Abstract
Introduction and Aims: To assess the tibiofemoral kinematics of the PCL deficient knee using vertical open-access ‘dynamic’ MRI.
Method: Tibiofemoral motion was assessed using open-access MRI, weight-bearing in a squat, through the arc of flexion from zero to 90 degrees in six patients with isolated rupture of the PCL in one knee [diagnosed from conventional MRI scanning and clinical assessment] and a normal contralateral knee. Mid-medial and mid-lateral sagittal images were analysed in all chosen positions of flexion in both knees to assess the relative tibiofemoral relationships. Passive sagittal laxity was assessed by performing the posterior and anterior drawer tests, while the knees were scanned, again using the same MRI scanner. The tibiofemoral positions during this stress MRI examination was measured from mid-medial and mid-lateral sagittal images of the knees.
Results: Rupture of the PCL leads to an increase in passive sagittal laxity in the medial compartment of the knee [P< 0.006]. In the weight-bearing scans, PCL rupture alters the kinematics of the knee with persistent posterior subluxation of the medial tibia so that the femoral condyle rides up the anterior upslope of the medial tibial plateau. This ‘fixed’ subluxation was observed throughout the extension-flexion arc being statistically significant at all flexion angles (P< 0.018 at 0°, P< 0.013 at 20°, P< 0.014 at 45°, P< 0.004 at 90°). The kinematics of the lateral compartment were not altered by PCL rupture to a statistically significant degree. The posterior drawer test showed increased laxity in the medial compartment.
Conclusion: PCL rupture alters the kinematics of the medial compartment of the knee resulting in ‘fixed’ anterior subluxation of the medial femoral condyle [posterior subluxation of the medial tibial condyle]. This study helps to explain the observation of increased incidence of osteoarthritis in the medial compartment and specifically femoral condyle, in PCL deficient knees.
These abstracts were prepared by Editorial Secretary, George Sikorski. Correspondence should be addressed to Australian Orthopaedic Association, Ground Floor, The William Bland Centre, 229 Macquarie Street, Sydney, NSW 2000, Australia.
At least one of the authors is receiving or has received material benefits or support from a commercial source.
