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软骨形成

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The histopathological findings of the partial ADD included the loss of chon- drocyte, horizontal splitting of the condylar cartilage and synovitis at early stage, and the hyperplasia of chondrocyte, the disarrangement of collagen fibers at late stage, but the articular surface remained intact.

完全性关节盘前移位和关节盘穿孔的组织病理研究发现,髁状突软骨变薄,部分区域软骨丧失,软骨细胞增生成族,肉芽组织形成,软骨及软骨下骨出现水平及垂直裂隙,软骨下骨纤维形成,甚至出现囊肿。

The defects of articular cartilage were repaired with cartilage without chondral degenerations in group A, which was similar to the normal chondral structure.

结果:B、C组软骨损伤区形成骨纤维组织修复,术后12周,C组出现明显的软骨退行性变,B组无明显退变:A组软骨缺损区形成软骨样组织修复,且与邻近正常软骨层相连续,未见明显的软骨退变。

Elastic fibers were well-distributed,and vascular endothelial cell did not immigrate.We suggested that expression of ectogenic VEGF triggered paracrine and autocrine of VEGF of chondrocyte and co-acted with VEGF receptor 2 to enhance permeability of chondrocyte and improve internal construct of engineering cartilage,and prevent vascularize proceed.

转VEGF基因软骨细胞作为组织工程的种子细胞与pluronic F-127复合后可于裸鼠体内形成转基因组织工程软骨,与对照组相比,转VEGF基因组织工程软骨具良好的生物学特性,结构均一且与正常软骨组织相似,软骨ECM的GAG、COLⅡ、COLⅩ增多,RunX2、Sox9表达增高,细胞处于增生期的肥大状态,初步分析其原因可能是转染后外源性的VEGF持续表达触发了软骨细胞VEGF自分泌,并通过VEGFR-2作用于软骨细胞,提高了软骨细胞活性,促进其存活与增殖,但未在软骨组织内引起血管内皮细胞的迁移及小血管形成。

Results Extensive and diffuse synovial hyperplasia can be seen in patients with RA;synovial pannus formation can be seen in 25 cases.

结果RA组病人均可见广泛、弥漫的滑膜增生,其中25例病人可见滑膜血管翳形成,而OA组仅7例病人可见轻度滑膜增厚,未见滑膜血管翳形成者(X2=55.78P.005);RA组关节软骨及软骨下骨改变较严重且弥漫,而OA组软骨退变则较局限,且以关节摩擦大的部位受损为著,其软骨下骨改变较为局限,常常见于IV软骨退变;关节腔积液、半月板及韧带改变,在OA组与RA组之间无差异。

TyPe II collagen induced arthritisln the rat ank1e joint andoVathumin as antigen induced arthritis WA in the rabbit knee joint wereestab1ish2 Qualitative evaluation of me in skin, muscle, synovium, cedilagearound joint and blood was performed by OMA3 The CIA rats were treated on day 7 after hind paw swelling and erythemaAnimals were injected intravenously with ase at a dose of 10mg/kg,tWenty minuots 1ater, one ankle of the rats random1y assigned was exPosedlaser irradiation at l00J/cm fOr l000 seconds, and another ankle wasM grouP wihout laser The other two groups is unmanipulatedcontrol group and untreated CIA group Bimaleolar ankle widthmeasuremellts were taken in all animals every tWo days using amicrometer The histopathology of the ank1e Joint was assessed at day 21after disease onset4 The pro1iferating cell nuclear antigen WCNA of CIA treated by PDT andthe HMME group without laser was doterdrined by immunohistochemiStry5 The AfA rabbits were treated on day 7 after knee swelling and erythemaThe theraPy invo1ved lntravenous injection of l0mg/kg HMME, fOl1owedby 20 minues period in dim light, and transdermal light treatment with\l00 J/cm2 fOr l000 seconds The inner sides of the treated Anees wereirradiated at first, and then the outer side did 24 hours later, the synovialtissue of the Anees joint were removed and in situ cel1 aPoptosis wasdetCCted With tednal deoxync1eotidyl transferase-mediated dUTP nickend labelingR6suIt8:l The pathologic changes of CIA and AIA include subsynovial inflammation,opovial hyPerplasia, pannus formation, cartilage and bone destructionresemble RA.2 The studies demonstrated that there are different uptake of HMME withinskin, muscle, synovium, cartilage and b1ood, and the synovium cou1draPidly uPtake more ase than skin and cartilage at the firSt 30 minuesaller intravenous injection of HMME3 The bimaleolar anke width had no different among PDT treated group,H group withollt 1aser and untreated CIA group But hlstologicalevaluation showed statiStical1y significallt reductions in synovialhyperplasia, pannus formation and cart1lage reosion, bone destruction andtotal score in PDT treated group4 Image analysis showed that the ratlo bforeen the areas of the coufltedobect to that of the entire area in PDTtreated grOup is lower than that in conirol group, but the integrated oPticaldensity had no different between the two groups5 Imape analysis showed that the ratio between the area of the countedobject to that of the e

治疗组在大鼠出现踝关节红肿后1周,炎症达到高峰时进行PDT治疗。随机治疗大鼠一侧的踝关节,另。2。一一侧作单纯HMME 对照。治疗方法是大鼠麻醉后尾静脉注入 HMME10ngkg,20分钟后踝关节照光,激光波长627.sum,功率密度 100mwcm',照射时间1000秒,能量密度100)/。治疗后避光喂养72 小时。隔日一次测量大鼠的踝关节左右横径,治疗后两周取关节进行病理d 观察。 4。大鼠CIA模型用上述方法进行PDT治疗后,治疗组和单纯HMME 组用兔疫组化SP法检测石蜡切片的核增殖抗原。 5。兔AIA模型在关节炎出现第七天进行PDT治疗,随机治疗一侧膝关节,另一侧作自身对照。兔耳静脉注入I'arrainrelomg/Kg,20分钟后,膝关节用金蒸气激光照射,激光能量密度100)儿旷。24 /J'时后取膝关节滑膜作病理检查,并用脱氧核昔酸末端转移酶介导的缺口末端标记法原位检测凋亡细胞。结果: 1。模型观察:CIA大鼠炎症高峰期滑膜下炎细胞浸润明显,滑膜细胞明显增殖,炎症达到高峰后二周,血管缀形成,并侵蚀和破坏软骨和骨, CIA模型病理改变与人类RA相似。兔AIA模型膝关节滑膜病理可见滑膜细胞增生,滑膜下炎细胞浸润,也与人类RA滑膜改变相似。 2。关节周围组织中光敏剂含量的测定结果表明,各组织对HMME 的吸收速度和吸收量不同,荧光值一时间曲线不同,滑膜组织比皮肤和软骨对 HMME的吸收多,在 2 0分钟时即有明显差异。 3.PDT对CIA模型的治疗结果表明:PDT治疗后关节炎组、单纯 HMME组和治疗组踝关节左右横径统计学检验差异没有显著性,但病理评分PDT治疗组滑膜增生、血管资形成及软骨破坏、骨破坏和总分比关节炎对照组和HMME对照组好,统计学检验差异有显著性。。3_军医进修学院硕士学位论文中文摘要 4.PDT治疗组PCNA阳性细胞较对照组少,图像分析结果表明面密度(阳性染色的面积总和与统计视野面积的比值)治疗组小于对照组,统计学检验差异有显著性。。 5.PDT治疗组凋亡阳性细胞较对照组明显增多,图像分析结果单位视野内阳性细胞数和面密度PDT治疗组高于对照组,统计学检验差异有显著性。凋亡细胞核直径PDT治疗组较小,与对照组相比,统计学检验差异有显著性。结论:二。CIA、AIA的病理改变类似人类RA,可作为研究RA病因、发病机制、检查及治疗方法的模型。 2。各组织对HMME的吸收速度和吸收量不同,滑膜组织比皮。

The human cartilages are composed of chondrocyte and extracellular matrix,the form of chondrocytes are hypertrophy and the quantity are less;the ECM of cartilage are compised of type II collagen and proteoglycan. Articular cartilages are all hyaline with little fibers. Trauma and arthritis are the main cause of cartilage injury,the ommilayer injury ofcartilage can be recovered by marrow,but because of without stimulation mechanism,the new tissues are merely fibrocartilages,they can not be coincide with hyaline cartilage in menchanics;the purely damage of articular cartilage can not stimulate chondrocyte to regenerate because of without blood circulation,thus,the plerosis of articular catilage can not depend on the proliferation of local chondrocyte.Ever since,people tried their best to find a way to reconstruct articular cartilage.

造成人体关节软骨损伤的原因主要为创伤和关节炎,关节软骨全层损伤可由于骨髓中间充质干细胞的高速增殖修复,但这种修复由于缺乏相应的刺激机制,只能形成纤维软骨,而不能形成符合关节生理、力学要求的透明软骨;单纯软骨部分损伤软骨组织内无血管,软骨细胞迁移迟缓,无法使损伤区域软骨细胞再生,因此,关节炎及关节创伤后的软骨修复不能依赖于软骨细胞的增殖和迁移。

The human cartilages are composed of chondrocyte and extracellular matrix , the form of chondrocytes are hypertrophy and the quantity are less; the ECM of cartilage are compised of type Ⅱ collagen and proteoglycan. Articular cartilages are all hyaline with little fibers. Trauma and arthritis are the main cause of cartilage injury, the ommilayer injury ofcartilage can be recovered by marrow, but because of without stimulation mechanism, the new tissues are merely fibrocartilages, they can not be coincide with hyaline cartilage in menchanics; the purely damage of articular cartilage can not stimulate chondrocyte to regenerate because of without blood circulation, thus, the plerosis of articular catilage can not depend on the proliferation of local chondrocyte.

造成人体关节软骨损伤的原因主要为创伤和关节炎,关节软骨全层损伤可由于骨髓中间充质干细胞的高速增殖修复,但这种修复由于缺乏相应的刺激机制,只能形成纤维软骨,而不能形成符合关节生理、力学要求的透明软骨;单纯软骨部分损伤软骨组织内无血管,软骨细胞迁移迟缓,无法使损伤区域软骨细胞再生,因此,关节炎及关节创伤后的软骨修复不能依赖于软骨细胞的增殖和迁移。

Totally 32 healthy New Zealand rabbits received design of 6 cm ×2 cm random flaps on trachelo-back and simultaneous implantation of central arterial and venous bundles of left ear as well as free PC chaffs of right ear into flaps, which formed in different time island-like PC flaps taking vascular bundle as pedicle.

健康新西兰大白兔32只,在项背部设计6cm 2cm的任意皮瓣,将左耳中央动、静脉束及右耳游离的软骨膜片同时植入皮瓣下,在不同时间形成以该血管束为蒂的岛状软骨皮瓣,观察血管化进程;另在不同时间取出预构软骨皮瓣中的软骨膜,观察其形成软骨情况。

Methods The cartilages derived from the sventh rib cartilage or septal cartilage and auricle cartilage were sculpted to different shapes such as willow leaf and strut and "bullet"shape to fill nasal back and column and tip for correcting nasal tip depression.

取右侧第7肋软骨或鼻中膈软骨、耳廓软骨,自体肋软骨塑形成柳叶形假体、鼻小柱支架和&子弹头&状软骨块、或鼻中隔软骨修成鼻小拄支架、耳廓软骨塑形成&子弹头&状充填鼻尖矫正鼻尖塌陷畸形。

Methods The chondrocytes isolated from mini swines' ears were mixed with injectable biocompatible matrix,and the density of cell suspensions were 10,20,30,40,50,60,70×10 6/ml.

结果在动物自体内形成的软骨组织,与正常软骨组织有相似的组织学特性,形成软骨组织最适细胞浓度为50×106/ml,最佳形成时间是第6周。

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