNA, N-cadherin, and PTH/PTHrP receptors was induced in cells at the center of the defects, where type II collagen-positive polygonal-shaped cells also begin to appear at day 7. Marrow-derived mesenchymal cells acquire higher levels of proliferative activity in induced cartilage cavities after their initial migration and filling of the smaller 0.7 mm defects. During the regenerative repair of articular cartilage in the rat, there is a distinctive step that appears to be analogous to the precartilaginous condensation that is pivotal during chondrogenesis in development.     

关节软骨损伤和缺损修复策略

关节软骨的损伤是临床中常见的疾病。由于关节软骨自身修复能力有限,采用关节镜下清创术、软骨移植、软骨细胞移植、组织工程技术及凝胶类关节软骨修复材料是目前对关节软骨损伤进行修复的主要手段。本文对目前用于关节软骨损伤和缺损修复的主要策略及各类修复技术的优缺点进行了综合评述。关节镜下清创术对早期骨性关节炎疗效显著;软骨及软骨细胞移植对小面积软骨缺损修复效果较为理想;组织工程技术是目前对关节软骨损伤和缺损修复的一个热点方向,但存在支架材料与软骨缺损区整合不紧密等问题;凝胶类关节软骨修复材料具有与自然关节软骨相似的力学和生物摩擦学特性,但其生物活性及与自然关节软骨间的结合强度有待进一步提高,如何实现材料生物活性、生物力学性能和生物摩擦学性能功能一体化是凝胶类关节软骨修复材料亟待解决的焦点问题。     

Surgical technique for articular cartilage transplantation to full-thickness cartilage defects in the knee joint

Focal arthritic defects in the knee lead to pain, swelling, and dysfunction. Treatment of the defects has includeddrilling, abrasion, and grafting. This report describes our surgical technique of autogenous articular cartilage grafting of arthritic and traumatic articular cartilage lesions. Articular cartilage grafting can be performed as a single arthroscopic outpatient procedure. The mixture of articular cartilage and cancellous bone appears to provide a supportive matrix for cartilage formation. Pain relief is excellent if careful surgical technique and a defined rehabilitation program is followed. Further collagen typing data and additional biopsies will reveal more about the durability of the newly formed cartilage.     

Injury and repair of articular cartilage: Related scientific issues

Articular cartilage (AC) is the soft tissue lining the ends of bones in diarthrodial joints. It is responsible for providinglubrication and compressive stiffness to the joint during articulation while responding viscoelastically to mechanical loading. Injury of the tissue caused by trauma or disease can be devastating to joint function as these mechanisms fail. Because of this, it is essential to review the basic science underlying the mechanical roles AC plays while healthy, the biomechanical and biological perspectives of the injury and repair processes, and the current repair techniques available for injured AC. This is done in an effort to further our understanding of the healing capacity of AC and facilitate new efforts into AC repair.     

镁元素及镁材料在关节软骨损伤修复中的作用及机制研究进展

软骨损伤是由炎症、创伤、肿瘤等造成的,由于关节软骨自身解剖因素,使其损伤后的愈合能力较差,制备组织工程材料促进软骨损伤修复备受研究者关注。镁元素及镁材料因其良好的生物安全性、生物相容性、可降解性及可获得性受到广泛关注,其在骨关节炎等软骨损伤修复中起到重要作用,笔者就镁元素及镁材料在关节软骨损伤修复中的作用及机制作一综述。     

壳聚糖在关节软骨组织工程中应用的研究进展

关节软骨一旦被损伤，因其缺乏自身血液循环系统，仅靠关节滑液提供大部分营养。随着年龄的增长，软骨细胞的合成能力下降，故关节软骨损伤后很难修复。虽然40多年来许多修复技术被广泛应用，但是至今还没有一种方法可以让受损软骨持续再生，从而达到完全修复的目的。组织工程的兴起在软骨的再生以及受损软骨的治疗方面显示出巨大的潜力。支架材料作为人工细胞外基质承载种子细胞是组织工程研究的重要内容之一。近年来，以壳聚糖为支架的材料及其在矫形组织工程中的应用正受到越来越多的关注。壳聚糖是一种理想的高分子生物材料，它具有机体反应小、天然抗菌性以及具有可任意塑性如多孔结构的特点，使其能够适合细胞的内在生长以及骨的传导，在组织工程中显示出巨大的应用价值。     

骨软骨移植联合rhBMP -2/bFGF修复软骨缺损

[目的]探讨采用冷冻同种异体骨软骨移植,配合骨形态发生蛋白(rhBMP-2)/碱性成纤维细胞生长因子(bFGF)修复软骨缺损的效果,为进一步应用于临床提供理论依据。[方法]48只日本大耳白兔,96个关节,随机分A、B、C、D组。A组采用骨软骨移植联合rhBMP-2/bFGF,B组单纯应用骨软骨移植,C组单纯局部注射rh-BMP-2/bFGF混悬液,D组用作空白对照。无菌条件下制作骨软骨缺损模型。术后第4、8、12周作解剖学观察、磁共振检查、组织学检查及软骨细胞记数、免疫组化检查。[结果]A组软骨缺损修复面光滑,呈瓷白色、半透明,B、C组未完全修复,D组无明显修复。A组修复软骨组织学评分与其他组比较差异有统计学意义(P<0.05),图像分析仪软骨细胞记数与其他组比较差异有统计学意义(P<0.05)。修复软骨Ⅱ型胶原免疫组化染色阳性。[结论]联合应用冷冻同种异体骨软骨移植、rhBMP-2/bFGF,能促进新生软骨的形成,提高软骨缺损修复的质量。     

一氧化氮合酶抑制剂对关节软骨缺损修复影响的形态学研究

目的　探讨诱导型一氧化氮合酶 (iNOS)抑制剂S 甲基异硫脲 (SMT)对关节软骨修复的影响。方法　将 2 0只新西兰大白兔双侧股骨髁关节面造成全层软骨缺损。随机分为 2组 :对照组 10例 ,缺损软骨面用纤维蛋白凝胶BMP复合物充填 ;给药组 10例 ,缺损软骨面用纤维蛋白凝胶BMP复合物充填后 ,皮下注射SMT(5mg·kg-1·12h-1)。术后 8周、16周、1年处死动物 ,按组织形态学分级标准 ,双盲法行 16周和 1年修复组织评价 ;化学比色法检测修复组织NO释放量和NOS活性。结果　形态学观察证实 ,术后 8周、16周及 1年后 ,给药组软骨缺损修复在缺损区结构、细胞形态和基质染色等评分方面优于对照组 (P <0 0 5 )。术后 16周及 1年对照组NO释放量和NOS活性明显高于给药组 (P <0 0 5 )。结论　iNOS抑制剂SMT可减少NO释放 ,降低iNOS活性 ,提高软骨修复质量。     

骨形态发生蛋白修复关节软骨的研究进展

【摘要】〓关节软骨损伤是一种常见疾病,其可导致关节炎的发生而严重影响人们的日常生活。但由于软骨缺乏血运,且不含祖干细胞,关节软骨的修复能力受到限制,至今临床上尚未有一个有效的方法来促进受损关节软骨的修复。目前,生长因子促进关节软骨修复和再生方面的研究日益受到重视,其中骨形态发生蛋白(BMP)是能够诱导骨组织形成的一个独特因子,对关节软骨的修复有促进作用。但是,BMP的作用尚处于研究阶段,仍有较多问题需解决,故有必要对BMP修复关节软骨作一综述。