背景:前交叉韧带(ACL)损伤使个体容易患上早发性膝关节骨关节炎(OA)。ACL损伤和重建后异常的关节负荷很明显。关节生物力学改变与膝关节OA发展之间的关系尚不清楚。
目的:损伤和重建后初始膝关节动力学和内侧室接触力的改变与重建后5年的影像学膝关节OA有关。
方法:病例对照研究;证据水平,3.
方法:急性,单侧ACL损伤术前(基线)和术后(训练后)以及6个月时完成步态分析,1年,重建2年后。表面肌电图和膝关节生物力学数据用作肌电图驱动的肌肉骨骼模型的输入,以估计膝关节接触力。重建后5年,患者完成了影像学检查。比较了有和没有影像学膝关节OA的患者之间膝关节动力学和接触力的差异。
结果:患有OA的患者在基线时的额平面间差异大于没有OA(非OA)的患者(峰值膝关节内收力矩差异:0.00±0.08N·m/kg·m[非OA]vs-0.15±0.09N·m/kg·m[OA],P=.014;膝关节内收力矩峰值脉冲差:-0.001±0.032N·m·s/kg·m[nonOA]vs-0.048±0.031N·m·s/kg·m[OA];P=.042)。在基线时,骨关节炎组的患肢膝关节内收力矩冲动也低于无骨关节炎组(0.087±0.023N·m·s/kg·m[nonOA]vs0.049±0.018N·m·s/kg·m[OA],P=.023)。训练后没有明显的组间差异,但在重建后6个月重新出现(峰值膝关节内收力矩差异:0.02±0.04N·m/kg·m[nonOA]vs-0.06±0.11N·m/kg·m[OA],P=.043)。此外,在6个月时,OA组的受累肢体的内侧室接触力峰值低于无OA组(2.89±0.52体重[nonOA]vs2.10±0.69体重[OA],P=.036)。
结论:ACL重建后5年有影像学膝关节OA的患者,在损伤和重建后早期没有OA的患者,其膝关节内收力矩和内侧室关节接触力较低。
BACKGROUND: Anterior cruciate ligament (ACL) injury predisposes individuals to early-onset knee joint osteoarthritis (OA). Abnormal joint loading is apparent after ACL injury and reconstruction. The relationship between altered joint biomechanics and the development of knee OA is unknown.
OBJECTIVE: Altered knee joint kinetics and medial compartment contact forces initially after injury and reconstruction are associated with radiographic knee OA 5 years after reconstruction.
METHODS: Case-control study; Level of evidence, 3.
METHODS: Individuals with acute, unilateral ACL injury completed gait analysis before (baseline) and after (posttraining) preoperative rehabilitation and at 6 months, 1 year, and 2 years after reconstruction. Surface electromyographic and knee biomechanical data served as inputs to an electromyographically driven musculoskeletal model to estimate knee joint contact forces. Patients completed radiographic testing 5 years after reconstruction. Differences in knee joint kinetics and contact forces were compared between patients with and those without radiographic knee OA.
RESULTS: Patients with OA walked with greater frontal plane interlimb differences than those without OA (nonOA) at baseline (peak knee adduction moment difference: 0.00 ± 0.08 N·m/kg·m [nonOA] vs -0.15 ± 0.09 N·m/kg·m [OA], P = .014; peak knee adduction moment impulse difference: -0.001 ± 0.032 N·m·s/kg·m [nonOA] vs -0.048 ± 0.031 N·m·s/kg·m [OA], P = .042). The involved limb knee adduction moment impulse of the group with osteoarthritis was also lower than that of the group without osteoarthritis at baseline (0.087 ± 0.023 N·m·s/kg·m [nonOA] vs 0.049 ± 0.018 N·m·s/kg·m [OA], P = .023). Significant group differences were absent at posttraining but reemerged 6 months after reconstruction (peak knee adduction moment difference: 0.02 ± 0.04 N·m/kg·m [nonOA] vs -0.06 ± 0.11 N·m/kg·m [OA], P = .043). In addition, the OA group walked with lower peak medial compartment contact forces of the involved limb than did the group without OA at 6 months (2.89 ± 0.52 body weight [nonOA] vs 2.10 ± 0.69 body weight [OA], P = .036).
CONCLUSIONS: Patients who had radiographic knee OA 5 years after ACL reconstruction walked with lower knee adduction moments and medial compartment joint contact forces than did those patients without OA early after injury and reconstruction.