Abstract:
Background Overuse tendinopathy is an important cause of noncombat attrition in the armed forces, however, the characterization of tendon injuries after overuse is unclear. Animal experiments will help us study its mechanisms and characteristics.
Objective To analyze the characteristics of tendon injuries caused by overuse from various perspectives, including etiology, ultrasonic imaging, histopathology, and cytokine levels.
Methods Sixteen Sprague-Dawley rats were randomly divided into normal group (n=8) and injury group (n=8). The overuse tendinopathy model was established through treadmill training, with a running protocol involving a 10° uphill inclination, 17 m/min speed, 1 hour of exercise per day, and a frequency of 5 days per week for 8 weeks. Normal rats were kept in cages and allowed unrestricted movement. After 8 weeks of treadmill training, the motor function of the rats was evaluated using the CatWalk gait analysis system. Inflammation and edema infiltration were observed using high-frequency ultrasound. Pathological staining was performed to observe histological changes in the tendon tissue. The expression levels of interleukin-1β (IL-1β) and transforming growth factor beta-1 (TGF-β1) were detected by ELISA.
Results Compared with the normal group, rats in the injury group had shorter stance (P<0.001), shorter paw print length (P=0.03), lower paw print area (P<0.001), and higher swing speed (P<0.001). Ultrasound images showed low echoes of inflammation and edema infiltration around the tendon in the injury group. Pathological staining showed that the tendon tissue in the injury group presented morphological alterations, including local collagen fiber destruction, abnormal blood vessel aggregation, and proteoglycan deposition. The Bonar score of rats in the injury group was higher than that of the normal group (P<0.001). The level of serum cytokine IL-1β in the injury group was significantly higher than that in the normal group (P=0.03), and there was a trend for TGF-β1 expression to be higher (P=0.09).
Conclusion Overuse tendinopathy leads to histopathological and structural changes in tendon tissue, which are manifested by peritendinous inflammatory edematous infiltrates and gait abnormalities. The up-regulation of proinflammatory cytokines and fibrosis-related cytokines may play an important role in the pathological changes of tendons.
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