Abstract:
Tendons, functionally categorized as positional or energy-storing, have differing structures and mechanical properties but are both susceptible to damage. Tendinopathy is a chronic condition that exhibits repetitive mechanical overuse damage. Despite the significant societal impact of tendinopathy, its development is poorly understood, generating a plethora of suboptimal treatment methods. This thesis investigated cyclic buckling, present in tendon unloading, as the potential root cause for the initiation and subsequent damage propagation, preceding tendinopathy. Associated structural effects were investigated from the nano-to-micro scales, using fluorescence microscopy with a collagen hybridizing peptide, second harmonic generation microscopy, and polarized light microscopy. Mechanical properties were measured via tensile testing. The results showed cyclic buckling caused structural changes, from molecular denaturation to fibre kinkbanding, accompanied by reduced ultimate tensile strength. Importantly, changes were seen in both tendon types, suggesting that cyclic buckling could be a loading mode responsible for damaging human tendons that frequently suffer tendinopathy.
Description:
1 online resource (xi,156, 9 unnumbered pages) : illustrations (some colour, charts (some colour), graphs (some colour)
Includes abstract and appendices.
Includes bibliographical references (pages 141-153).