Power production in the terminal stance phase is essential for propelling the body forward during walking and is generated primarily by ankle plantarflexion. Osteoarthritis (OA) of the ankle restricts joint range of motion and is expected to reduce power production at that ankle. This loss of power may be compensated for by unaffected joints on both the ipsilateral and contralateral limbs resulting in overloading of the asymptomatic joints. Total ankle arthroplasty (TAA) has been shown to reduce pain and has the potential to restore range of motion and therefore increase ankle joint power, which could reduce overloading of the unaffected joints and increase walking speed. The purpose of this study was to test the hypothesis that ankle OA causes a loss of power in the affected ankle, compensatory power changes in unaffected lower limb joints, and that TAA will increase ankle power in the repaired ankle and reduce compensatory changes in other joints.

One hundred and eighty-three patients (86 men, 97 women with average ages 64.1 and 62.4 years respectively) requiring surgical intervention for ankle OA were prospectively enrolled. Implant selection of either a fixed (INBONE or Salto Talaris) or mobile (STAR) bearing implant was based on surgeon preference. Three-dimensional kinematics and kinetics were collected prior to surgery and one year post-operatively during self-selected speed level walking using an eight-camera motion capture system and a series of force platforms. Subject walking speed and lower extremity joint power during the last third of stance at the ankle, knee, and hip were calculated bilaterally and compared before and after surgical intervention across the entire group and by implant type (fixed vs. mobile), and gender using a series of ANOVAs (JMP SAS, Cary, NC), with statistical significance defined as p < 0 .05.

There were no gender differences in age, walking speed, or joint power. All patients increased walking as a result of surgery (0.87 m/s±0.26 prior to surgery and 1.13 m/s±0.24 after surgery, p < 0 .001) and increased total limb power. Normalized to total power (which accounts for changes in speed and distribution of power production across joints), prior to surgery the affected ankle contributed 19%±10% of total power while the unaffected ankle contributed 42%±12% (P < 0 .001). After surgery, the affected ankle increased to 25%±9% of total power and the unaffected ankle decreased to 38%±9% of total (P < 0.001). Other joints showed no significant power changes following surgery. Fixed bearing implants provide greater surgical ankle power improvement (61% versus 29% increase, p < 0 .002). Much of that change was due to the fact that those that received fixed-bearing implants had significantly lower walking speed and power before surgery.

Ankle OA reduced ankle power production, which was partially compensated for by the unaffected ankle. TAA increases walking speed and power at the affected ankle while lowering power production on the unaffected side. The modifications in power production could lead to increased physical activity and reduced overloading of asymptomatic joints.