中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2013年
4期
796-798
,共3页
王光达%张祚福%曹春妮%齐晓军%林春华
王光達%張祚福%曹春妮%齊曉軍%林春華
왕광체%장조복%조춘니%제효군%림춘화
膝关节%前交叉韧带%有限元分析%生物力学
膝關節%前交扠韌帶%有限元分析%生物力學
슬관절%전교차인대%유한원분석%생물역학
Knee joint%Anterior cruciate ligament%Finite element analysis%Biomechanics
目的 对膝关节前交叉韧带(ACL)进行生物力学分析,探讨ACL的生物力学作用.方法 建立膝关节三维有限元模型,施加1150 N的轴向压力和100 N胫骨前向力,对膝关节进行以下2个方面生物力学分析:具有完整ACL的膝关节、切除ACL的膝关节.结果 ACL完整时,胫骨水平前向移位4.5 mm,ACL承受全部前向负荷的78%,轴向负荷的57%由膝关节外侧间室承载.切断ACL后,胫骨水平前向位移增至16.5 mm,轴向负荷70%由内侧间室承载,半月板及关节软骨应力增大.结论 ACL为限制胫骨前移的首要的结构,ACL切除后,膝关节明显不稳定,因此在ACL损伤后要及时修复以恢复膝关节正常的功能.
目的 對膝關節前交扠韌帶(ACL)進行生物力學分析,探討ACL的生物力學作用.方法 建立膝關節三維有限元模型,施加1150 N的軸嚮壓力和100 N脛骨前嚮力,對膝關節進行以下2箇方麵生物力學分析:具有完整ACL的膝關節、切除ACL的膝關節.結果 ACL完整時,脛骨水平前嚮移位4.5 mm,ACL承受全部前嚮負荷的78%,軸嚮負荷的57%由膝關節外側間室承載.切斷ACL後,脛骨水平前嚮位移增至16.5 mm,軸嚮負荷70%由內側間室承載,半月闆及關節軟骨應力增大.結論 ACL為限製脛骨前移的首要的結構,ACL切除後,膝關節明顯不穩定,因此在ACL損傷後要及時脩複以恢複膝關節正常的功能.
목적 대슬관절전교차인대(ACL)진행생물역학분석,탐토ACL적생물역학작용.방법 건립슬관절삼유유한원모형,시가1150 N적축향압력화100 N경골전향력,대슬관절진행이하2개방면생물역학분석:구유완정ACL적슬관절、절제ACL적슬관절.결과 ACL완정시,경골수평전향이위4.5 mm,ACL승수전부전향부하적78%,축향부하적57%유슬관절외측간실승재.절단ACL후,경골수평전향위이증지16.5 mm,축향부하70%유내측간실승재,반월판급관절연골응력증대.결론 ACL위한제경골전이적수요적결구,ACL절제후,슬관절명현불은정,인차재ACL손상후요급시수복이회복슬관절정상적공능.
Objective To analyze the biomechanics of the anterior cruciate ligament (ACL).Methods An intact three-dimensional finite model of knee joint was established.With the model to have a finite element analysis of biomechanics of the knee joint.Two cases were simulated under a axial compressive load of 1150 N and an anterior tibial load of 134 N:a knee with:(a) Native ACL,(b) No ACL.Results With native ACL,the tibia shift forward 4.5 mm,the ACL bears 78% of the anterior tibial load,and the lateral compartment bears 57% of the axial compressive load.With no ACL,the tibia shift forward 16.5 mm,and the medial compartment bears 70% of the axial compressive load,the stress of the menisci and cartilage increased.Conclusion The ACL is the principle structure in retaining stability of the knee joint,it is essential to be adequately repaired or replaced after injury to restore its normal function.