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Age-Related Changes in Structure and Biomechanics of Human Sartorius Tendon Collagen
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Injuries to soft tissues such as tendons affect millions of people annually. Injuries produced by in vitro mechanical overload result in damage to constituent collagen. Using bovine models, it has been found that damage to tendon results in serial kink formation within collagen fibrils in low-load tendons – a mechanism called discrete plasticity. Injuries to soft tissues such as tendons affect millions of people annually. Injuries produced by in vitro mechanical overload result in damage to constituent collagen. Using bovine models, it has been found that overload results in serial kink formation within collagen fibrils in low-load tendons -- a mechanism called discrete plasticity. Despite the prevalence of injury and our aging population, the exact mechanism behind the failure of collagen in aging human tendons has not been investigated until now. In this study, fresh contralateral human sartorius tendons from donors aged 20 to 60 were used to assess potential age-related changes in failure mechanics. Thermal stability of tendon collagen was examined and was expected to increase with age due to increased crosslinking. Damage motifs were investigated following tendon rupture using scanning electron microscopy. It was thought that discrete plasticity kinks would form following rupture in younger samples, but that the mechanism would dissipate with age. The thermal stability results suggest that there is a high density of mature crosslinks present. The exact relationship between crosslinking and age remains inconclusive. Despite these structural changes, the mechanical properties did not change with age. Discrete plasticity was not found in any tendon sample, likely due to heavy crosslinking. Individual fibrils displayed sites of local damage with exposed substructure, and kinks/turns that propagated across fibrils. These failure motifs along with the thermal stability test results support the notion that discrete plasticity is a feature of tendons that are sparsely crosslinked. This study was the first to examine how the nanoscaled, structuro-mechanical features of overload failure in human tendons varies with age. As we increase our understanding of the effect of tendon type and age on damage motifs, we will also better understand how injury occurs on the nanoscale and how healing is mediated in the body.