Biomedical Engineering, University of Calgary, 2500 University Drive NW, Calgary, AB T2N 1N4, Canada; Human Performance Laboratory, Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada.
Human Performance Laboratory, Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada; Advanced Imaging and Histopathology Core, Qatar Biomedical Research Institute, Hamad Bin Khalifa University, Qatar Foundation, Doha, Qatar.
Clin Biomech (Bristol). 2020 Aug;78:105095. doi: 10.1016/j.clinbiomech.2020.105095. Epub 2020 Jun 17.
Mechanical stimulation of joints regulates the biosynthetic activity of chondrocytes. It has been argued that excessive loading might cause chondrocyte death, leading to degeneration of cartilage and cause osteoarthritis. The aims of this study were to apply a high, short-term loading, and a low intensity, long-term loading protocol to intact joints in life animals and determine changes in synovial fluid and the percentage of dead cells in rabbit knee cartilage.
Nine rabbits were subjected to unilateral exercise loading consisting of five sets of 10 maximal eccentric knee contractions. Another 6 rabbits were subjected to submaximal concentric contractions for 30 min at 20% of the maximum isometric knee extensor force. Contralateral joints served as unloaded controls. Cell viability was assessed using confocal microscopy. Synovial fluid was analyzed for total protein concentration and total number of identifiable proteins and was compared to protein content of control rabbits (n = 4).
Neither the high-intensity, short-term nor the low-intensity, long-term loading protocol caused increased chondrocyte death compared to the unloaded control joints. Total synovial fluid protein concentration was the same before and after exercise. Following the high-intensity exercise protocol, the number of identifiable proteins was decreased, while following the low-intensity exercise protocol, the number of identifiable proteins was increased compared to control.
Chondrocytes are well protected in the intact joint and withstood maximal eccentric muscular loading, and maximal endurance loading. Synovial fluid protein content was changed after exercise, and these changes depended crucially on the type of loading.
关节的机械刺激调节软骨细胞的生物合成活性。有人认为，过度负荷可能导致软骨细胞死亡，导致软骨退化并引发骨关节炎。本研究的目的是在活体动物的完整关节上应用高、短期负荷和低强度、长期负荷方案，并确定兔膝关节软骨滑膜液和细胞死亡百分比的变化。
9 只兔子进行了单侧运动负荷，包括 5 组 10 次最大的离心膝关节收缩。另外 6 只兔子进行了 30 分钟 20%最大等长膝关节伸肌力的次最大向心收缩。对侧关节作为未加载对照。使用共聚焦显微镜评估细胞活力。分析滑膜液的总蛋白浓度和总可识别蛋白数量，并与对照兔（n=4）的蛋白含量进行比较。
高强度、短期和低强度、长期负荷方案均未导致软骨细胞死亡增加与未加载对照关节相比。运动前后总滑膜液蛋白浓度相同。高强度运动方案后，可识别蛋白数量减少，而低强度运动方案后，可识别蛋白数量增加与对照相比。
完整关节中的软骨细胞受到很好的保护，可以承受最大的离心肌肉负荷和最大的耐力负荷。运动后滑膜液蛋白含量发生变化，这些变化取决于负荷的类型。
