Kinetic gait adaptations following anterior cruciate ligament reconstruction: Implications for post-traumatic knee osteoarthritis

Abstract

Purpose: Anterior cruciate ligament injury and reconstruction surgery (ACLR) incur a 3-5x increase in the risk of developing post-traumatic knee osteoarthritis (PTOA). This OA phenotype progresses rapidly, with as many as 25% of patients developing radiographic joint changes within 5 years. Furthermore, these injuries typically occur in individuals 15-25 years of age, thus PTOA resulting from ACLR represents a long-term health concern. While development of PTOA is multifactorial, loading characteristics of the articular cartilage have received substantial attention in the literature, with greater loading hypothesized to result in greater cartilage degradation. Given the repetitive nature of walking and its integral role in human locomotion, gait biomechanics are commonly evaluated in efforts to identify loading characteristics that influence cartilage degradation. While cartilage loading cannot be directly quantified in vivo, peak impact forces and joint moments are commonly evaluated as biomechanical surrogates. Additionally, animal models suggest that the rate of loading may play a more important role in cartilage degradation than the magnitude of loading. While loading rates during gait have been evaluated in individuals diagnosed with knee OA, we are unaware of any literature evaluating the potential role of loading rates in the development of PTOA following ACLR. Therefore, the purpose of this investigation was to compare gait kinetics between the healthy and surgically reconstructed limbs following ACLR. We hypothesized that greater loading and loading rates would be observed in the ACLR limb compared to the healthy limb. Methods: Three-dimensional gait biomechanics were obtained from twenty-three individuals with a history of unilateral ACLR (15 females, 8 males; age = 22±4 years, mass = 74±20 kg, height = 1.70±0.12 m, time since ACLR = 39±29 months) via an optoelectric motion capture system integrated with force plates. Subjects walked along a 6m walkway at a self-selected speed. The force plates were staggered such that data for both limbs could be obtained in a single trial. Peak vertical ground reaction force (vGRF; N) and instantaneous loading rate (vGRF-LR; N/s), internal knee extension moment (KEM; Nm), and sagittal plane knee stiffness (KS; Nm/°) were identified during the first 50% of the stance phase. vGRF-LR was calculated as the 1st time-derivative of the vGRF; KEM was calculated via standard inverse dynamics; and KS was calculated as the ratio of the change in KEM to the change in knee flexion angle. Forces were normalized to body weight (xBW) and moments were normalized to the product of body weight and height (%BW*Ht). All dependent variables were compared between healthy and ACLR limbs via paired-samples t-tests (p≤0.05). Results: No differences were observed between limbs for peak vGRF (1.13±0.07 xBW vs. 1.14±0.09 xBW, p=0.318) or peak vGRF-LR (59.97±17.51 BW/s vs. 55.44±17.59 BW/s, p=0.216). However, peak KEM (4.4±1.2 %BW*Ht vs. 5.0±1.5 %BW*Ht, p=0.003) and KS (0.35±0.11 %BW*Ht/° vs. 0.40±0.12 %BW*Ht/°, p=0.003) were significantly greater in the healthy limb compared to the ACLR limb. Conclusions: While ground reaction force characteristics did not differ between the ACLR and healthy limbs, knee extension moment and stiffness were greater in the healthy limb than in the ACLR limb. The vGRF reflects the summative loading of all lower extremity joints. In contrast, KEM and KS are joint-specific. Reduced knee joint-specific loading in the ACLR limb in the presence of similar vGRF characteristics between-limbs suggests that contributions from the ankle and hip extensors to the vGRF are increased in the ACLR limb to compensate for reduced contributions from the knee extensors. These data may also suggest that insufficient, rather than excessive, loading may contribute to PTOA following ACLR. Insufficient loading may alter nutrient and waste exchange characteristics, thus resulting in a cellular energy imbalance due to the avascular nature of articular cartilage. Furthermore, altered joint-specific loading may disrupt the normal catabolic and anabolic processes that are necessary to regulate articular cartilage remodeling. Quadriceps dysfunction is a common, lingering complication following ACLR. As the quadriceps is the primary contributor KEM and KS, future research is necessary to determine if interventions targeting quadriceps dysfunction improve gait biomechanics in manners that would reduce the risk of PTOA following ACLR.