The hypothesis that the involved limb of patients with medial knee OA would demonstrate less varied knee motion during gait was partially supported by these data. The frontal plane variability of the involved limb was significantly lower than the variability of the uninvolved knee but not different from the control group. Frontal plane knee laxity and medial co-contraction partially influenced the amount of joint motion variability in the involved knee in individuals with unilateral knee OA. Pain did not influence variability in this sample.
The frontal plane knee variability findings were somewhat perplexing. Was the variability of the involved knee diminished or was the variability of the uninvolved knee increased? Perhaps the control, uninvolved, and involved knees represent a spectrum of health and disease. The uninvolved knees of the OA group, while showing no overt signs of OA, had somewhat greater medial laxity and higher VMMG co-contraction values than the control knees, but normal knee excursions. The involved knees also had higher co-contraction values but stiffened the knee during weight acceptance.2,3
These data may reflect a continuum of control strategies for patients with knee OA, where an initial increase in laxity, as seen in the uninvolved knee, is met with an increase in the variability of the knee joint’s motion. Such an increase may indicate either inadequate control or may reflect inter-limb compensations for the involved knee. As OA progresses, a substantial reduction in joint motion variability may occur, mediated by higher medial co-contraction values and observed as a truncated knee flexion excursion during gait ,which may ultimately result in disease progression.12
Our subjects already had knee OA, meaning that we are unable to determine whether observed differences in knee motion variability are the cause or the result of the knee OA.
We had hypothesized that the presence of pain would reduce the variability of the knee joint’s motion. The subjects may have learned to use only knee motions that minimized pain, effectively eliminating movement options. Pain, however, was not related to knee motion variability for this group of subjects.
Recent work has also demonstrated that knee instability is a significant problem in patients with knee OA,10
as instability can result from an inability to control excessive joint laxity. The presence of instability in this population raises the possibility that the CNS is unable to deviate from a few similar knee joint motions because of the tightly constrained muscular requirements necessary for controlling greater laxity. In the involved limb, frontal plane laxity significantly influenced frontal plane variability so that individuals with greater laxity exhibited less variable knee motions. Presumably, the greater medial co-contraction was used to control laxity to minimize instability. Therefore, therapeutic interventions that target joint laxity and the subsequent instability may be successful.22
At any given moment during gait, many combinations of knee angles and angular velocities are available, controlled by multiple muscles crossing the knee joint. Although the involved side’s motion variability was not different from the control group, the uninvolved limb demonstrated many different combinations of frontal plane knee angle and angular velocity, possibly reflecting decreased joint control with each step. Increased variability has previously been observed in the uninvolved limb of children with spastic hemiplegic cerebral palsy.23
The authors attributed the increased variability on the uninvolved side to be a compensatory mechanism for impairments on the involved side. In patients with knee OA, greater variability in the uninvolved knee has important clinical implications as the joint may be at greater risk of joint damage. This is particular important, as many individuals with unilateral knee OA eventually develop symptoms of knee OA on the contralateral side.24
We can speculate that the increased variability of the uninvolved knee joint’s motion, undetectable by examining joint kinematics at discrete time points, may lead to a greater risk of articular cartilage damage and may provide insight into the mechanism underlying the high incidence of bilateral knee OA. It remains unclear, however, which factors predispose an individual with unilateral knee OA to increase variability on the uninvolved side. The establishment of these factors may aid in the determination of who may progress to bilateral knee OA.
In summary, this study provides important information about how individuals with unilateral knee OA walk and about the potential consequences of more variable knee joint motion of the uninvolved limb during gait. Patients with unilateral medial knee OA display altered knee kinematics and kinetics on the involved side, although stride-to-stride variability of knee motion was unchanged on the involved side. Evidence of excessive joint motion variability on the uninvolved side, however, may provide insight into the development of OA in the contralateral cognate joint.