New work being done by Dr. Robert Mauck's Lab at UPenn utilized CHPs to examine the effect that fatigue loading has on localized tissue mechanics. Their team discovered that although fatigue loading resulted in collagen kinking and denaturation, there was no difference in the local tissue modulus when compared to fresh controls. The image below shows how CHPs were used to visualize the collagen denaturation from fatigue loading and compare with the fresh control. There was a significant increase in collagen degradation in the fatigued tissues (B vs D). They also found that the level of collagen kinking was evenly distributed in areas with and without collagen denaturation, suggesting these two structural defects are a result of independent damage mechanisms. Great read, well-done everyone!
Abstract: Fatigue loading is a primary cause of tendon degeneration, which is characterized by the disruption of collagen fibers and the appearance of abnormal (e.g., cartilaginous, fatty, calcified) tissue deposits. The formation of such abnormal deposits, which further weakens the tissue, suggests that resident tendon cells acquire an aberrant phenotype in response to fatigue damage and the resulting altered mechanical microenvironment. While fatigue loading produces clear changes in collagen organization and molecular denaturation, no data exist regarding the effect of fatigue on the local tissue mechanical properties. Therefore, the objective of this study was to identify changes in the local tissue stiffness of tendons after fatigue loading. We hypothesized that fatigue damage would reduce local tissue stiffness, particularly in areas with significant structural damage (e.g., collagen denaturation). We tested this hypothesis by identifying regions of local fatigue damage (i.e., collagen fiber kinking and molecular denaturation) via histologic imaging and by measuring the local tissue modulus within these regions via atomic force microscopy (AFM). Counter to our initial hypothesis, we found no change in the local tissue modulus as a consequence of fatigue loading, despite widespread fiber kinking and collagen denaturation. These data suggest that immediate changes in topography and tissue structure – but not local tissue mechanics – initiate the early changes in tendon cell phenotype as a consequence of fatigue loading that ultimately culminate in tendon degeneration.
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