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11:30
15 mins
Analysis of the Factors of Patellofemoral Instability Using Musculoskeletal Modelling and Simulation
Marco Marra, Sebastiaan van de Groes, Dennis Janssen, Nico Verdonschot, Bart Koopman
Session: Neuromuscular – lower extremities 1
Session starts: Friday 25 January, 10:30
Presentation starts: 11:30
Room: Lecture room 536


Marco Marra (University of Twente)
Sebastiaan van de Groes (Radboudumc)
Dennis Janssen (Radboudumc)
Nico Verdonschot (Radboudumc and University of Twente)
Bart Koopman (University of Twente)


Abstract:
Patellofemoral instability affects very young patients (incidence 21–45%), and causes pain, (sub-)luxation and a general sense of instability in the patellofemoral joint. Many factors play a role in this pathology: trochlear dysplasia, patella alta, rupture of the medial patellofemoral ligament (MPFL), tightness of the lateral retinaculum, and vastus medialis obliquuus (VMO) deficiency. The current surgical treatment aims at correcting the patellar tracking, and includes tibial tubercle transfer, trochleoplasty, and MPFL reconstruction. However, the pre-operative information available is scarce, as it is based on static measurements on X-rays and physical examination. The aim of this research is to use musculoskeletal modelling to understand how the abovementioned factors influence patellofemoral instability. CT and MR images of a cadaver specimen were acquired and segmented using Mimics to reconstruct the 3 D models of femur, patella and tibia, and tibiofemoral and patellofemoral articular cartilage. A specimen-specific 12-DoF knee model was developed using the AnyBody Modeling System, and simulated during a simple knee extension using Force Dependent Kinematics (FDK). Four additional cases were created by manual editing of the 3 D shapes, representing four types (A–D) of trochlear dysplasia. In addition, a combination of MPFL rupture, tightness of lateral retinaculum and VMO deficiency was simulated. Compared to the intact case, trochlear dysplasia (Type B) resulted in 6 mm more lateral patellar translation at knee extension, but no clear dislocation was observed. Patellofemoral contact pressures were altered (Types B–D), showing pressure concentrations in the lowest portion of the patellar cartilage. Only the combination of Type B dysplasia, MPFL rupture, lateral tightness and VMO insufficiency showed patellar sub-luxation during the FDK simulations. Patellofemoral instability is a complex phenomenon and these findings confirm its highly multifactorial nature. Whereas trochlear dysplasia alone did not lead to any (sub-)luxation – although it did change both kinematic and kinetic patterns in the patellofemoral joint – the combination of multiple risk factors clearly led to instability. In further research, bone morphology and soft tissues properties will be studied extensively to identify risky combinations, and a clinical tool for pre-operative planning will be implemented, which will help optimizing the surgery to restore joint stability.