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基于三维有限元方法探索ACL断裂后胫股关节轨迹异常对半月板和软骨应力分布的影响
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摘要
研究背景
     前交叉韧带(anterior cruciate ligament,ACL)断裂可导致膝关节运动不稳,引起胫骨与股骨之间的位移和旋转异常。胫骨与股骨之间的运动关系比较复杂,包括6个自由度的位移和旋转,以及股骨内外侧髁的前后、内外和远近位移。ACL是维持膝关节正常活动的关键纽带。当ACL断裂后,膝关节在屈曲过程中会出现胫骨前移、内移和内旋增加。以往许多关于ACL断裂后膝关节运动的研究,把股骨的运动作为一个整体来看待,而忽略了内侧髁和外侧髁的运动。因此,ACL断裂对内外侧髁运动的影响在目前仍认识不足,表现在ACL断裂对内外侧髁前后位移的影响仍存在分歧,而且尚未有文献报道ACL断裂对内外侧髁内外和远近位移的影响。全面地了解ACL断裂后胫股关节6个自由度运动以及股骨内外侧髁运动的异常变化,将有助于进一步认识ACL断裂对股骨运动产生的影响,有助于改进ACL重建术的外科技术。
     ACL断裂引起的胫股关节运动轨迹改变可进一步引发半月板和软骨继发性损伤。随着ACL断裂后胫股关节位移和旋转的改变,胫股软骨接触点在屈曲过程中出现后移和外移增加,从而引起关节负荷从负重区转移到非负重区,造成非负重区软骨应力增加。此外,ACL断裂后内侧半月板所承受的应力也明显增加。可见,ACL断裂会引起关节间应力重新分配,容易导致半月板和软骨继发性损伤。既往的研究很少对ACL断裂后半月板(前角、体部和后角)和软骨(胫骨软骨和股骨软骨)各部分的应力情况进行细分观察。临床观察显示,ACL断裂对半月板和软骨各部分的影响并不完全相同。因此,全面地了解ACL断裂后半月板和软骨各部分异常的应力分布,将有助于了解半月板和软骨上出现继发性损伤的好发部位以及了解潜在的损伤机制。
     有限元分析法是获得膝关节半月板和软骨上应力分布的有效方法。该方法以研究对象的几何结构为基础构建生物力学模型,赋予恰当的材料属性后,加载负荷和边界条件,对研究对象进行受力分析和运动分析。有限元分析法可以克服体外实验中标本不易获得、标本不能重复使用等缺点,而且能获得体外实验不易获得的数据,如韧带张力,关节间的接触力、接触面积,半月板和软骨的应力、应变等。有限元分析法已成为研究关节生物力学的可靠手段。
     在本文中,我们应用双平面X光技术全面地测量直立负重屈曲过程中,胫股关节6个自由度的运动以及股骨内外侧髁前后、内外和远近位移。直立负重比非负重能更好地反映和评估ACL断裂病理状态下的胫股关节运动。本文先建立应用该技术测量胫股关节运动的方法,以及验证该技术测量的准确性;接着,我们使用该技术全面地测量并分析膝关节在直立负重屈曲过程中,ACL断裂后胫股关节位移和旋转的变化;然后,我们把ACL断裂后胫股关节运动轨迹改变的数据应用到有限元模型中,模拟分析ACL断裂后内外侧半月板前角、体部和后角,以及内外侧胫骨软骨和股骨软骨上应力分布的变化。
     研究方法
     1.双平面X光技术测量胫股关节位移和旋转方法的建立与体外实验的验证。使用两台X光机从正交方向同时采集膝关节6个屈曲位置的双平面X光影像,CT扫描伸直位的膝关节并重建成胫股关节三维模型,然后用三维模型与双平面X光影像进行图像配准,获得6个屈曲位置的胫股关节模型,通过建立在模型上的关节坐标系测量出胫股关节在屈曲过程中的位移和旋转。验证过程如下:CT直接扫描处于6个屈曲位置的同一个膝关节,并重建成6个位置的胫股关节模型,通过同一个坐标系测量出胫股关节的位移和旋转,并以此运动数据作为参考标准,考查双平面X光技术所获得的胫股关节运动数据的准确性。
     2.测量ACL断裂后直立负重屈曲过程中胫股关节的位移和旋转。应用双平面X光技术,测量单侧ACL断裂患者从伸直位到120°屈曲的弓步下蹲过程中,ACL断裂膝和正常对侧膝的胫股关节位移和旋转,然后对比分析患膝与健膝之间胫股关节位移和旋转的差异,获得ACL断裂后胫股关节运动轨迹改变的数据。
     3.探讨ACL断裂对半月板和软骨应力分布的影响。应用有限元分析法计算出ACL断裂膝和正常膝中半月板和软骨各部分上的应力分布。构建胫股关节有限元模型,并对此模型的有效性进行验证。创建ACL断裂有限元模型,把ACL断裂后胫股关节运动轨迹改变的数据作为边界条件应用到该模型中。计算出伸直位、15°和30°屈曲时ACL断裂模型和正常模型中半月板和软骨上的应力分布,并对比分析两个模型之间半月板和软骨各部分上应力的差异。
     研究结果
     1.双平面X光技术能较准确地测量胫股关节的位移和旋转。该技术的精确度在前后、内外和远近位移上分别为0.88mm、0.65mm和0.61mm,在屈伸、内外旋转和内外翻转上分别为1.03°、1.09°和0.76°。
     2.膝关节在下蹲屈曲过程中,在伸直位和15°屈曲时,ACL断裂后股骨外侧髁的后移增加,伴随着股骨的后移和外旋增加。而对于内侧髁的前后位移,内外侧髁和股骨的内外、远近位移,以及股骨的内外翻转在ACL断裂后均与正常膝相似。
     3.膝关节从15°到60°的下蹲屈曲阶段中,ACL断裂后外侧髁后移的幅度显著减少,这使得股骨后移和外旋的幅度也随之减少。而对于内侧髁前后移动的幅度,内外侧髁和股骨内外、远近移动的幅度,以及股骨内外翻转的幅度在ACL断裂后均与正常膝相似。
     4.在伸直位到30°屈曲之间,ACL断裂后内外侧半月板上的应力均增加。在伸直位时,ACL断裂造成内侧半月板前角的应力增加明显,外侧半月板前角和体部的应力也有所增加;在15°和30°屈曲时,ACL断裂后内侧半月板后角的应力增加明显,而外侧半月板各部位的应力增加不明显。
     5. ACL断裂后内外侧胫股软骨在伸直位到30°屈曲之间所承受的应力均增加,其中,内侧股骨软骨的应力增幅随着屈曲的增加而逐渐升高,内侧胫骨软骨的应力增幅随着屈曲逐渐下降,外侧间室中胫股软骨的应力增幅比较小。
     研究结论
     1.建立了双平面X光技术全面测量胫股关节位移和旋转的方法,经过验证,该技术有效可行。
     2.在膝关节从伸直位到120°的下蹲屈曲过程中,ACL断裂主要改变了股骨外侧髁的前后运动,引起外侧髁在早期屈曲范围内向后松动,而且造成外侧髁在屈曲过程的中间阶段向后移动的幅度显著少于正常膝。
     3.在膝关节从伸直位到30°屈曲之间,ACL断裂主要改变了胫股关节内侧间室的应力分布,引起内侧半月板前角和后角的应力分别在伸直位和屈曲位时明显大于正常膝,并造成内侧股骨软骨应力的增加幅度随着屈曲的加深不断升高。
Introduction
     Anterior cruciate ligament (ACL) rupture leads to the motion instability of the knee,resulting in changed tibiofemoral kinematics. Tibiofemoral motion is relatively complexand includes components of6degrees of freedom kinematics and femoral condylar motion(anterior-posterior, medial-lateral, and proximal-distal translations). ACL is the keyligament for normal knee motion. After ACL rupture, anterior and medial translations andinternal rotation of the tibia increase abnormally during knee flexion. Many previousstudies on tibiofemoral motion after ACL deficiency regarded femoral motion as onemovement, neglecting the motion of the medial and lateral condyles. Therefore, the effectof ACL deficiency on femoral condylar motion remains poorly understood at present.Inconsistent results still exist about the effect of ACL deficiency on femoral condylaranterior-posterior motion. Furthermore, there is no report in documents about the effect ofACL deficiency on femoral condylar medial-lateral and proximal-distal motions. Athorough knowledge of abnormal tibiofemoral6degrees of freedom kinematics andcondylar motion in ACL-deficient knees might further understand the influence of ACLdeficiency on femoral motion, and contribute to improving ACL reconstructive surgicaltechniques.
     The changed tibiofemoral kinematics caused by ACL deficiency might lead tosecondary injury of the meniscus and cartilage. With the changed tibiofemoral translationand rotation in ACL deficiency, posterior and lateral translations of tibiofemoral cartilagecontact point increase abnormally during flexion, resulting in a load shift fromweight-bearing area to non-weight-bearing area, which causes increased cartilage contactstress on the non-weight-bearing area. In addition, the stress on the medial meniscus alsoincreases obviously after ACL deficiency. So it is clear that ACL rupture leads to a redistribution of the interarticular stress, which predisposes the meniscus and cartilage tosecondary injury. Few previous studies have discussed the stress on each part of themeniscus (the anterior horn, the body and the posterior horn) and cartilage (tibial cartilageand femoral cartilage) after ACL rupture. Clinical observations have showed that the effectof ACL deficiency on each part of the meniscus and cartilage is not exactly the same.Therefore, a thorough knowledge of the abnormal stress on each part of the meniscus andcartilage in ACL deficiency might contribute to understanding the frequent areas ofsecondary injury in the meniscus and cartilage and the potential injury mechanism.
     The finite element analysis should be an effective method to obtain the stressdistributions of knee meniscus and cartilage. The work process of this method is as follows:A finite element model is created based on the geometric structure of the object. After themodel is given the right material property, load and boundary conditions, the finite elementanalysis of the force and motion is conducted for the object. The finite element analysis canovercome some disadvantages of in-vitro experiments, such as specimens being not readilyavailable or not used repeatedly. Furthermore, it can obtain the data which are not easy toobtain in in-vitro experiments, such as ligament tension, joint contact force and area, stressand strain on the meniscus and cartilage. The finite element analysis has become a reliablemethod to study the joint biomechanics.
     In the present article, we used biplane radiography technique to measure the thoroughtibiofemoral translation and rotation during upright weight-bearing flexion. The uprightweight-bearing condition is better than the non-weight-bearing condition to reflect andevaluate the pathological knee motion caused by ACL deficiency. The biplane radiographytechnique was first developed to measure the tibiofemoral motion, and accuracy of thistechnique was evaluated. Next, we used biplane radiography to measure and analyze thechanged tibiofemoral6degrees of freedom kinematics and femoral condylar motion(anterior-posterior, medial-lateral, and proximal-distal translations) in ACL-deficient kneesduring upright weight-bearing flexion. Then, we inputted the changed tibiofemoralkinematics after ACL deficiency into the finite element model, so as to analyze the changedstress distributions of the medial and lateral menisci, including the anterior horn, the bodyand the posterior horn, and of the medial and lateral tibiofemoral cartilages in ACL-deficient knees.
     Methods
     1. Biplane radiography technology was developed to measure tibiofemoral kinematicsand was validated in an in-vitro experiment. Two X-ray machines were used tosimultaneously capture the biplane X-ray images of the knee at6flexion positions. Next,the knee at extension was scanned by CT, and the three-dimensional tibiofemoral modelwas reconstructed using CT data. Then, the tibiofemoral model was matched to the biplanetibiofemoral images at6flexion positions, obtaining6tibiofemoral models based onbiplane radiography (BR models). The tibiofemoral kinematics of BR models was measuredthrough a joint coordinate system established on the model. The process of validation is asfollows: The same knee at6flexion positions was directly scanned by CT, and6tibiofemoral models were reconstructed (CT models). The tibiofemoral kinematics of CTmodels was also measured through the same joint coordinate system. Then, the accuracy ofbiplane radiography was evaluated by comparing the tibiofemoral kinematics of BR modelsto CT models (as a reference standard).
     2. The tibiofemoral motion after ACL rupture was measured during uprightweight-bearing flexion. Biplane radiography was used to measure the tibiofemoral motionin ACL-deficient knees and contralateral normal knees during squatting from extension to120°in patients with unilateral ACL rupture. And the tibiofemoral motion between the twosides was compared to obtain the changed kinematics after ACL rupture.
     3. To investigate the effect of ACL rupture on the stress distributions of the meniscusand cartilage, the finite element analysis was used to obtain the changed stress on each partof the meniscus and cartilage in ACL-deficient knees. The finite element tibiofemoralmodel was created, and the model‘s validity was verified. Next, the ACL-deficient modelwas created using the changed kinematics after ACL deficiency as boundary conditions.Then, the stress on each part of the meniscus and cartilage was calculated in theACL-deficient model and the normal model and compared between the two models atextension,15°, and30°flexions.
     Results
     1. Biplane radiography was able to accurately measure the tibiofemoral kinematics. The accuracy of biplane radiography was0.88mm,0.65mm, and0.61mm inanterior-posterior, medial-lateral, and proximal-distal translation, respectively; and1.03°,1.09°and0.76°in flexion-extension, internal-external and adduction-abduction rotation,respectively.
     2. At extension and15°of flexion, increased posterior translation of the lateral condylewas found in ACL-deficient knees, which was accompanied by excess posterior translationand external rotation of the femur during squatting. The anterior-posterior translation of themedial condyle, the medial-lateral and proximal-distal translations of femoral condyles andthe femur, and the femoral adduction-abduction were all comparable betweenACL-deficient knees and normal knees.
     3. On flexion phase from15°to60°during squatting, ACL deficiency led to asignificantly reduced extent of posterior movement of the lateral condyle, which wasaccompanied by reduced extents of posterior movement and external rotation of the femur.The extents of anterior-posterior movement of the medial condyle, of medial-lateral andproximal-distal movements of femoral condyles and the femur, and of femoraladduction-abduction were all comparable between ACL-deficient knees and normal knees.
     4. Between extension and30°of flexion, the stress increased on the medial and lateralmenisci after ACL deficiency. At extension, ACL rupture led to markedly increased stresson the anterior horn of the medial meniscus and slightly increased stress on the anteriorhorn and body of the lateral meniscus. At15°and30°of flexion, the stress increasedobviously on the posterior horn of the medial meniscus, and increased slightly on each partof the lateral meniscus after ACL rupture.
     5. ACL rupture led to increased stress on the medial and lateral tibiofemoral cartilagesbetween extension and30°of flexion. The growth rate of the stress increased gradually onthe medial femoral cartilage but decreased gradually on the medial tibial cartilage in theACL-deficient model during flexion. The growth rate of the stress was small ontibiofemoral cartilage in the lateral compartment after ACL rupture.
     Conclusions
     1. Biplane radiography technology was developed successfully to measure the thoroughtibiofemoral motion and was valid and feasible after verification.
     2. During squatting from extension to120°, ACL deficiency primarily changed theanterior-posterior motion of the lateral condyle, producing not only posterior subluxation atearly flexion positions but also reduced extent of posterior movement on the middle flexionphase.
     3. Between extension and30°of flexion, ACL deficiency primarily changed the stressdistribution of the medial tibiofemoral compartment. After ACL rupture, the stress increasedobviously on the anterior and posterior horns of the medial meniscus at extension and atflexion, respectively. The growth rate of the stress increased gradually on the medialfemoral cartilage in the ACL-deficient model during flexion.
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    4Defrate LE, Papannagari R, Gill TJ, et al. The6degrees of freedom kinematics of the knee after anterior cruciateligament deficiency: an in vivo imaging analysis. Am J Sports Med,2006,34(8):1240-1246.
    5Shefelbine SJ, Ma CB, Lee KY, et al. MRI analysis of in vivo meniscal and tibiofemoral kinematics in ACL-deficientand normal knees. J Orthop Res,2006,24(6):1208-1217.
    1Olsen OE, Myklebust G, Engebretsen L, Bahr R. Injury mechanisms for anterior cruciate ligament injuries in teamhandball: a systematic video analysis. Am J Sports Med,2004,32(4):1002-1012.
    2Logan MC, Williams A, Lavelle J, et al. Tibiofemoral kinematics following successful anterior cruciat e ligamentreconstruction using dynamic multiple resonance imaging. Am J Sports Med,2004,32(4):984-992.
    3Defrate LE, Papannagari R, Gill TJ, et al. The6degrees of freedom kinematics of the knee after anterior cruciateligament deficiency: an in vivo imaging analysis. Am J Sports Med,2006,34(8):1240-1246.
    4Georgoulis AD, Papadonikolakis A, Papageorgiou CD, et al. Three-dimensional tibiofemoral kinematics of the anteriorcruciate ligament-deficient and reconstructed knee during walking. Am J Sports Med,2003,31(1):75-79.
    5Brandsson S, Karlsson J, Eriksson BI, Karrholm J. Kinematics after tear in the anterior cruciate ligament: dynamicbilateral radiostereometric studies in11patients. Acta Orthop Scand,2001,72(4):372-378.
    6Scarvell JM, Smith PN, Refshauge KM, et al. Comparison of kinematic analysis by mapping tibiofemoral contact withmovement of the femoral condylar centres in healthy and anterior cruciate ligament injured knees. J Orthop Res,2004,22(5):955-962.
    1Nicholson JA, Sutherland AG, Smith FW, Kawasaki T. Upright MRI in kinematic assessment of the ACL-deficient knee.Knee,2012,19(1):41-48.
    2Scarvell JM, Smith PN, Refshauge KM, et al. Comparison of kinematics in the healthy and ACL injured knee usingMRI. J Biomech,2005,38(2):255-262.
    3Kozanek M, Hosseini A, Liu F, et al. Tibiofemoral kinematics and condylar motion during the stance phase of gait. JBiomech,2009,42(12):1877-1884.
    4Kozanek M, Van de Velde SK, Gill TJ, Li G. The contralateral knee joint in cruciate ligament deficiency. Am J SportsMed,2008,36(11):2151-2157.
    1Freeman MA, Pinskerova V. The movement of the normal tibio-femoral joint. J Biomech,2005,38(2):197-208.
    1Georgoulis AD, Papadonikolakis A, Papageorgiou CD, et al. Three-dimensional tibiofemoral kinematics of the anteriorcruciate ligament-deficient and reconstructed knee during walking. Am J Sports Med,2003,31(1):75-79.
    Logan M, Dunstan E, Robinson J, et al. Tibiofemoral kinematics of the anterior cruciate ligament (ACL)-deficientweightbearing, living knee employing vertical access open "interventional" multiple resonance imaging. Am J SportsMed,2004,32(3):720-726.
    1Dennis DA, Mahfouz MR, Komistek RD, Hoff W. In vivo determination of normal and anterior cruciateligament-deficient knee kinematics. J Biomech,2005,38(2):241-253.
    2Logan M, Dunstan E, Robinson J, et al. Tibiofemoral kinematics of the anterior cruciate ligament (ACL)-deficientweightbearing, living knee employing vertical access open "interventional" multiple resonance ima ging. Am J SportsMed,2004,32(3):720-726.
    3Yamaguchi S, Gamada K, Sasho T, et al. In vivo kinematics of anterior cruciate ligament deficient knees during pivotand squat activities. Clin Biomech (Bristol, Avon),2009,24(1):71-76.
    4Defrate LE, Papannagari R, Gill TJ, et al. The6degrees of freedom kinematics of the knee after anterior cruciateligament deficiency: an in vivo imaging analysis. Am J Sports Med,2006,34(8):1240-1246.
    5Nicholson JA, Sutherland AG, Smith FW, Kawasaki T. Upright MRI in kinematic assessment of the ACL-deficient knee.Knee,2012,19(1):41-48.
    6Logan M, Dunstan E, Robinson J, et al. Tibiofemoral kinematics of the anterior cruciate ligament (ACL)-deficientweightbearing, living knee employing vertical access open "interventional" multiple resonance imaging. Am J SportsMed,2004,32(3):720-726.
    1Sakane M, Fox RJ, Woo SL, et al. In situ forces in the anterior cruciate ligament and its bundles in response to anteriortibial loads. J Orthop Res,1997,15(2):285-293.
    2Nicholson JA, Sutherland AG, Smith FW, Kawasaki T. Upright MRI in kinematic assessment of the ACL-deficient knee.Knee,2012,19(1):41-48.
    3von Eisenhart-Rothe R, Bringmann C, Siebert M, et al. Femoro-tibial and menisco-tibial translation patterns in patientswith unilateral anterior cruciate ligament deficiency--a potential cause of secondary meniscal tears. J Orthop Res,2004,22(2):275-282.
    4Shefelbine SJ, Ma CB, Lee KY, et al. MRI analysis of in vivo meniscal and tibiofemoral kinematics in ACL-deficientand normal knees. J Orthop Res,2006,24(6):1208-1217.
    5Scarvell JM, Smith PN, Refshauge KM, et al. Comparison of kinematics in the healthy and ACL injured knee usingMRI. J Biomech,2005,38(2):255-262.
    1Yamaguchi S, Gamada K, Sasho T, et al. In vivo kinematics of anterior cruciate ligament deficient knees during pivotand squat activities. Clin Biomech (Bristol, Avon),2009,24(1):71-76.
    2Allen CR, Wong EK, Livesay GA, et al. Importance of the medial meniscus in the anterior cruciate ligament-deficientknee. J Orthop Res,2000,18(1):109-115.
    3Defrate LE, Papannagari R, Gill TJ, et al. The6degrees of freedom kinematics of the knee after anterior cruciateligament deficiency: an in vivo imaging analysis. Am J Sports Med,2006,34(8):1240-1246.
    1Slauterbeck JR, Kousa P, Clifton BC, et al. Geographic mapping of meniscus and cartilage lesions associated withanterior cruciate ligament injuries. J Bone Joint Surg Am,2009,91(9):2094-2103.
    2Papageorgiou CD, Gil JE, Kanamori A, et al. The biomechanical interdependence between the anterior cruciateligament replacement graft and the medial meniscus. Am J Sports Med,2001,29(2):226-231.
    3Lee MS, Trindade MC, Ikenoue T, et al. Regulation of nitric oxide and bcl-2expression by shear stress in humanosteoarthritic chondrocytes in vitro. J Cell Biochem,2003,90(1):80-86.
    4Pena E, Calvo B, Martinez MA, Doblare M. A three-dimensional finite element analysis of the combined behavior ofligaments and menisci in the healthy human knee joint. J Biomech,2006,39(9):1686-1701.
    5Moglo KE, Shirazi-Adl A. Biomechanics of passive knee joint in drawer: load transmission in intact and ACL-deficientjoints. Knee,2003,10(3):265-276.
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    7Yao J, Snibbe J, Maloney M, Lerner AL. Stresses and strains in the medial meniscus of an ACL deficient knee underanterior loading: a finite element analysis with image-based experimental validation. J Biomech Eng,2006,128(1):135-141.
    8Yao J, Funkenbusch PD, Snibbe J, et al. Sensitivities of medial meniscal motion and deformation to material propertiesof articular cartilage, meniscus and meniscal attachments using design of experiments methods. J Biomech Eng,2006,128(3):399-408.
    1Moglo KE, Shirazi-Adl A. Biomechanics of passive knee joint in drawer: load transmission in intact and ACL-deficientjoints. Knee,2003,10(3):265-276.
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    1谢锋. ACL功能缺失对膝半月板、关节软骨影响的临床和有限元仿真研究.重庆:第三军医大学,2010.
    2Donahue TL, Hull ML, Rashid MM, Jacobs CR. A finite element model of the human knee joint for the study oftibio-femoral contact. J Biomech Eng,2002,124(3):273-280.
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    1Donahue TL, Hull ML, Rashid MM, Jacobs CR. A finite element model of the human knee joint for the study oftibio-femoral contact. J Biomech Eng,2002,124(3):273-280.
    2McPherson A, Karrholm J, Pinskerova V, et al. Imaging knee position using MRI, RSA/CT and3D digitisation. JBiomech,2005,38(2):263-268.
    1Li G, Gil J, Kanamori A, Woo SL. A validated three-dimensional computational model of a human knee joint. JBiomech Eng,1999,121(6):657-662.
    2林祥波.固定与旋转平台膝关节假体有限元、体外生物力学分析及临床应用研究.上海:第二军医大学,2009.
    1Li G, Gil J, Kanamori A, Woo SL. A validated three-dimensional computational model of a human knee joint. JBiomech Eng,1999,121(6):657-662.
    1林祥波.固定与旋转平台膝关节假体有限元、体外生物力学分析及临床应用研究.上海:第二军医大学,2009.
    1Yao J, Snibbe J, Maloney M, Lerner AL. Stresses and strains in the medial meniscus of an ACL deficient knee underanterior loading: a finite element analysis with image-based experimental validation. J Biomech Eng,2006,128(1):135-141.
    2Moglo KE, Shirazi-Adl A. Biomechanics of passive knee joint in drawer: load transmission in intact and ACL-deficientjoints. Knee,2003,10(3):265-276.
    3Andriacchi TP, Briant PL, Bevill SL, Koo S. Rotational changes at the knee after ACL injury cause cartilage thinning.Clin Orthop Relat Res,2006,442:39-44.
    1Moglo KE, Shirazi-Adl A. Biomechanics of passive knee joint in drawer: load transmission in intact and ACL-deficientjoints. Knee,2003,10(3):265-276.
    2姚杰,樊瑜波,张明,等.前交叉韧带损伤的继发性生物力学影响.力学学报,2010,42(1):102-108.
    3Tandogan RN, Taser O, Kayaalp A, et al. Analysis of meniscal and chondral lesions accompanying anterior cruciateligament tears: relationship with age, time from injury, and level of sport. Knee Surg Sports Traumatol Arthrosc,2004,12(4):262-270.
    4Chhadia AM, Inacio MCS, Maletis GB, et al. Are Meniscus and Cartilage Injuries Related to Time to Anterior CruciateLigament Reconstruction? Am J Sports Med,2011,39(9):1894-1899.
    5罗令.前交叉韧带功能性分束及其断裂对内侧半月板影响的研究.长沙:中南大学,2008.
    6冯华,张辉,郭铁能,等.膝关节前十字韧带切断对内侧半月板后角应力的影响.中华骨科杂志,2006,26(7):476-478.
    7谢锋. ACL功能缺失对膝半月板、关节软骨影响的临床和有限元仿真研究.重庆:第三军医大学,2010.
    8Slauterbeck JR, Kousa P, Clifton BC, et al. Geographic mapping of meniscus and cartilage lesions as sociated withanterior cruciate ligament injuries. J Bone Joint Surg Am,2009,91(9):2094-2103.
    1Moglo KE, Shirazi-Adl A. Biomechanics of passive knee joint in drawer: load transmission in intact and ACL-deficientjoints. Knee,2003,10(3):265-276.
    2Tandogan RN, Taser O, Kayaalp A, et al. Analysis of meniscal and chondral lesions accompanying anterior cruciateligament tears: relationship with age, time from injury, and level of sport. Knee Surg Sports Traumatol Arthrosc,2004,12(4):262-270.
    3Andriacchi TP, Briant PL, Bevill SL, Koo S. Rotational changes at the knee after ACL injury cause cartilage thinning.Clin Orthop Relat Res,2006,442:39-44.
    4Moglo KE, Shirazi-Adl A. Biomechanics of passive knee joint in drawer: load transmission in intact and ACL-deficientjoints. Knee,2003,10(3):265-276.
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