论文部分内容阅读
[目的]通过增加软骨下骨硬度模拟软骨下骨硬化,诱发骨关节炎的发生,探讨骨关节炎发病机制.[方法]调整聚甲基丙烯酸甲酯粉剂(polymethylmethacrylate,PMMA)、甲基丙烯酸甲酯液剂(methylmethacrylate,MMA)、羟基磷灰石(hydroxyapatite,HA)和蒸馏水的比例,使反应温度低于40℃,测量该比例下聚合后的极限强度和刚度并与软骨下骨比较,制得PMMA/HA复合材料.刮除兔胫骨平台内侧软骨下骨后置入复合材料,对术后3、6、9、12周的关节软骨进行组织学观察,免疫组化法榆测Ⅱ型胶原和基质会属蛋白酶-1(matrix metallo proteinase-1,MMP-1)在软骨中的表达和分布,并与空白、对照组比较.透射电镜观察空白、6、12周组软骨细胞改变.[结果]该复合材料置入软骨下骨后,随观察时间延长实验组逐渐出现退变,Mankin分级逐渐升高,电镜也显示实验组软骨细胞退变表现.免疫组化显示Ⅱ型胶原表达增加主要在移行层和深层上部,MMP-1表达以软骨表层及中上层居多,随观察时间延长二者染色强度均逐渐升高.[结论]增加软骨下骨硬度后,诱发了兔膝骨关节炎.提示软骨下骨硬化可引起软骨退变,其可能是骨关节炎的病因之一.“,”[Objective]To investigate the pathogenesis of osteoarthritis by increasing stiffness of subchondral bone to simu-late subchondral bone sclerosis to induce the osteoarthritis. [Methods]The proportion between polymethylmethacrylate (PM-MA), methylmethacrylate (MMA), hydroxyapatite (HA) and distilled water was adjusted to keep the maximum reaction tem-perature under 40℃. The composite material PMMA/HA was obtained and compressed on a mechanical material machine to de-termine its ultimate strength and stiffness, which were compared with those of subchondral bone. The subehondral bone of medial tibial plateau was scraped, where the composite material PMMA/HA was implanted into. Rabbits were sacrificed at 3, 6, 9 and 12 weeks, respectively. The articular cartilages of the medial tibia]plateau were harvested for histological observation. Immuno-histochemical analysis was adopted to record the expression and distribution of collagen type Ⅱ and MMP-1 in cartilage at pro-tein level, which were compared with the blank and control groups. Transmission electron microscope was used to examine the ultramicroscopic changes of chondrocytes in blank and 6, 12-week-postsurgery groups. [Results]With the time going, the experimental groups gradually presented degeneration, and had increased histological Mankin score. TEM demonstrated degenera-tive changes of chondrocytes. Collagen type Ⅱ expressed mainly in transition zone and upper deep zone, and MMP-1 expressed predominantly in the superficial and upper intermediate layers of cartilage. Both expressions steadily increased with time passing. [Conclusion]The increased stiffness of subchondral bone induced osteoarthritis in rabbits, which suggests that subcondral bone sclerosis may induce cartilage damage, and that subcondral bone sclerosis is one of the initial pathogenesis of osteoarthritis.