A multibody workflow to investigate ACL biomechanics.

Van Niekerk, J. E. (2019-12)

Thesis (MEng)--Stellenbosch University, 2019.

Thesis

ENGLISH ABSTRACT: Anterior cruciate ligament (ACL) injury often occurs in high intensity sports involving contact or sudden changes of direction. Knee biomechanics change due to ACL injury and cause other ligaments and structures such as the medial collateral ligament (MCL) and the menisci to be at risk of concurrent injury. Presented in this study is a joint-level model of a human knee that was developed using a multibody modelling workflow and experimental data from the Open Knee(s) project. The model was developed in MSC Adams and simulated knee biomechanics between 0° and 30° of flexion for an intact and ACL deficient (ACLd) knee. Three different loading conditions were applied to the joint: (1) 100 N anterior-posterior (AP) tibial drawer, applied in 10 N increments, (2) 10 Nm varus-valgus (VV) torque, applied in 2.5 Nm increments and (3) 5 Nm internalexternal (IE) tibial torque, applied in 1 Nm increments. These loading conditions were applied individually as isolated degree of freedom loads, and simultaneously as combined degree of freedom loads. Loading conditions were applied to measure model predicted joint kinematics, ligament forces and tibiofemoral and meniscofemoral contact force. A sensitivity analysis was performed to investigate the sensitivity of modelling output to changes in modelling parameters. One parameter was changed at a time. Kinematic output was validated against experimental tibiofemoral testing data and had root mean square (RMS) errors of less than 4.50 mm for position and less than 6.5° for orientation. Predicted model outputs were the most sensitive to changes in the zero-load length (ZLL) of ligaments (> 30 % change in output parameter for 20 % change in ZLL). Changes in compliant contact stiffiness also resulted in changes in predicted output, but to a lesser extent than changes in ZLL (< 20 % change in output for 50 % change in contact stifiness). The model was least sensitive to changes in ligament stifiness (< 10 % change in output for a 30 % change in ligament stifiness). For the intact knee, the greatest force in the ACL was predicted for a combination of anterior tibial loading, valgus torque and internal tibial torque (151 N). For the ACLd knee, the model predicted that AP and IE laxity increased by 343 % and 28 % respectively when a 100 N tibial drawer load was applied. For a combination of 100 N tibial drawer load, 10 Nm valgus torque and 5 Nm internal tibial torque, AP and IE laxity increased by 261 % and 37 % respectively. ACL defiency resulted in an increase in MCL force (56 N at 30° flexion) and meniscus contact force for tibial drawer loading (33.9 N and 14.7 N at 30° flexion on the medial and lateral sides respectively). The increase in meniscus contact force coincided with joint motion that has been reported to result in meniscus injury. This study developed a multibody model of the knee using a multibody modelling approach. The model showed how anterior-posterior laxity, internalexternal tibial rotation, meniscal contact force and MCL force increased due to ACL deficiency. The model was most sensitive to changes in the ligament zero-load length and least sensitive to changes in ligament stifiness. The model confirmed previous findings describing the mechanism of meniscal ramp lesions, and the predicted meniscofemoral contact force was similar to what was measured experimentally and predicted by other models.

AFRIKAANSE OPSOMMING: Anterior kruisligament (ACL) beserings kom dikwels voor in hoë intensiteit sportsoorte wat kontak of skielike rigtingveranderinge behels. Kniebiomeganika verander as gevolg van 'n ACL-besering en veroorsaak dat ander ligamente en strukture, soos die mediale kollaterale ligament (MCL) en die menisci, die risiko loop vir gepaartgaande besering. In hierdie studie word 'n multiliggaam-model ('multibody model') van 'n menslike knie aangebied wat ontwikkel is met behulp van eksperimentele data van die 'Open Knee(s)' projek. Die model is ontwikkel in MSC Adams en was gebruik om knie-biomeganika tussen 0° en 30° fleksiehoeke vir 'n ongeskonde en ACL-lose (ACLd) knie te ondersoek. Drie verskillende lastoestande was op die knie toegepas: (1) 100 N anterior-posterior (AP) tibiale las ('tibial drawer'), aangewend in inkremente van 10 N, (2) 10 Nm varus-valgus (VV) draaimoment, aangewend in inkremente van 2.5 Nm en (3) 5 Nm interne-eksterne (IE) tibiale draaimoment, aangewend in 1 Nm inkremente. Hierdie lastoestande is afsonderlik toegepas as geïsoleerde vryheidsgraad belading, en gesaamentlik as gekombineerde vryheidsgraad beladings. Lastoestande is toegepas om die voorspelde gewrigskinematika, ligamentkragte, tibiofemorale en meniscofemorale kontakkrag te meet. 'n Parametriese studie is uitgevoer om die sensitiwiteit van modelleringsuitsette vir veranderinge in modelleringsparameters te ondersoek. Een parameter is op 'n slag verander. Kinematiese uitset is gevalideer op grond van eksperimentele tibiofemorale toetsdata en het 'root mean square' (RMS) foute van minder as 4.5 mm vir posisie en minder as 6.5° vir oriëntasie. Voorspelde modeluitsette was die sensitiefste vir veranderinge in die nulbelastinglengte ('zero-load length', ZLL) van ligamente (> 30 % verandering in die uitsetparameter vir 20 % verandering van die ZLL). Veranderings in die kontakstyfheidparameter het ook gelei tot veranderinge in die voorspelde uitset, maar tot 'n mindere mate as veranderinge in ZLL (< 20 % verandering in uitset vir 50 % verandering in kontakstyfheidparameter). Die model was die minste sensitief vir veranderinge in ligamentstyfheid (< 10 % verandering in uitset vir 30 % verandering in ligamentstyfheid). Vir die ongeskonde knie is die grootste krag in die ACL voorspel vir 'n kombinasie van anterior tibiale las, valgus-draaimoment en interne tibiale draaimoment (151 N), wat groter is as wat in die literatuur gemeld word. Vir die ACLdknie het die model voorspel dat die laksheid ('laxity') van AP translasie en IE rotasie onderskeidelik met 343 % en 28 % toegeneem het toe 'n anterior tibiale las van 100 N aangewend is. Vir 'n kombinasie van 100 N tibiale las, 10 Nm valgus-draaimoment en 5 Nm interne tibiale draaimoment, het AP en IE-laksiteit onderskeidelik met 261 % en 37 % toegeneem. ACL-tekort het gelei tot 'n toename in MCL-krag (56 N by 30° eksie) en meniscus-kontakkrag vir die aangewende anterior tibiale las (33.9 N vir die mediale en 14.7 N vir die laterale meniscus by 30° eksie). Die toename in die kontakkrag van die menisci het gepaard gegaan met die kniebewegings wat na bewering tot meniscus besering lei. Hierdie studie het 'n multi-liggaam model van die knie ontwikkel. Die model het voorspel hoe anterior-posterior laksheid, interne-eksterne tibiale rotasie, meniscus kontakkrag en MCL-krag toegeneem het as gevolg van 'n anterior kruisligament-tekort. Die model was die mees sensitief vir veranderinge in die nulbelastinglengte van ligamente en die minste sensitief vir veranderinge in die ligamentstyfheid. Die model kon die meganisme van meniscus skeure ('meniscal ramp-lesions') wat in die literatuur beskryf is bevestig, en die voorspelde krag was soortgelyk aan wat eksperimenteel gemeet is en deur ander modelle voorspel is.

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