Development of a continuum damage model to predict accumulation of sub-failure damage in tendons.

Many painful and physically debilitating conditions involve sub-failure mechanical damage to seemingly intact connective tissues such as tendons and ligaments. We found that the amount of denatured collagen in rat tail tendon (RTT) fascicles increased over experiments of cyclic loading to a constant load level (creep cyclic fatigue) with fluorescently tagged collagen hybridizing peptides (CHPs) that bind to denatured collagen. To better understand tendon sub-failure damage progression, computational modeling of tendon materials via finite element analysis in FEBio has been conducted. The objective of this project was to develop, implement, and test the ability of a new continuum damage mechanics (CDM) model in FEBio to represent the sub-failure damage behavior seen in our RTT fascicle creep cyclic fatigue experimental data. There appeared to be two distinct mechanisms responsible for the creep cyclic fatigue softening behavior of RTT fascicles over the number of cycles to failure: the preconditioning effect and overall collagen damage. In our finite element (FE) models, the RTT fascicle undamaged elastic constitutive material was composed of a matrix and fibers described by the Coupled Veronda-Westmann and exponential-linear materials. This undamaged elastic material was convolved with a modified CDM model adapted from Balzani et al., in 2012. The novelty of the Balzani damage model is the inclusion of two interrelated mechanisms described as continuous and discontinuous damage. The continuous damage formulation calculates damage accumulation during the loading and reloading of each new cycle, while the discontinuous damage approach accumulates damage from the maximum strain over the loading history to the current time. We modified the Balzani damage model formulations to represent exponential and sigmoidal increases in damage marked by the preconditioning effect and collagen damage in RTT fascicles as functions of continuous and discontinuous damage. The original Balzani damage model was first verified, then the modified CDM model was implemented into FEBio and used to reproduce the sample specific experimental creep cyclic fatigue stress-strain data as well as predict incremental cyclic fatigue. The resulting model will be useful for future experimental and computational studies of damage mechanics to understand tendon pathologies.

Characterization and finite element validation of transchondral strain in the human hip during static and dynamic loading.

Distribution of strain through the thickness of articular cartilage, or transchondral strain, is highly dependent on the geometry of the joint involved. Excessive transchondral strain can damage the solid matrix and ultimately lead to osteoarthritis. Currently, high-resolution transchondral strain distribution is unknown in the human hip. Thus, knowledge of transchondral strain patterns is of fundamental importance to interpreting the patterns of injury that occur in prearthritic hip joints. This study had three main objectives. We sought to 1) quantify high-resolution transchondral strain in the native human hip, 2) determine differences in transchondral strain between static and dynamic loading conditions to better understand recovery and repressurization of cartilage in the hip, and 3) create finite element (FE) models of the experimental testing to validate a modeling framework for future analysis. The transchondral strain patterns found in this study provide insight on the localization of strain within cartilage of the hip. Most notably, the chondrolabral junction experienced high tensile and shear strain across all samples, which explains clinical data reporting it as the most common region of damage in cartilage of the hip. Further, the representative FE framework was able to match the experimental static results and predict the dynamic results with very good agreement. This agreement provides confidence for both experimental and computational measurement methods and demonstrates that the specific anisotropic biphasic FE framework used in this study can both describe and predict the experimental results.

Collagen denaturation is initiated upon tissue yield in both positional and energy-storing tendons.

Tendons are collagenous soft tissues that transmit loads between muscles and bones. Depending on their anatomical function, tendons are classified as positional or energy-storing with differing biomechanical and biochemical properties. We recently demonstrated that during monotonic stretch of positional tendons, permanent denatured collagen begins accumulating upon departing the linear region of the stress-strain curve. However, it is unknown if this observation is true during mechanical overload of other types of tendons. Therefore, the purpose of this study was to investigate the onset of collagen denaturation relative to applied strain, and whether it differs between the two tendon types. Rat tail tendon (RTT) fascicles and rat flexor digitorum longus (FDL) tendons represented positional and energy-storing tendons, respectively. The samples were stretched to incremental levels of strain, then stained with fluorescently labeled collagen hybridizing peptides (CHPs); the CHP fluorescence was measured to quantify denatured collagen. Denatured collagen in both positional and energy-storing tendons began to increase at the yield strain, upon leaving the linear region of the stress-strain curve as the sample started to permanently deform. Despite significant differences between the two tendon types, it appears that collagen denaturation is initiated at tissue yield during monotonic stretch, and the fundamental mechanism of failure is the same for the two types of tendons. At tissue failure, positional tendons had double the percentage of denatured collagen compared to energy-storing tendons, with no difference between 0% control groups. These results help to elucidate the etiology of subfailure injury and rupture in functionally distinct tendons.