Investigation of the Biomechanical, Structural, and Cellular Response to Fatigue Damage Accumulation in a Novel In Vitro Tail Tendon Injury Model

Tendinopathy is a highly prevalent degenerative pathology of tendons that affects the elderly and working population. Accumulation of matrix damage over time is thought to lead to this pathology, however, little is known about the effect of fatigue damage on the ability of tenocytes to repair injury and remodel. To better understand the biomechanical processes of damage accumulation and tendon degradation in subrupture fatigue, as well as the repair response after injury, this thesis focuses on the development and characterization of an in vitro fatigue damage model in the rat tail tendon fascicle. This work provides novel insight into the biomechanics of tendon injury and describes tendon matrix damage at the macro-, micro-, and ultra-structural levels. Furthermore, a novel technique for quantitative image analysis and segmentation of tendon damage using edge detection was developed for this work. Lastly, the effect of fatigue injury on cellular response was investigated using quantitative gene expression analysis and found increased catabolic processes in fatigue damaged tendons. Together, studies provide a solid foundation for future work on studying the effect of fatigue damage on tenocyte response to matrix injury.