CAJ | 학술논문

背景:以往对髋臼发育不良的研究集中在X射线形态学,关于机械应力如何影响髋臼发育及解除机械压力后,髋臼发育不良修复的演变规律研究较少.目的:阐明异常机械应力对髋臼发育,尤其对髋臼软骨生长板内软骨细胞增殖的影响,探讨髋臼发育不良的修复方法.设计:随机对照的实验研究.地点和对象:实验地点为中国医科大学.对象:清洁级Wistar大鼠60只,体质量150～200 g,均为雌性,周龄为3周,由中国医科大学实验动物部提供.饲养温度18～25℃,湿度40%～70%.干预:将3周龄的Wistar大鼠随机数字表法分成3组,每组20只,左侧髋关节为实验侧,右侧为对照侧.A组:2周内反复将髋关节手法脱位,而后将其复位;B组:膝关节伸直位钢针固定,制作髋臼发育不良的动物模型,2周后拔出钢针;C组:持续伸直位固定膝关节.主要观察指标:分别于5,7,9,12周龄时进行钼靶软X射线、组织形态学及透射电镜观察.结果:A组:5周龄时髋臼角比对侧增大约5°,软骨生长板内增殖层软骨细胞极向紊乱,7,9,12周龄时变化轻,两侧无差异;B组:5周龄时髋臼角比对侧明显增大,7周龄时柱状细胞层极性紊乱,肥大的细胞层增多,9,12周龄时近正常;C组:髋臼角比对侧持续增大,没有任何改善倾向,12周龄时臼缘内翻扁平,无明显柱状细胞排列,细胞核变小,细胞器减少,空泡形成.结论:髋臼发育旺盛期解除异常机械应力,恢复头臼同心性,髋臼发育不良有治愈倾向.造成髋臼发育不良的直接原因是软骨生长板内增殖层软骨细胞代谢功能发生改变,造成骨化延迟.
배경:이왕대관구발육불량적연구집중재X사선형태학,관우궤계응력여하영향관구발육급해제궤계압력후,관구발육불량수복적연변규률연구교소.목적:천명이상궤계응력대관구발육,우기대관구연골생장판내연골세포증식적영향,탐토관구발육불량적수복방법.설계:수궤대조적실험연구.지점화대상:실험지점위중국의과대학.대상:청길급Wistar대서60지,체질량150～200 g,균위자성,주령위3주,유중국의과대학실험동물부제공.사양온도18～25℃,습도40%～70%.간예:장3주령적Wistar대서수궤수자표법분성3조,매조20지,좌측관관절위실험측,우측위대조측.A조:2주내반복장관관절수법탈위,이후장기복위;B조:슬관절신직위강침고정,제작관구발육불량적동물모형,2주후발출강침;C조:지속신직위고정슬관절.주요관찰지표:분별우5,7,9,12주령시진행목파연X사선、조직형태학급투사전경관찰.결과:A조:5주령시관구각비대측증대약5°,연골생장판내증식층연골세포겁향문란,7,9,12주령시변화경,량측무차이;B조:5주령시관구각비대측명현증대,7주령시주상세포층겁성문란,비대적세포층증다,9,12주령시근정상;C조:관구각비대측지속증대,몰유임하개선경향,12주령시구연내번편평,무명현주상세포배렬,세포핵변소,세포기감소,공포형성.결론:관구발육왕성기해제이상궤계응력,회복두구동심성,관구발육불량유치유경향.조성관구발육불량적직접원인시연골생장판내증식층연골세포대사공능발생개변,조성골화연지.
BACKGROUND: The previous researches on the hypogenesis of acetabulum concentrated on X-ray morphology. And there are few researches on the impact of mechanical stress force on the development of acetabulum and the evolution disciplinarian in the restoration of acetabular dysplasia after the removal of mechanical pressure.OBJECTIVE: To clarify the impact of abnormal mechanical stress force on the development of acetabulum, especially on the proliferation of chondrocytes in the chondral growth plate of acetabulum, for the discussion of the restorative methods in acetabular dysplasia.DESIGN: A randomized controlled study was conducted.SETTING and PARTICIPANTS: Setting was in China Medical University. Subjects were 60 females, 3-week old Wistar rats in cleanness grade with a body mass from 150 g to 200 g obtained from the Experimental Animal Center of China Medical University, which were fed at 18 - 25 ℃ and in the humidity of 40% to 70%.INTERVENTION: Three-week old Wistar rats were randomly allocated into 3 groups according to random number table with 20 rats each. The left hip joint was set as study side and the right side was set as control side. Group A: hit joint was repeated dislocated and repositioned by manipulation within 2 weeks; Group B: the knee joint was straightened for fixation by Kirschner wire to establish the animal model of acetabular dysplasia. Kirschner wire was removed after 2 weeks; Group C: the knee joint was straightened for continuous fixation.MAIN OUTCOME MEASURES: Molybdenum X-ray, histomorphologyand transmision electron microscope observations were operated at age of 5,7, 9 and 12 weeks respectively.RESULTS: Group A: at 5-week old, the acetabular angle increased about 5° compared with the other side, and polar derangement of chondrocyte was found in the proliferation layer of the chondral growth plate. The changes at age 7, 9 and 12 weeks were mild with no difference between two sides. Group B: at 5-week old, the acetabular angle significantly increased compared with the other side. At 7-week old, the columnar cell layer was in polar derangement with increased hypertrophic cell layers. At age 9 and 12 weeks, the cells were close to normal. Group C: the acetabular angle continuously increased compared with the other side with no improvement tendency. At age 12 weeks, the acetabular border was entropion and applanation with no obvious arrangement of columnar cells. The nucleus became smaller and the cell organs decreased with the formation of vacuole.CONCLUSION: The removal of abnormal mechanical stress force and restore the concentricity between femoral head and acetabulum in the development bloom phase could hopefully cure the acetabular dysplasia. The direct reason of acetabular dysplasia is the alteration in the metabolism of chondrocyte in the proliferation layer of the chondral growth plate, which causes the delay in the ossification.