Hinterwimmer S, Baumgart R, Plitz W
Chirurgische Klinik und Poliklinik der LMU München, Standort Innenstadt, Nussbaumstrasse 20, 80336 Munich, Germany.
Arch Orthop Trauma Surg. 2002 Nov;122(8):454-8. doi: 10.1007/s00402-002-0432-5. Epub 2002 Sep 20.
The biomechanical changes in the cruciate ligament-deficient knee are still widely unexplained. By producing a model of cruciate ligament insufficiency in the knee joint, we wanted to provide an experimental explanation for the great amount of secondary injuries to the knee joint after conservative treatment of an anterior cruciate ligament rupture.
The forces exerted on the medial and lateral collateral ligament were measured in ten fresh human cadaver knees. While simulating muscle force and body weight, the ligamentous loading patterns were determined before and after the anterior cruciate ligament was transected. The specimens were moved in a special apparatus from 0 degrees extension to 100 degrees flexion. Strain gauges were used to measure the ligament forces. They were fixed at the bony origins and insertions of the examined ligaments. The method allowed all ligamentous and capsular structures to be kept intact, thereby creating nearly physiological conditions by simulating muscular strength and axial force.
During the quasistatic measurements, the relative changes of the ligament forces were determined from one angle position to the next. The variability of these relative values were very small among the ten specimens. The method yielded reproducible ligament force data. The values obtained in the intact knee joints were markedly similar to those reported in the literature. Cutting the anterior cruciate ligament led to a general increase of the ligament forces on both collateral ligaments.
Our results show excess stress of the main ligamentous stabilisers after anterior cruciate ligament transection. This is an explanation for the secondary injuries often seen after conservative treatment of anterior cruciate ligament rupture as a result of impaired knee biomechanics.
交叉韧带损伤膝关节的生物力学变化仍未得到充分解释。通过建立膝关节交叉韧带功能不全模型，我们旨在为前交叉韧带断裂保守治疗后膝关节大量继发损伤提供实验性解释。
在10个新鲜人体尸体膝关节上测量施加于内外侧副韧带的力。在模拟肌肉力量和体重的同时，确定前交叉韧带横断前后的韧带负荷模式。标本在特殊装置中从伸直0度移动到屈曲100度。使用应变片测量韧带力。应变片固定在所检查韧带的骨附着点处。该方法可使所有韧带和关节囊结构保持完整，从而通过模拟肌肉力量和轴向力创造接近生理的条件。
在准静态测量过程中，确定了从一个角度位置到下一个角度位置韧带力的相对变化。这10个标本中这些相对值的变异性非常小。该方法产生了可重复的韧带力数据。在完整膝关节中获得的值与文献报道的值明显相似。切断前交叉韧带导致两侧副韧带的韧带力普遍增加。
我们的结果显示前交叉韧带横断后主要韧带稳定结构存在应力过度。这解释了前交叉韧带断裂保守治疗后因膝关节生物力学受损而常见的继发损伤。
