Abstract
PURPOSE The inherent variability of joint motions during gait provides flexibility to adapt to unexpected perturbations, and may be beneficial in preventing injury because joint structures are stressed differently with each repetition. The pain and knee joint laxity in patients with knee osteoarthritis (OA) may influence their choice of knee joint movement patterns during gait. Muscular co-contraction is a crude method of controlling joint laxity, resulting in reduced angular joint motion and joint stiffening. This stiffening strategy may limit the number of available motor patterns during gait, despite the numerous movement plans theoretically available. The purpose of this study was to determine if knee pattern variability is diminished in a group of subjects with symptomatic knee OA. METHODS Eleven subjects with symptomatic medial knee OA and 9 healthy age-matched control subjects underwent 3D lower extremity gait analysis for 10 trials. Knee joint pattern variability was calculated from a phase plot of the knee's position and velocity during stance, from initial contact to the peak knee adduction moment. Knee laxity was measured from stress radiographs taken of the medial and lateral compartments of the knee. RESULTS The OA group had a mean pattern variability measurement of 9.0±1.7°, which was significantly reduced compared to the control group whose variability measured 14.2±7.7° (p = 0.04). Significantly greater medial joint laxity was observed from the stress radiographs in the OA group compared to the control group (p = 0.02). CONCLUSIONS These data indicate that subjects with knee OA exhibit reduced variability in knee motion patterns over repeated cycles. These subjects appear unwilling or unable to utilize more diverse movement patterns. This may be a strategy to avoid pain, or may indicate a muscular compensation necessary to maximize joint stability. Such a result could predispose the knee joint to further damage through an inability to adequately adjust to external perturbations. Supported by ACSM (Foundation Student Research Grant), NIH (P20 RR016458), and FPT (PODS II).
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