股骨头坏死早期的关节软骨改变

目的:探讨早期股骨头坏死关节软骨的改变,为深入了解股骨头坏死的病理机制及制定合理治疗提供实验与临床依据。方法:采用软骨延迟增强核磁成像(delayed gado1inium-enhanced magnetic resonance i maging ofcartilage-dGEMRIC)技术,对Ⅱ、Ⅲ期成人股骨头坏死的关节软骨进行检测。20髋激素性股骨头坏死患者中,以国际骨坏死与循环协会(ARCO)分期标准,股骨头坏死Ⅱ期患者为11髋,股骨头坏死Ⅲ期患者为9髋,5名健康志愿者作测试为对照组。对每名受试者进行钆增强延迟核磁共振(1.5T)扫描,分别获得T1Gd数据,应用Matlab和mri mapper软件对每位受试者的影像数据进行分析。结果:股骨头坏死Ⅱ期患者的MRITl Gd值(441.13士41.32)与健康志愿者的T1Gd值(544.2士27.83)有显著差别(P0.001)。股骨头坏死Ⅲ期患者的T1Gd值(363,11士56.39)与健康志愿者的T1Gd值也有显著差别(P0.001)。股骨头坏死Ⅲ期与股骨头坏死Ⅱ期患者的T1Gd值比较下降17.7%,两者有显著性差别(P0.05)。结论:股骨头坏死早期患者的关节软骨已经开始发生代谢变化。说明骨坏死早期可以影响软骨的代谢和功能,并随着坏死程度加重而加大。     

低磁场磁共振成像诊断股骨头缺血坏死的临床价值

股骨头缺血坏死(AFHN)是临床常见的病症，因股骨头缺血导致骨坏死，影响局部或整个髋关节，引起软骨坏死、股骨头塌陷变形、关节功能丧失。磁共振成像(MRI)对股骨头坏死早期诊断有很高的敏感性，能准确描述骨坏死的形态、区域，尤其是对早期AFHN患者，可以为临床治疗争取时间，最大限度保存关节功能。     

犬股骨头软骨下骨缺损对关节软骨结构与代谢的影响

目的 应用股骨头骨缺损模型研究骨缺损对其上部邻近关节软骨结构与代谢的变化,以期说明骨坏死对关节软骨的可能影响.方法 将18只杂种成年犬一侧股骨头制造骨缺损模型,对侧作为对照.分别于4、12、24周各处死5、5、8只动物取材.取材前行股骨头X线检查及大体标本检查.应用HE染色、天狼星红染色及甲苯胺蓝染色方法行关节软骨组织学检查,应用氨基酸分析仪及分光光度计行关节软骨组织化学定量检测并行统计学分析.结果 造模术后12周,可见到骨缺损上部邻近软骨细胞减少,细胞核变小,软骨基质染色变浅.术后24周可见到细胞排列不整齐,呈细胞簇状.紧邻骨缺损开口处软骨浅表层出现裂隙及纤维化改变.潮线模糊、中断,部分切片出现软骨血管形成改变,可见血管突破潮线现象.邻近骨缺损处软骨葡胺聚糖(GAG)减少.结论 与骨坏死的结构强度和血运损害有相似之处的模型骨缺损,对邻近软骨的结构与代谢有影响,提示骨坏死塌陷前期可能会有邻近软骨的变化.     

股骨头缺血性坏死治疗的研究进展

骨坏死(Osteonecrosis,0N)又称无菌性坏死、无血管性坏死或缺血性坏死,指由于各种原因(机械、生物等)使骨循环中断、骨的活性成分死亡及随后修复的一系列复杂的病理过程。骨坏死可累及全身许多关节,其中以股骨头缺血性坏死(Osteonecrosis of the Femoral Head,ONFH)最常见。2006年4月在北京召开的"首届全国骨坏死与关节保留重     

兔激素性股骨头缺血性坏死血管变化及对关节软骨的影响

目的:探讨早期激素性股骨头缺血性坏死关节软骨损伤的发病机制。方法:健康成年日本大耳白兔60只,随机分为模型组(大剂量注射醋酸泼尼松龙,n=42)与对照组(n=18)。观察模型组及对照组第6周X线、MRI变化及光镜下关节软骨、软骨下区骨组织、血管(Masson三色染色、Weigert间苯二酚品红染色法)的组织病理学变化。结果:光镜观察到模型组第6周股骨头软骨下区骨小梁稀疏、变细,甚至骨小梁断裂,死骨形成,关节软骨区域性软骨细胞丢失。髓腔内造血组织减少,肥大脂肪细胞增多,后期脂肪细胞液化坏死、基质水肿、出血。小动脉壁结构破坏,软骨下静脉及毛细血管扩张、淤血。偶见毛细血管内透明血栓形成。结论:早期激素性股骨头缺血性坏死关节软骨的损伤可能与局部血液循环障碍有密切关系。     

生长分化因子治疗股骨头坏死

股骨头坏死是缺血所造成的股骨头部骨和骨髓组织坏死 ,其病因和发病机制尚不完全清楚。在股骨头坏死的病变发展过程中伴随有骨修复 (爬行替代 ) :坏死区周围骨组织中的破骨细胞受各种调节因子影响向坏死区迁徙 ,吸收坏死骨 ;周围血管长入坏死区 ;周围正常骨组织中的成骨细胞启动成骨过程形成新骨而逐步取代死骨。除非股骨头坏死范围较小(小于股骨头体积的 15 %且仅位于内侧 ) ,这种骨修复的效果很微弱。结果是关节软骨下骨由于力学性能逐渐减弱而发生频繁的疲劳骨折 ,继而发生关节软骨面塌陷 ,造成髋关节结构的破坏。股骨头坏死的确切发病率…     

缺血性坏死区位置和大小对股骨头应力的影响

为研究股骨头缺血性坏死区域位置和大小对股骨头软骨下骨板应力的影响。采用实验应力分析的光测弹性力学方法，设计环氧树脂平面光弹模型。计算软骨下骨板的应力，结果表明紧邻软骨下骨板的或坏死区较大的骨坏死将对骨板产生很大应力，说明对因坏死或钻孔等造成的股骨头空洞进行植骨术是必要的。     

健康中国人股骨头软骨下骨及股骨头缺血性坏死软骨下骨胶原、蛋白聚糖含量的测定及意义

作者对２０例健康中国人股骨头软骨下骨及２０例股骨头缺血性坏死股骨头软骨下骨的胶原及蛋白聚糖的含量进行了测定及比较，确立了健康中国人股骨头软骨下骨胶原及蛋白聚糖的正常参考范围，为研究疾病状态下股骨头软骨下骨胶原及蛋白聚糖含量的变化提供了正常参数。同时，通过对股骨头缺血性坏死的股骨头软骨下骨的胶原和蛋白聚糖的定量分析，进一步弄清了股骨头缺血性坏死过程中的病理改变基础，发现了股骨头缺血性坏死后软骨下骨胶原及蛋白聚糖均降低，骨修复机能减弱这一代谢的基本病理变化。     

健康中国人股骨头软骨下骨及股骨头缺血性坏死软骨下骨胶原,蛋白…

作者对２０例健康中国人股骨头软骨下骨及２０例股骨头缺血性坏死股骨头软骨下骨的胶原及蛋白聚糖的含量进行了测定及比较，确立了健康中国人股骨头软骨下骨胶原及蛋白聚糖的正常参考范围，为研究疾病状态下股骨头软骨下骨胶原及蛋白糖含量的变化提供了正常参数。同时，通过对股骨头缺血性坏死的股骨头软骨下骨的胶原和蛋白聚糖的定量分析，进一步弄清了股骨头缺血性坏死过程中的病理改变基础，发现了股骨头缺血性坏死后软骨下骨胶原     

股骨头缺血性坏死介入疗法的实验研究和临床应用

本研究采用介入疗法对骨头缺血性坏死进行了动物模型复制和１５２例患者的临床应用，动物实验治疗组与模型组比较，前者股骨头软骨下区损伤程度较骨复较明显。临床观察介入治疗对改善症状，缓解疼痛和恢复骨关节功能有较明显疗效。本研究的作用机理是通过局部给药，保证了病变部位血管内药物浓度，达到扩张血管，溶解脂肪栓子，改善血供的目的，对延缓骨坏死的发展，促进股骨头的修复和新生骨形成起一定的作用，为治疗股骨头坏死提供     

Effects of Structural Changes in Subchondral Bone on Articular Cartilage in a Beagle Dog Model

Objective Using MR T2-mapping and histopathologic score for articular cartilage to evaluate the effect of structural changes in subchondral bone on articular cartilage. Methods Twenty-four male Beagle dogs were randomly divided into a subchondral bone defect group(n = 12) and a bone cement group(n = 12). Models of subchondral bone defectin the medial tibial plateau and subchondral bone filled with bone cement were constructed. In all dogs, the left knee joint was used as the experimental sideand the right knee as the sham side. The T2 value for articular cartilage at the medial tibial plateau was measured at postoperative weeks 4, 8, 16, and 24. The articular cartilage specimens were stained with hematoxylin and eosin, and evaluated using the Mankin score. Results There was a statistically significant difference(P 0.05) in Mankin score between the bone defect group and the cement group at postoperative weeks 16 and 24. There was a statistically significant difference in the T2 values between the bone defect group and its sham group(P 0.05) from week 8, and between the cement group and its sham group(P 0.05) from week 16. There was significant difference in T2 values between the two experimental groups at postoperative week 24(P 0.01). The T2 value for articular cartilage was positively correlated with the Mankin score(ρ = 0.758, P 0.01). Conclusion Structural changes in subchondral bone can lead to degeneration of the adjacent articular cartilage. Defects in subchondral bone cause more severe degeneration of cartilage than subchondral bone filled with cement. The T2 value for articular cartilage increases with the extent of degeneration. MR T2-mapping images and the T2 value for articular cartilage can indicate earlycartilage degeneration.     

自体骨-骨膜移植修复关节软骨缺损的实验研究

目的　通过自体骨 -骨膜移植修复兔关节软骨缺损 ,探讨骨膜间充质细胞对关节透明软骨组织全层缺损修复的作用与机制。方法　以成年兔胫骨内上侧的骨 -骨膜组织作为供体 ,镶嵌式植入兔自体髌股关节之股骨滑车关节软骨等大、相同形状的全层缺损区 ,术后 4～ 2 4周分别对缺损修复情况进行大体、组织学及电镜观察。结果　自体骨 -骨膜移植组织与缺损周围组织完全愈合 ,组织学及电镜观察显示修复组织为透明软骨组织。结论　自体骨 -骨膜组织移植修补关节软骨缺损可以诱导关节软骨缺损以透明软骨方式进行修复 ,这为临床应用自体骨 -骨膜组织移植修复关节软骨缺损提供了理论依据     

Repair of articular cartilage defects in minipigs by microfracture surgery and BMSCs transplantation

Objective：To investigate the feasibility of minimal invasive repair of cartilage defect by arthroscope-aided microfracture surgery and autologous transplantation of mesenchymal stem cells. Methods： Bone marrow of minipigs was taken out and the bone marrow derived mesenchymal stem cells （BMSCs） were isolated and cultured to passage 3. Then 6 minipigs were randomly divided into 2 groups with 6 knees in each group. After the articular cartilage defect was induced in each knee, the left defect received microfracture surgery and was injected with 2.5 ml BMSCs cells at a concentration of 3×107 cells/ml into the articular cavity; while right knee got single microfracture or served as blank control group. The animals were killed at 8 or 16 weeks, and the repair tissue was histologically and immunohistochemically examined for the presence of type Ⅱ collagen and glycosaminoglycans （GAGs） at 8 and 16 weeks. Results： Eight weeks after the surgery, the overlying articular surface of the cartilage defect showed normal color and integrated to adjacent cartilage. And 16 weeks after surgery, hyaline cartilage was observed at the repairing tissues and immunostaining indicated the diffuse presence of this type Ⅱ collagen and GAGs throughout the repair cartilage in the treated defects. Single microfracture group had the repairing of fibrocartilage, while during the treatment, the defects of blank group were covered with fewer fiber tissues, and no blood capillary growth or any immunological rejection was observed. Conclusion： Microfracture technique and BMSCs transplantation to repair cartilage defect is characterized with minimal invasion and easy operation, and it will greatly promote the regeneration repair of articular cartilage defect.     

兔膝关节软骨缺损修复的初步研究

目的　通过髓腔细胞的分化、生长及应用生长因子 ,修复穿透软骨下骨的关节软骨损伤。方法　采用胶原凝胶与髓腔细胞相混 ,植入兔膝关节实验性软骨缺损区 ,并加入少量细胞生长因子 ,观察软骨缺损修复情况。结果　胶原凝胶移植后的修复组织为透明软骨样组织 ,表面光滑 ,基底部骨小梁形成良好 ,且与碱性成纤维细胞生长因子相混合后 ,其修复组织生长似乎更好一些 ;而单纯钻孔组的修复则是不完全的 ,形成以纤维组织为主的修复组织。结论　关节软骨下髓腔内的间叶细胞在胶原凝胶载体支架的保护下 ,关节腔内特定的局部微环境使其向软骨细胞转化 ,形成修复组织     

急性膝关节软骨损伤的MRI表现

目的:分析急性膝关节软骨损伤的MRI表现,以提高对MRI诊断的认识。方法:回顾性分析35例有明确膝关节外伤史,且经关节镜和手术证实为关节软骨损伤患者的膝关节MRI表现,着重观察关节软骨及软骨下骨髓的改变。结果:35例患者共发现52处软骨损伤,其中软骨形态正常,信号异常7处(5例),软骨局限性变薄6处(4例),软骨压迹5处(3例),软骨凹凸不平7处(4例),软骨裂隙状中断10处(6例),软骨缺损11处(9例),软骨缺损伴关节内游离软骨体6处(4例)。MRI还发现软骨损伤附近骨挫伤、隐匿性骨折、半月板及韧带等其他关节结构的损伤。结论:MRI检查能较准确的显示急性膝关节软骨损伤的部位、范围和类型,是急性软骨损伤较佳的无创性检查方法。     

关节软骨下骨移植后对关节软骨影响的实验研究

目的：探讨关节软骨下大块骨缺损骨移植后，局部成骨活动的发生与演变、关节软骨的活性变化及术后关节面塌陷、关节软骨退变等并发症的原因。方法：在家兔胫骨上端内侧，模拟临床骨肿瘤刮除，建立关节软骨下大块骨缺损动物模型，采用新鲜自体骨与同种异体脱钙骨移植后，通过大体观察、组织学观察、放射自显影方法进行动态观察。结果：模型建立２周后，软骨下骨完全坏死，出现吸收腔；４周时吸收腔内出现新的毛细血管，新骨开始沉积；到１２周时，坏死软骨下骨中毛细血管完全恢复，有８２５％的死骨被新骨替代。结论：（１）关节软骨下骨移植时，大量刮除软骨下骨，会增高术后关节软骨退变的发生率。（２）在关节软骨下骨移植时，如果大量刮除软骨下骨，将引起软骨下骨的缺血坏死，坏死的软骨下骨将逐渐被新生骨爬行替代。（３）用新鲜自体骨与异体脱钙骨移植修复关节软骨下大块骨缺损相比较，均经历了被吸收、血管长入、新骨形成取代移植骨的过程，愈合及修复程度均无显著差异。     

带阔筋膜张肌蒂胫骨骨膜移植术治疗骨关节炎症骨不连

目的　探讨带阔筋膜张肌蒂胫骨骨膜移植术修复骨关节软骨缺损及骨不连。方法　对 4例髋关节结核行病灶清除而有软骨缺损 ;1例股骨骨髓炎行病灶清除 ,开窗 ,减压 ,肌瓣填塞 ;1例股骨骨不连 ,采用带阔筋膜张肌蒂胫骨骨膜 游离骨膜移植。结果　髋关节功能不同程度恢复 ,无融合或强直 ,恢复正常工作 ,日常生活可自理 ,疼痛完全缓解。带阔筋膜张肌蒂胫骨骨膜移植血运建立快 ,成软骨作用强 ,修复骨缺损并具有抗炎及关节外成骨作用。结论　带阔筋膜张肌蒂胫骨骨膜移植术对关节软骨缺损、骨不连、骨髓炎均具有成软骨、成骨及增强抗感染的作用 ,修复重建关节功能效果好 ,在髋关节软骨缺损重建头臼功能中可作为首选术式。     

Scanning electron microscopic study of subchondral bone tissues in osteoarthritic femoral head.

During total hip replacement for 12 cases of advanced osteoarthritis of the hip joint in aged women, three types of diseased or abnormal articular cartilage with different degrees of severity (white articular cartilage, white and hyperplastic articular cartilage, and yellowish articular cartilage) and ivory bone were obtained together with their subchondral bone tissues. These specimens were processed and studied under scanning electron microscope and were compared with sex- and age-matched non-osteoarthritic femoral head articular cartilage specimens. The following findings were observed: 1. In non-osteoarthritic femoral head, the subchondral bone plate was quite thin. The bone plate connected on its deep surface with the lattice-work of trabeculae of the epiphyseal region. The trabeculae were fine and smooth and some revealed round or spindle-shaped callus resulted from microfracture. 2. In osteoarthritic femoral heads, with increased the severity of the articular lesion, the articular cartilage gradually became thinned out and eventually lost. The subchondral bone plate was markedly thickened. The epiphyseal trabeculae were also thickened and turned rough so that the lattice-work pattern gradually disappeared. The thickened trabeculae finally fused into a large piece of dense bone tissue. No microfracture was detected. These changes were attributable to the increased stress imposed on the subchondral bone tissues as a result of defective articular cartilage. Consequently, the changes on the part of the subchondral bone tissues of the osteoarthritic femoral heads were the sequent, rather than the cause, of the articular lesions.

     

骨不连与骨形成蛋白

研究骨不连发生的原理及骨不连与骨诱导因子的关系是抗击有不连发生机理的重要课题。方法：将兔桡骨中段告成ｃｍ的缺损，Ａ组术后即放入ＢＭＰ，Ｂ组术后４周放入ＢＭＰ，Ｃ组为在Ａ组术后８周放入ＢＭＰ。结果：发现ＢＭＰ植入８周时形成骨小梁。Ｂ组和Ｃ组，骨缺损修复仍然取得满意的效果。