Basic mechanisms of tendon fatigue damage.

Abstract

Pathologic processes intrinsic and extrinsic to the tendons have been proposed as the underlying cause of rotator cuff disease, but the precise etiology is not known. Tear formation is, in part, attributable to the accumulation of subrupture tendon fatigue damage. We review the molecular, mechanical, and structural changes induced in tendons subjected to controlled amounts of fatigue loading in an animal model of early tendinopathy. The distinct tendon responses to low and moderate levels of loading, as opposed to high levels, provide insight into the potential mechanisms for the therapeutic benefits of exercise in the treatment of rotator cuff tendinopathy. The progression of damage accumulation leading to fiber rupture and eventual tendon tearing seen with higher loading illustrates the progression from tendinopathy to full-thickness tearing. We hope that this more realistic animal model of tendon fatigue damage will allow better assessment of biologic, mechanical, tissue-engineering, and rehabilitation strategies to improve repair success.