CAJ | 학술논문

背景：研究发现，在灵长类动物尺骨缺损模型中外源性重组人骨形态发生蛋白7能治愈自体骨不能愈合的缺损。 　　目的：观察兔髋臼软骨局部损伤对髋臼发育及髋臼软骨中骨形态发生蛋白7含量的影响。 　　方法：选用4周龄家兔36只，麻醉后暴露左侧髋关节。用刮勺在髋臼 Y 型软骨后上部刮除约1.5 mm×2 mm×0.5 mm髋臼软骨作为实验侧；同时按上述方法暴露兔右侧髋关节，不损伤软骨作为对照侧。术后第4，6，8周分别拍摄骨盆平片观察髋关节发育状况。并且每次处死12只兔并对标本进行大体观察、组织学、免疫组织化学法检测。 　　结果与结论：实验侧术后4，6，8周X射线测定示髋臼逐渐变浅且形态不规则，股骨头变得扁平，出现髋关节半脱位和脱位。苏木精-伊红染色示髋臼软骨缺损区再生填充组织表面微薄层的纤维组织向深层逐渐移行为纤维软骨，软骨增殖层和肥大层软骨细胞失去正常的柱状结构，排列较乱。免疫组织化学检测示随着时间增加，标本中骨形态发生蛋白7染色由呈强阳性渐变淡。对照侧具有典型的关节透明软骨结构。结果提示，髋臼软骨破坏可引起发育性髋关节发育不良表现，并且髋臼软骨破坏区骨形态发生蛋白7含量随时间的延长而减少。
배경：연구발현，재령장류동물척골결손모형중외원성중조인골형태발생단백7능치유자체골불능유합적결손。 　　목적：관찰토관구연골국부손상대관구발육급관구연골중골형태발생단백7함량적영향。 　　방법：선용4주령가토36지，마취후폭로좌측관관절。용괄작재관구 Y 형연골후상부괄제약1.5 mm×2 mm×0.5 mm관구연골작위실험측；동시안상술방법폭로토우측관관절，불손상연골작위대조측。술후제4，6，8주분별박섭골분평편관찰관관절발육상황。병차매차처사12지토병대표본진행대체관찰、조직학、면역조직화학법검측。 　　결과여결론：실험측술후4，6，8주X사선측정시관구축점변천차형태불규칙，고골두변득편평，출현관관절반탈위화탈위。소목정-이홍염색시관구연골결손구재생전충조직표면미박층적섬유조직향심층축점이행위섬유연골，연골증식층화비대층연골세포실거정상적주상결구，배렬교란。면역조직화학검측시수착시간증가，표본중골형태발생단백7염색유정강양성점변담。대조측구유전형적관절투명연골결구。결과제시，관구연골파배가인기발육성관관절발육불량표현，병차관구연골파배구골형태발생단백7함량수시간적연장이감소。
BACKGROUND:In a primate model of ulna defect, exogenous recombinant human bone morphogenetic protein-7 can promote the healing of autologous bone defect. OBJECTIVE:To probe into the variation of the development of acetabulum and the content of bone morphogenetic protein 7 after local lesion of cartilage acetabularis in rabbits. METHODS:Thirty-six rabbits (4-week-old) were anesthetized to expose the left hip joint by the anterolateral approach. A 1.5 mm×2.0 mm×0.5 mm sample of the cartilago acetabularis was scraped from each rabbit as experimental group;and the right hip joint was also exposed as control group. To evaluate the hip development, X-rays were used at 4, 6, 8 weeks after the operation, 12 rabbits were kil ed randomly at 4, 6, 8 weeks after operation for general observation, histological examination and immunohistochemical assay. RESULTS AND CONCLUSION:By the radiographic examination, the acetabulums became shal ow and irregular in morphology. The shape of these femoral heads was applanate. Semiluxation and dislocation could be observed in some cases. Hematoxylin-eosin staining showed the regenerated fibrous tissue in the lesion region gradual y migrated from the meager layer to the deep layer to form fibrous cartilage, cartilage cells from proliferative and hypertrophic layers lost their normal columnar structure and arranged disorderly. Immunohistochemistry detection showed that over time, the dyeing of bone morphogenetic protein 7 became light in color. In the control group, a typical structure of articular hyaline cartilage was observed. The results suggest that damaging the cartilago acetabularis led to developmental hip dysplasia, and the content of bone morphogenetic protein 7 from al regions decreased by the extension of time.