Characterization of Tendon Loading Mechanisms: Shear Loading at Different Hierarchical Levels.

摘要

This dissertation contains three general components, each investigating an aspect of internal shear load redistribution within tendon, especially around defects. In the first section, cyclic and stress relaxation tests were performed on tendons before and after partial laceration. Average stress within the remaining intact portion of the tendon exhibited a large increase in stress concentration with a laceration depth greater than 50% of the tendon width. Nominal stress (calculated with the intact cross-sectional area) and stiffness decreased with increasing laceration depth; although the decrease was not proportional to the percent loss of cross-sectional area. This result suggests the presence of a loading mechanism, i.e. shear, within tendon in addition to axial loading of individual components of the tendon hierarchy. In the second portion of this dissertation, various aspects of shear load transfer within tendon were investigated by testing tendons and their fascicles. Porcine flexor (high stress) and rat tail (low stress) tendons maintained about 20% of the intact tendon stress when subject to overlapping lacerations (no intact fascicles end-to-end). Low stress tendons had a more rapid decline in maximum stress and modulus with increasing laceration depth and more linear, less tightly packed fascicles. Comparing shear transfer between hierarchical components, greater failure load and stiffness were seen between fibers than fascicles. Within fascicles, shear deformation mechanisms were shear-lag and sliding between fibers, with more sliding visualized. Conversely, sliding occurred at the inter-fascicular interface, with negligible shear-lag present. The final dissertation component investigated the viability of tenocytes within mechanically tested and control intact and lacerated fascicles. Fascicles were subject to either a partial, mid-substance laceration (single laceration), longitudinally separated overlapping lacerations (double laceration), or remained intact for testing. Peak and steady state load and stiffness decreased from the intact to single laceration to double laceration groups. Approximately 45% of intact values were maintained in double laceration fascicles (eliminating all intact fibers end-to-end). Cellularly, a large decrease in viability was seen in both laceration groups, the cell death primarily occurring within a longitudinal plane, which corresponded to high shear load transfer and extended far from the laceration site.