Effect of ACL deficiency on MCL strains and joint kinematics

The knee joint is partially stabilized by the interaction of multiple ligament structures. This study tested the interdependent functions of the anterior cruciate ligament (ACL) and the medial collateral ligament (MCL) by evaluating the effects of ACL deficiency on local MCL strain while simultaneously measuring joint kinematics under specific loading scenarios. A structural testing machine applied anterior translation and valgus rotation (limits 100 N and 10 N m, respectively) to the tibia of ten human cadaveric knees with the ACL intact or severed. A three-dimensional motion analysis system measured joint kinematics and MCL tissue strain in 18 regions of the superficial MCL. ACL deficiency significantly increased MCL strains by 1.8% (p<0.05) during anterior translation, bringing ligament fibers to strain levels characteristic of microtrauma. In contrast, ACL transection had no effect on MCL strains during valgus rotation (increase of only 0.1%). Therefore, isolated valgus rotation in the ACL-deficient knee was nondetrimental to the MCL. The ACL was also found to promote internal tibial rotation during anterior translation, which in turn decreased strains near the femoral insertion of the MCL. These data advance the basic structure-function understanding of the MCL, and may benefit the treatment of ACL injuries by improving the knowledge of ACL function and clarifying motions that are potentially harmful to secondary stabilizers.     

Pathology of the Calcified Zone of Articular Cartilage in Post-Traumatic Osteoarthritis in Rat Knees

Objectives

This study aimed to investigate the pathology occurring at the calcified zone of articular cartilage (CZC) in the joints afflicted with post-traumatic osteoarthritis (PTOA).

Methods

Rats underwent bilateral anterior cruciate ligament (ACL) transection and medial meniscectomy to induce PTOA. Sham surgery was performed on another five rats to serve as controls. The rats were euthanized after four weeks of surgery and tibial plateaus were dissected for histology. The pathology of PTOA, CZC area and the tidemark roughness at six pre-defined locations on the tibial plateaus were quantified by histomorphometry.

Results

PTOA developed in the knees, generally more severe at the medial plateau than the lateral plateau, of rats in the experimental group. The CZC area was unchanged in the PTOA joints, but the topographic variations of CZC areas that presented in the control knees were reduced in the PTOA joints. The tidemark roughness decreased in areas of the medial plateau of PTOA joints and that was inversely correlated with the Mankin’s score of PTOA pathology.

Conclusion

Reduced tidemark roughness and unchanged CZC area differentiate PTOA from primary osteoarthritis, which is generally believed to have the opposite pathology at CZC, and may contribute to the distinct disease progression of the two entities of arthropathy.     

Endothelial dysfunction and decreased vascular responsiveness in the anterior cruciate ligament-deficient model of osteoarthritis.

Chronic inflammation associated with osteoarthritis (OA) may alter normal vascular responses and contribute to joint degradation. Vascular responses to vasoactive mediators were evaluated in the medial collateral ligament (MCL) of the anterior cruciate ligament (ACL)-deficient knee. Chronic joint instability and progressive OA were induced in rabbit knees by surgical transection of the ACL. Under halothane anesthesia, laser speckle perfusion imaging (LSPI) was used to measure MCL blood flow in unoperated control (n = 12) and 6-wk ACL-transected knees (n = 12). ACh, bradykinin, histamine, substance P (SP), and prostaglandin E(2) (PGE(2)) were applied to the MCL vasculature in topical boluses of 100 microl (dose range 10(-14) to 10(-8) mol). In normal joints, ACh, bradykinin, histamine, and PGE(2) evoked a dilatory response. Substance P caused a biphasic response that was dilatory from 10(-14) to 10(-11) mol and constricting at higher doses. In ACL-deficient knees, ACh, bradykinin, histamine, and SP decreased perfusion, whereas PGE(2) had a biphasic response that decreased perfusion at 10(-14) to 10(-11) mol and was dilatory at higher concentrations. Sodium nitroprusside increased perfusion in resting and phenylephrine-precontracted vessels with no significant differences between ACL-transected and control knees. Femoral artery occlusion and release increased perfusion by 74.3 +/- 11.1% in control knees but only by 25.8 +/- 4.4% in ACL-deficient knees. The altered responsiveness of the MCL vasculature to these inflammatory mediators may indicate endothelial dysfunction in the MCL, which may contribute to the progression and severity of OA and to the adaptation of the joint in an altered mechanical environment.     

A spatial mechanism with higher pairs for modelling the human knee joint

By generalizing a previous model proposed in the literature, a new spatial kinematic model of the knee joint passive motion is presented. The model is based on an equivalent spatial parallel mechanism which relies upon the assumption that fibers within the anterior cruciate ligament (ACL), the medial collateral ligament (MCL) and the posterior cruciate ligament (PCL) can be considered as isometric during the knee flexion in passive motion (virtually unloaded motion). The articular surfaces of femoral and tibial condyles are modelled as 3-D surfaces of general shapes. In particular, the paper presents the closure equations of the new mechanism both for surfaces represented by means of scalar equations that have the Cartesian coordinates of the points of the surface as variables and for surfaces represented in parametric form. An example of simulation is presented in the case both femoral condyles are modelled as ellipsoidal surfaces and tibial condyles as spherical surfaces. The results of the simulation are compared to those of the previous models and to measurements. The comparison confirms the expectation that a better approximation of the tibiofemoral condyle surfaces leads to a more accurate model of the knee passive motion.     

ACL/MCL transection affects knee ligament insertion distance of healing and intact ligaments during gait in the Ovine model

The objective of this study was to assess the impact of combined transection of the anterior cruciate and medial collateral ligaments on the intact and healing ligaments in the ovine stifle joint. In vivo 3D stifle joint kinematics were measured in eight sheep during treadmill walking (accuracy: 0.4±0.4 mm, 0.4±0.4°). Kinematics were measured with the joint intact and at 2, 4, 8, 12, 16 and 20 weeks after either surgical ligament transection (n=5) or sham surgery without transection (n=3). After sacrifice at 20 weeks, the 3D subject-specific bone and ligament geometry were digitized, and the 3D distances between insertions (DBI) of ligaments during the dynamic in vivo motion were calculated. Anterior cruciate ligament/medial collateral ligament (ACL/MCL) transection resulted in changes in the DBI of not only the transected ACL, but also the intact lateral collateral ligament (LCL) and posterior cruciate ligament (PCL), while the DBI of the transected MCL was not significantly changed. Increases in the maximal ACL DBI (2 week: +4.2 mm, 20 week: +5.7 mm) caused increases in the range of ACL DBI (2 week: 3.6 mm, 20 week: +3.8 mm) and the ACL apparent strain (2 week: +18.9%, 20 week: +24.0%). Decreases in the minimal PCL DBI (2 week: −3.2 mm, 20 week: −4.3 mm) resulted in increases in the range of PCL DBI (2 week: +2.7 mm, 20 week: +3.2 mm). Decreases in the maximal LCL DBI (2 week: −1.0 mm, 20 week: −2.0 mm) caused decreased LCL apparent strain (2 week: −3.4%, 20 week: −6.9%). Changes in the mechanical environment of these ligaments may play a significant role in the biological changes observed in these ligaments.     

Differential response to CoCl2-stimulated hypoxia on HIF-1α, VEGF, and MMP-2 expression in ligament cells

The adult human anterior cruciate ligament (ACL) has a poor functional healing response, whereas the medial collateral ligament (MCL) does not. The difference in intrinsic properties of these ligament cells can be due to their different response to their located microenvironment. Hypoxia is a key environmental regulator after ligament injury. In this study, we investigated the differential response of ACL and MCL fibroblasts to hypoxia on hypoxia-inducible factor-1α, vascular endothelial growth factor, and matrix metalloproteinase-2 (MMP-2) expression. Our results show that ACL cells responded to hypoxia by up-regulating the HIF-1α expression significantly as compared to MCL cells. We also observed that in MCL fibroblasts response to hypoxia resulted in increase in expression of VEGF as compared to ACL fibroblasts. After hypoxia treatment, mRNA and protein levels of MMP-2 increased in both ACL and MCL. Furthermore we found in ACL pro-MMP-2 was converted more into active form. However, hypoxia decreased the percentage of wound closure for both ligament cells and had a greater effect on ACL fibroblasts. These results demonstrate that ACL and MCL fibroblasts respond differently under the hypoxic conditions suggesting that these differences in intrinsic properties may contribute to their different healing responses and abilities.     

Matrix metalloproteinase-13 expression in rabbit knee joint connective tissues: influence of maturation and response to injury.

The hypothesis of the present work was that expression of matrix metalloproteinase-13 (MMP-13, collagenase-3) would be induced during conditions involving important matrix remodeling such as ligament maturation, scar healing and joint instability. Therefore, MMP-13 expression in the medial collateral ligament (MCL) during the variable situations of tissue maturation and healing was assessed. MMP-13 expression in three intra-articular connective tissues of the knee (i.e. articular cartilage, menisci and synovium) following the transection of the anterior cruciate ligament of the knee was evaluated at 3 and 8 weeks post-injury. MMP-13 mRNA (semi-quantitative RT-PCR) and protein (immunohistochemistry and Western blotting) were detected in all of the tissues studied. Significantly higher MCL mRNA levels for MMP-13 were detected during the early phases of tissue maturation (i.e. 29 days in utero and 2-month-old rabbits) compared to later phases (5- and 12-month-old rabbits). This pattern of expression was recapitulated following MCL injury, with very high levels of expression in scar tissue at 3 weeks post-injury and then a decline to levels not significantly different from control values by 14 weeks. Elevated mRNA levels correlated with increased protein levels for MMP-13 in both menisci and synovium following the transection of the anterior cruciate ligament and during medial collateral ligament healing. These results indicate that MMP-13 expression is regulated by a number of variables and that high levels of expression occur in situations when connective tissue remodeling is very active.     

Interactions between kinematics and loading during walking for the normal and ACL deficient knee

The relationships between extrinsic forces acting at the knee and knee kinematics were examined with the purpose of identifying specific phases of the walking cycle that could cause abnormal kinematics in the anterior cruciate ligament (ACL) deficient knee. Intersegmental forces and moments in directions that would produce anterior-posterior (AP) translation, internal-external (IE) rotation and flexion-extension (FE) at the knee were compared with the respective translation and rotations of the tibia relative to the femur during four selected phases (heel strike, weight acceptance, terminal extension and swing) of the walking cycle. The kinematic changes associated with loss of the ACL occurred primarily during the terminal portion of swing phase of the walking cycle where, for the ACL deficient knee, the tibia had reduced external rotation and anterior translation as the knee extended prior to heel strike. The kinematic changes during swing phase were associated with a rotational offset relative to the contralateral knee in the average position of the tibia towards internal rotation. The offset was maintained through the entire gait cycle. The abnormal offsets in the rotational position were correlated with the magnitude of the flexion moment (balanced by a net quadriceps moment) during weight acceptance. These results suggest that adaptations to the patterns of muscle firing during walking can compensate for kinematic changes associated with the loss of the ACL. The altered rotational position would cause changes in tibiofemoral contact during walking that could cause the type of degenerative changes reported in the meniscus and the articular cartilage following ACL injury.     

ACL deficiency impairs the vasoconstrictive efficacy of neuropeptide Y and phenylephrine in articular tissues: a laser speckle perfusion imaging study.

Sympathetic-derived neuropeptide Y (NPY) helps regulate inflammatory responses in injury and disease, is a vasoconstrictor, and stimulates angiogenesis. Rupture of the anterior cruciate ligament (ACL) is a common clinical presentation that results in tissue inflammation, hyperemia, and angiogenesis in the intact medial collateral ligament (MCL). This study is the first to examine the vasoregulatory role of NPY in ACL-deficient knee joints by using the newly developed technique of laser speckle perfusion imaging (LSPI). MCL blood flow was measured in two groups of adult rabbits: unoperated control (n = 6), and 6-wk ACL transected (n = 5). Under anesthesia, the MCL was surgically exposed and tissue blood flow was imaged at high resolution using LSPI. NPY was applied to the MCL vasculature in topical boluses of 100 mul (dose range 10(-14) to 10(-9) mol), and the alpha-adrenoceptor agonist phenylephrine was applied in doses of 10(-14), 10(-10), and 10(-7) mol. In control rabbits, topical administration of NPY or phenylephrine produced dose-dependent vasopressor responses (maximal effect at 10(-9) mol NPY and 10(-7) mol phenylephrine). In ACL-transected knees, there was little or no vasoconstrictive response to NPY at any dose. The response to phenylephrine was significantly reduced compared with control ligaments. Possible causes of the reduced vasoconstrictive response to NPY in the MCL after 6 wk of ACL deficiency include development of tolerance to the peptide due to a prolonged increase in sympathetic nerve activity or change in the distribution or functionality of the NPY Y(1) receptors. Chronic ACL deficiency leads to profound and protracted hyperemia in associated articular tissues. Abrogation of a vasoconstrictor response to both NPY and phenylephrine in the MCL indicates that ACL deficiency induces major changes in the vascular physiological homeostasis.     

Effects of medial collateral ligament release,limb correction,and soft tissue laxity on knee joint contact force distribution after medial opening wedge high tibial osteotomy: a computational study

In this study, the effects of medial collateral ligament (MCL) release and the limb correction strategies with pre-existing MCL laxity on tibiofemoral contact force distribution after high tibial osteotomy (HTO) were investigated. The medial and lateral contact forces of the knee were quantified during simulated standing using computational modeling techniques. MCL slackness had a primary influence on contact force distribution of the knee, while there was little effect of simulated limb correction. Anterior and middle bundle release, which involved the partial release of two-thirds of the superficial MCL, was shown to be an optimal surgical method in HTO, achieving balanced contact distribution in simulated weight-bearing standing.     

骨关节炎软骨细胞发生内质网应激

目的：研究骨关节炎软骨细胞是否发生内质网应激现象。方法：对关节置换术后的人类骨关节炎软骨标本和正常关节软骨标本切片进行内质网应激标志分子免疫球蛋白重链结合蛋白（BiP）的免疫组织化学检测;对小鼠膝关节进行半月板切断术诱发实验性骨关节炎,在术后1、3和6周取材,对组织切片进行番红花“O”染色、Mankin评分及BiP的免疫组织化学检测。结果：所有人类骨关节炎标本中软骨细胞BiP的表达明显升高。番红花“O”染色结果表明,在小鼠骨关节炎模型中,全部手术侧关节表面发生磨损,且随着术后时间延长关节表面磨损范围逐步扩大,手术侧Mankn分值显著高于对照侧;此外,手术侧的软骨细胞内BiP呈阳性表达,且表达量随术后时间延长而增加。结论：在人类骨关节炎标本和实验性小鼠骨关节炎模型中,关节软骨细胞均发生明显的内质网应激现象。     

Animal models of osteoarthritis

Animal models of osteoarthritis are used to study the pathogenesis of cartilage degeneration and to evaluate potential antiarthritic drugs for clinical use. Animal models of naturally occurring osteoarthritis (OA) occur in knee joints of guinea pigs, mice and other laboratory animal species. Transgenic models have been developed in mice. Commonly utilized surgical instability models include medial meniscal tear in guinea pigs and rats, medial or lateral partial meniscectomy in rabbits, medial partial or total meniscectomy or anterior cruciate transection in dogs. Additional models of cartilage degeneration can be induced by intra-articular iodoacetate injection or by administration of oral or parenteral quinolone antibiotics. None of these models have a proven track record of predicting efficacy in human disease since there are no agents that have been proven to provide anything other than symptomatic relief in human OA. However, agents that are active in these models are currently in clinical trials. Methodologies, gross and histopathologic features and comparisons to human disease will be discussed for the various models.     

Three-dimensional in vivo kinematics and finite helical axis variables of the ovine stifle joint following partial anterior cruciate ligament transection

Partial anterior cruciate ligament (p-ACL) rupture is a common injury, but the impact of a p-ACL injury on in vivo joint kinematics has yet to be determined in an animal model. The in vivo kinematics of the ovine stifle joint were assessed during ‘normal’ gait, and at 20 and 40 weeks after p-ACL transection (Tx). Gross morphological scoring of the knee was conducted. p-ACL Tx creates significant progressive post-traumatic osteoarthritis (PTOA)-like damage by 40 weeks. Statistically significant increases for flexion angles at hoof-strike (HS) and mid-stance (MST) were seen at 20 weeks post p-ACL Tx and the HS and hoof-off (HO) points at 40 weeks post p-ACL-Tx, therefore increased flexion angles occurred during stance phase. Statistically significant increases in posterior tibial shift at the mid-flexion (MF) and mid-extension (ME) points were seen during the swing phase of the gait cycle at 40 weeks post p-ACL Tx. Correlation analysis showed a strong and significant correlation between kinematic changes (instabilities) and gross morphological score in the inferior-superior direction at 40 weeks post p-ACL Tx at MST, HO, and MF. Further, there was a significant correlation between change in gross morphological combined score (ΔGCS) and the change in location of the helical axis in the anterior direction (ΔsAP) after p-ACL Tx for all points analyzed through the gait cycle. This study quantified in vivo joint kinematics before and after p-ACL Tx knee injury during gait, and demonstrated that a p-ACL knee injury leads to both PTOA-like damage and kinematic changes.     

Epidermal growth factor differentially affects integrin-mediated adhesion and proliferation of ACL and MCL fibroblasts

The anterior cruciate ligament (ACL) and the medial collateral ligament (MCL) are two commonly injured structures in the human knee. While the MCL heals post-traumatically, the ACL does not. Since growth factors play a major role in the proliferation phase of wound healing, we compared the differential effects of epidermal growth factor (EGF) on adhesion and proliferation of ACL and MCL fibroblasts. Using a micropipette/micromanipulator system we found that cells subjected to shorter incubation periods (15 minutes) with EGF (5, 10, 50 ng/ml) showed a general increase in adhesion to the extracellular matrix fibronectin while cells subjected to longer incubation periods (4, 6, 10, and 24 hr) with EGF (5 ng/ml) showed decreases in adhesion. For both incubation durations, MCL fibroblasts displayed a greater change in adhesion than ACL fibroblasts, when compared to control. Investigation of integrin expression showed no fluctuation in cell surface expression of the alpha5 subunit of the FN-binding integrin alpha5beta1 for all EGF (5 ng/ml) incubation times. MCL cells showed a significant increase in proliferation upon stimulation with EGF compared to ACL cells when cultured in FN coated wells. The results found in this study help provide a better understanding of EGF's role in adhesion and proliferation, two events that may contribute to the differential healing response between ACL and MCL fibroblasts. Following exposure to EGF, ACL and MCL cells initially respond by increasing their adhesion strength. MCL cells respond to all concentrations of EGF while ACL cells appear to have a threshold concentration after which EGF effects plataeu. After this initial response period (<10 hr) cells exhibit lower adhesion strength and higher proliferation rate. It is possible that the release from FN serves to enhance the ability of the cells to proliferate. These results may aid in understanding the ligament healing process.     

New parameters describing how knee ligaments carry force in situ predict interspecimen variations in laxity during simulated clinical exams

Knee laxity, defined as the net translation or rotation of the tibia relative to the femur in a given direction in response to an applied load, is highly variable from person to person. High levels of knee laxity as assessed during routine clinical exams are associated with first-time ligament injury and graft reinjury following reconstruction. During laxity exams, ligaments carry force to resist the applied load; however, relationships between intersubject variations in knee laxity and variations in how ligaments carry force as the knee moves through its passive envelope of motion, which we refer to as ligament engagement, are not well established. Thus, the objectives of this study were, first, to define parameters describing ligament engagement and, then, to link variations in ligament engagement and variations in laxity across a group of knees. We used a robotic manipulator in a cadaveric knee model (n = 20) to quantify how important knee stabilizers, namely the anterior and posterior cruciate ligaments (ACL and PCL, respectively), as well as the medial collateral ligament (MCL) engage during respective tests of anterior, posterior, and valgus laxity. Ligament engagement was quantified using three parameters: (1) in situ slack, defined as the relative tibiofemoral motion from the neutral position of the joint to the position where the ligament began to carry force; (2) in situ stiffness, defined as the slope of the linear portion of the ligament force–tibial motion response; and (3) ligament force at the peak applied load. Knee laxity was related to parameters of ligament engagement using univariate and multivariate regression models. Variations in the in situ slack of the ACL and PCL predicted anterior and posterior laxity, while variations in both in situ slack and in situ stiffness of the MCL predicted valgus laxity. Parameters of ligament engagement may be useful to further characterize the in situ biomechanical function of ligaments and ligament grafts.     

Repeated application of incremental landing impact loads to intact knee joints induces anterior cruciate ligament failure and tibiofemoral cartilage deformation and damage: A preliminary cadaveric investigation

Anterior cruciate ligament (ACL) injury is a major problem worldwide and prevails during high-impact activities. It is not well-understood how the extent and distribution of cartilage damage will arise from repetitive landing impact loads that can lead to ACL failure. This study seeks to investigate the sole effect of repetitive incremental landing impact loads on the induction of ACL failure, and extent and distribution of tibiofemoral cartilage damage in cadaveric knees. Five cadaveric knees were mounted onto a material testing system at 70° flexion to simulate landing posture. A motion-capture system was used to track rotational and translational motions of the tibia and femur, respectively. Each specimen was compressed at a single 10 Hz haversine to simulate landing impact. The compression trial was successively repeated with increasing actuator displacement till a significant compressive force drop was observed. All specimens underwent ACL failure, which was confirmed via magnetic resonance scans and dissection. Volume analysis, thickness measurement and histological techniques were employed to assess cartilage lesion status. For each specimen, the highest peak compressive force (1.9–7.8 kN) was at the final trial in which ACL failure occurred; corresponding posterior femoral displacement (7.6–18.0 mm) and internal tibial rotation (0.6°–4.7°) were observed. Significant compressive force drop (79.8–90.9%) was noted upon ACL failure. Considerable cartilage deformation and damage were found in exterior, posterior and interior femoral regions with substantial volume reduction in lateral compartments. Repeated application of incremental landing impact loads can induce both ACL failure and cartilage damage, which may accelerate the risk of developing osteoarthritis.     

Loss of ACL function leads to alterations in tibial plateau common dynamic contact stress profiles

It has been suggested that the repetitive nature of altered joint tissue loading which occurs after anterior cruciate ligament (ACL) rupture can contribute to the development of osteoarthritis (OA). However, changes in dynamic knee joint contact stresses after ACL rupture have not been quantified for activities of daily living. Our objective was to characterize changes in dynamic contact stress profiles that occur across the tibial plateau immediately after ACL transection. By subjecting sensor-augmented cadaveric knees to simulated gait, and analyzing the resulting contact stress profiles using a normalized cross-correlation algorithm, we tested the hypothesis that common changes in dynamic contact stress profiles exist after ACL injury. Three common profiles were identified in intact knees, occurring on the: (I) posterior lateral plateau, (II) posterior medial plateau, and (III) central region of the medial plateau. In ACL-transected knees, the magnitude and shape of the common dynamic stress profiles did not change, but their locations on the tibial plateau and the number of knees identified for each profile changed. Furthermore, in the ACL transected knees, a unique common contact stress profile was identified in the posterior region of the lateral plateau near the tibial spine. This framework can be used to understand the regional and temporal changes in joint mechanics after injury.     

The symmetry of the medial collateral and anterior cruciate ligament properties: a biochemical study in the rat hind limb

The medial collateral (MCL) and the anterior cruciate ligament (ACL) of the rat's knee are frequently used in biomedical research and occasionally in ligament healing studies. The contralateral normal ligament serves as a control. In this study the presence of symmetry in the biomechanical properties of the MCL and the ACL was investigated. Bilateral femur-MCL-tibia and femur-ACL-tibia preparations were obtained from the hind limbs of sixty rats and were subjected to tensile testing to failure under the same loading conditions. Tensile load to failure, stiffness and energy absorption capacity were measured and the mode of failure was recorded. All biomechanical parameters were not significantly different between the two knees of the same animal, although significant individual variation was evident. The most common mechanism of failure was mid-substance tear. Symmetry seems to exist in the biomechanical properties of the MCL and the ACL in the rat knee. When ligament healing is evaluated, increased group size is necessary and the use of a normal control group may be advisable. The contralateral normal knee ligament may serve as a control when the properties of an injured ligament are evaluated and when the parameters of tensile testing failure under similar load conditions are applied.     

The effect of isolated valgus moments on ACL strain during single-leg landing: A simulation study

Valgus moments on the knee joint during single-leg landing have been suggested as a risk factor for anterior cruciate ligament (ACL) injury. The purpose of this study was to test the influence of isolated valgus moment on ACL strain during single-leg landing. Physiologic levels of valgus moments from an in vivo study of single-leg landing were applied to a three-dimensional dynamic knee model, previously developed and tested for ACL strain measurement during simulated landing. The ACL strain, knee valgus angle, tibial rotation, and medial collateral ligament (MCL) strain were calculated and analyzed. The study shows that the peak ACL strain increased nonlinearly with increasing peak valgus moment. Subjects with naturally high valgus moments showed greater sensitivity for increased ACL strain with increased valgus moment, but ACL strain plateaus below reported ACL failure levels when the applied isolated valgus moment rises above the maximum values observed during normal cutting activities. In addition, the tibia was observed to rotate externally as the peak valgus moment increased due to bony and soft-tissue constraints. In conclusion, knee valgus moment increases peak ACL strain during single-leg landing. However, valgus moment alone may not be sufficient to induce an isolated ACL tear without concomitant damage to the MCL, because coupled tibial external rotation and increasing strain in the MCL prevent proportional increases in ACL strain at higher levels of valgus moment. Training that reduces the external valgus moment, however, can reduce the ACL strain and thus may help athletes reduce their overall ACL injury risk.     

Comparison of shear forces and ligament loading in the healthy and ACL-deficient knee during gait

The purpose of this study was to predict and explain the pattern of shear force and ligament loading in the ACL-deficient knee during walking, and to compare these results to similar calculations for the healthy knee. Musculoskeletal modeling and computer simulation were combined to calculate ligament forces in the ACL-deficient knee during walking. Joint angles, ground-reaction forces, and the corresponding lower-extremity muscle forces obtained from a whole-body dynamic optimization simulation of walking were input into a second three-dimensional model of the lower extremity that represented the knee as a six degree-of-freedom spatial joint. Anterior tibial translation (ATT) increased throughout the stance phase of gait when the model ACL was removed. The medial collateral ligament (MCL) was the primary restraint to ATT in the ACL-deficient knee. Peak force in the MCL was three times greater in the ACL-deficient knee than in the ACL-intact knee; however, peak force sustained by the MCL in the ACL-deficient knee was limited by the magnitude of the total anterior shear force applied to the tibia. A decrease in anterior tibial shear force was brought about by a decrease in the patellar tendon angle resulting from the increase in ATT. These results suggest that while the MCL acts as the primary restraint to ATT in the ACL-deficient knee, changes in patellar tendon angle reduce total anterior shear force at the knee.