| Non-insertional disorders of the Achilles tendon cause pain, disability, may predispose to catastrophic rupture, and are increasing in frequency. Currently, the pathobiology of Achilles tendon disease is poorly understood. This thesis seeks to improve the understanding of Achilles tendon disease biology by establishing an animal model for Achilles tendon disease. The animal model is based on an over-exercise uphill treadmill running regime imposed on rats. It has been validated as providing tendon samples with histological characteristics similar to those commonly cited in the literature for human Achilles tendon disease. These include increased cellularity, and more disorganized, more intensely stained collagen fibers. Immunohistochemical staining of the diseased tendons show that the increased cell numbers are principally fibroblasts and/or endothelial cells---not leukocytes. This is suggestive that the underlying biological response is more reparative than inflammatory. Biochemical testing revealed that the tendons had increased levels of glycosaminoglycans but no increase in collagen content. The collagen thermomechanics of the Achilles tendons from running rats demonstrated decreased intrahelical crosslinking that was similar to the features observed in maturing rat tendons. These biochemical changes did not translate into altered biomechanical properties when the tendons were subjected to mechanical testing. In summary, an animal model for Achilles tendon disease has been established that produces rat Achilles tendons with histological characteristics similar to those observed in human Achilles tendon disease. The underlying histology and biochemistry is suggestive that overuse-exercise running in the rat may induce biological repair or remodeling of the Achilles tendon. |
