中文摘要：

背景关节的软骨损害是普通疾病，和发生关节穿，退化，损伤和运动损害正在增加，它经常导致残疾并且减少生活的质量。不幸地，关节的软骨缺点的修理总是不提供令人满意的 outcomes.Methods Chondrocyte，造骨细胞 composites 用一个生物反应器是 co 有教养的。软骨缺点与房间被对待-- tricalcium 磷酸盐(植入进 osteochondral 的-TCP) composites 在狗背叛在 vivo ，用 mosaicplasty ，由放 chondrocyte --在缺点和造骨细胞上的 TCP 支架 composites --在 defect.Results 电子显微镜学下面的 TCP 支架 composites 表明导致的 chondrocytes 和造骨细胞在 -TCP 支架显示出好粘合剂前进和增长。在试验性的组的修理纸巾维持了他们的厚度到原来的缺点的完整的深度，作为与否定控制组相比(q=12.3370， P 0.01；q=31.5393， P 0.01 ) 提供的 .Conclusions 灌注文化支撑了滋养的供应和煤气的交换进大支架的中心。这个灌注生物反应器使 chondrocytes 和造骨细胞能在三维的脚手架幸存并且增殖。

英文摘要：

Background Articular cartilage injury is a common disease, and the incidence of articular wear, degeneration, trauma and sports injury is increasing, which often lead to disability and reduced quality of life. Unfortunately repair of articular cartilage defects do not always provide satisfactory outcomes. Methods Chondrocyte and osteoblast composites were co-cultured using a bioreactor. The cartilage defects were treated with cell-β-tricalcium phosphate （β-TCP） composites implanted into osteochondral defects in dogs, in vivo, using mosaicplasty, by placing chondrocyte-β-TCP scaffold composites on top of the defect and osteoblast-β-TCP scaffold composites below the defect.Results Electron microscopy revealed that the induced chondrocytes and osteoblast showed fine adhesive progression and proliferation in the β-TCP scaffold. The repaired tissues in the experimental group maintained their thickness to the full depth of the original defects, as compared with the negative control group （q=12.3370, P 〈0.01; q=31.5393, P 〈0.01）. Conclusions Perfusion culture provided sustained nutrient supply and gas exchange into the center of the large scaffold. This perfusion bioreactor enables the chondrocytes and osteoblasts to survive and proliferate in a three-dimensional scaffold.