Date on Master's Thesis/Doctoral Dissertation
Bertocci, Gina E.
Computer simulation; Dogs--Anatomy
Background - Cranial cruciate ligament (CrCL) rupture in the canine stifle is a leading cause of orthopedic lameness in the dog. Several corrective surgical procedures have been developed to return dogs to pre-injury function following CrCL rupture, but no one technique has fully shown superiority in terms of functional outcomes. A complete understanding of canine stifle biomechanics prior to and following CrCL rupture is needed to evaluate the biomechanical rationale of surgical corrective procedures being employed. Research Question - The goals of this study were to 1) develop a three dimensional rigid body canine hind limb computer model to simulate both a CrCL intact and CrCL deficient stifle during the stance phase of gait, 2) describe the stifle biomechanics in the CrCL intact and CrCL deficient stifle, and 3) to systematically assess model parameters which may influence CrCL deficiency. Methods - A three dimensional rigid body computer model representing the skeletal structure of a 32 kg Labrador Retriever was developed using SolidWorks based on boney landmarks. Canine hind limb kinetic and kinematic parameters associated with the stance phase of gait were incorporated into the model from the scientific literature. Model simulation of the stance phase was implemented in COSMOSMotion for the CrCL intact and CrCL deficient stifle. Outcome measures assessed include stifle ligament forces and tibial translation. Parameters thought to be associated with CrCL deficiency were systematically altered to determine the model outcome measure sensitivity. Verification of the model was attempted by comparison to a previously reported hind limb mathematical model and an in vitro study. Results - The CrCL was found to be the primary load-bearing ligament during the stance phase in the CrCL intact stifle. The peak CrCL load of 26% body weight occurred at 40% stance in the intact stifle. The caudal cruciate ligament (CaCL) was found to be the primary load-bearing ligament in the CrCL deficient stifle. The peak CaCL load of 219% body weight occurred at 40% stance in the deficient stifle. Suppression of the CrCL consistently increased CaCL load profiles during stance. The medial collateral ligament and lateral collateral ligament were generally not loaded in the CrCL intact or CrCL deficient stifle. The peak relative cranial tibial translation following suppression of the CrCL in the baseline model was 17.8 mm. These outcome measures were verified through reasonable agreement with a hind limb mathematical model and an in vitro study. Tibial plateau angle (TPA), patellar ligament line of action angle (PLLAA) and femoral condyle radius (FCR) were parameters for which model outcomes were most sensitive. In the CrCL intact stifle the CrCL peak load during stance increased with increasing TPA and increasing PLLAA. In the CrCL deficient stifle the CaCL peak load during stance increased with increasing TPA, increasing PLLAA, increasing FCR, increasing ground reaction force magnitude, increasing muscle force magnitude and increasing body mass. Additionally, the peak relative tibial translation during stance increased with increasing TPA, increasing PLLAA and increasing FCR. Parameters for which model outcome measures were less sensitive include ligament stiffness (all ligaments), CrCL stiffness, ligament prestrain (all ligaments), CrCL prestrain and femoromeniscal friction coefficients. Conclusions - A three dimensional rigid body canine hind limb computer model was developed to simulate both a CrCL intact and a CrCL deficient stifle during the stance phase of gait. This is the first 3D computer model to our knowledge capable of determining ligament forces in the CrCL intact and CrCL deficient stifle and visually describing tibial translation. This study attempts to assess several clinically relevant biomechanical parameters thought to be related to CrCL deficiency.
Brown, Nathan 1984-, "Development of a canine stifle computer model to investigate cranial cruciate ligament deficiency." (2009). Electronic Theses and Dissertations. Paper 164.