Biomechanical study of the canine stifle: an in vitro comparison of the intact and cranial cruciate ligament deficient stifle

Abstract

Rupture of the cranial cruciate ligament (CrCL) is a common injury. There are few studies that address the biomechanics of the intact, CRCL deficient, and reconstructed stifle. The purpose of this study was to measure the range of motion of the intact and CRCL deficient stifle so that a reconstruction could be identified that would maintain a range of motion similar to the intact stifle. Six canine rear limbs (3 right, 3 left) were harvested from dogs weighing between 15 and 25 kg. The limbs were mounted in an instrumented linkage apparatus that allowed 5 degrees of freedom and measured cranial-caudal translation, axial rotation, and varus-valgus rotation. These parameters were measured at 15' intervals from 15' to 90'. Each stifle served as a positive control (intact CRCL) and a negative control (CRCL deficient). Then each stifle was reconstructed with 12 different intra-articular reconstruction combinations. This was done by varying three parameters: 1.) two tibial insertion sites (tibial insertion site of the patellar ligament and the tibial insertion site of the CRCL), 2.) two graft preloads (5 N and 20 N), and 3.) three flexion angles at the time of graft fixation (15', 30', and 90'). The model demonstrated a significant difference between the intact and CRCL deficient stifle in cranial translation (p=0.0001), internal rotation (p=0.0002), and varus rotation (p=0.0004). When reconstructed, tensile graft force was higher in extension than flexion in measuring tension. Graft forces never exceeded 52.6 N with an average of 40.5 N. Reconstructions done with the limb at 90 ' at time of graft fixation, at the CRCL insertion site, and with a 20 N preload produced higher graft forces than the other reconstructions. This model demonstrated a difference in the intact and CRCL deficient stifle in measuring cranial translation, internal rotation, and varus rotation. Further, this study demonstrates that grafts do not have to be secured with a high preload. This study, in agreement with other studies, indicates that graft failure is more a biological factor of the graft itself and not a failure at the graft fixation site.