Department of Biomedical Engineering, Pennsylvania State University, University Park, PA, United States.
Department of Biomedical Engineering, Pennsylvania State University, University Park, PA, United States; Department of Orthopaedics and Rehabilitation, Pennsylvania State University, Hershey, PA, United States.
J Biomech. 2023 Apr;151:111545. doi: 10.1016/j.jbiomech.2023.111545. Epub 2023 Mar 12.
While overuse is a prominent risk factor for tendinopathy, the fatigue-induced structural damage responsible for initiating tendon degeneration remains unclear. Denaturation of collagen molecules and collagen fiber disorganization have been observed within certain tendons in response to fatigue loading. However, no studies have investigated whether these forms of tissue damage occur in Achilles tendons, which commonly exhibit tendinopathy. Therefore, the objective of this study was to determine whether mouse Achilles tendons undergo collagen denaturation and collagen fiber disorganization when cyclically loaded to failure. Consistent with previous testing of other energy-storing tendons, we found that cyclic loading of mouse Achilles tendons produced collagen disorganization but minimal collagen denaturation. To determine whether the lack of collagen denaturation is unique to mouse Achilles tendons, we monotonically loaded the Achilles and other mouse tendons to failure. We found that the patellar tendon was also resistant to collagen denaturation, but the flexor digitorum longus (FDL) tendon and tail tendon fascicles were not. Furthermore, the Achilles and patellar tendons had a lower tensile strength and modulus. While this may be due to differences in tissue structure, it is likely that the lack of collagen denaturation during monotonic loading in both the Achilles and patellar tendons was due to failure near their bony insertions, which were absent in the FDL and tail tendons. These findings suggest that mouse Achilles tendons are resistant to collagen denaturation in situ and that Achilles tendon degeneration may not be initiated by mechanically-induced damage to collagen molecules.
虽然过度使用是腱病的一个突出危险因素,但导致肌腱退化的疲劳引起的结构损伤仍不清楚。在某些疲劳负荷下的肌腱中,已经观察到胶原分子的变性和胶原纤维的紊乱。然而,尚无研究调查这些组织损伤是否发生在常见腱病的跟腱中。因此,本研究的目的是确定在周期性加载至失效时,小鼠跟腱是否会发生胶原变性和胶原纤维紊乱。与先前对其他储能肌腱的测试一致,我们发现周期性加载小鼠跟腱会导致胶原纤维紊乱,但胶原变性最小。为了确定胶原变性的缺乏是否是小鼠跟腱所特有的,我们单调地加载跟腱和其他小鼠肌腱至失效。我们发现髌腱也不易发生胶原变性,但屈趾长肌(FDL)肌腱和尾腱束则不然。此外,跟腱和髌腱的拉伸强度和模量较低。虽然这可能是由于组织结构的差异,但在 FDL 和尾腱中,单调加载时跟腱和髌腱均缺乏胶原变性,很可能是由于它们靠近骨插入处发生了失效,而 FDL 和尾腱中则没有骨插入处。这些发现表明,小鼠跟腱在原位不易发生胶原变性,并且跟腱退化可能不是由机械诱导的胶原分子损伤引发的。