Overuse injuries and other tendon disorders represent a common challenge in orthopaedic medicine, resulting in chronic pain, functional disability and even tendon rupture. Most chronic tendon injuries and disorders are believed to start from repeated exposure to low-magnitude forces that 'injure' the tissue microscopically. However, the role of repetitive loading-- so-called 'overuse'-- in the pathogenesis of chronic tendon injury is not well-understood. In particular, tendinosis is a condition where degenerative changes occur in the absence of inflammation. In these cases it is speculated that fatigued tendon loses its endogenous reparative ability. Repetitive microtrauma may overwhelm the ability of tendon cells to repair damage, or even incite them to respond in a manner that is degradative to their local extracellular matrix. Continued repetitive activity may lead to an accumulation of damage that eventually disrupts the structure of the tendon. Because chronic tendon injuries are believed to start from repeated exposure to low-magnitude forces, we hypothesize that they are the result of cell-mediated processes (e.g., aberrant repair and/or directed degradation) rather than material fatigue. We will explore this hypothesis in an organ culture model where tendon cells can be maintained in their native three-dimensional environment. To differentiate between damage that is cell-mediated and damage due to material fatigue alone, we will first establish and then cyclically load a devitalized tendon explant to assess material damage. We will then investigate if cyclic mechanical load will instigate a damage response in vital tendon explants and whether the loads are less than those required to acutely damage devitalized tendon. A role for intrinsic tendon cells in the pathogenesis of tendon overuse injury would be implied by a lower damage threshold in vital tendon.
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