Abstract
Tendon disease causes widespread morbidity ranging from mild pain to catastrophic end-stage rupture. The pathophysiology of tendon disease is not certain. An overuse exercise model was developed using rats with the aim of developing tissue with histological, biochemical and biomechanical features similar to those in human tendinosis. Results indicate that the biological response to over-exercise of the rat Achilles tendon is similar to the literature description of pathological specimens of human with disease. Biochemical and histological analysis of the rat Achilles tendons suggest that the patho-physiology is more consistent with a repair response than with a classical inflammatory response.
Tendon disease causes widespread morbidity ranging from mild pain to catastrophic end-stage rupture and the pathophysiology of tendon disease is not certain.
To develop an overuse exercise animal model to study the pathophysiology of Achilles tendon disease.
Experimental rats were subjected to an over-exercise running regime, while control rats were maintained under normal cage activity. Achilles tendons were analyzed for histological features, glycosaminoglycan content, collagen content, collagen subtype, collagen crosslinking (hydrothermal isometric tension testing), and mechanical properties.
Experimental rat Achilles tendons demonstrated: increased nuclear numbers per high-power field (527 vs. 392, p < 0.05), decreased semi-quantitative grade for collagen organization (2.9 vs. 3.7, p < 0.05) and decreased semi-quantitative grade for collagen staining (1.9 vs 3.5, p < 0.05). The total collagen content remained unchanged (84.3 vs. 89.0% p=0.38), while the glycosaminoglycan content was increased (17.5 vs. 9.0% p=0.02). Increased levels of collagen type III were not demonstrated, however. Experimental tendons were determined to have distinct differences in the collagen crosslinking patterns, with reduced total cross links and a greater population of immature, hydrolytically unstable cross links. These differences did not, however, translate into a decrease in ultimate tensile failure during mechanical testing (UTS of 77.8 vs. 88.8 N, p=0.26).
The histology and biochemistry observed in the experimental rat Achilles tendons were similar to those described in the literature on human Achilles tendon disease.
The rat Achilles tendon over-exercise model has demonstrated histopathology that was different from a control group and was consistent with the human literature for Achilles tendon disease.
Research Grants were received from the following organizations:
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Canadian Orthopaedics Foundation
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American Foot and Ankle Society
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Dalhousie University Department of Surgery
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Nova Scotia Capitol District Health Authority Research Fund
Correspondence should be addressed to Cynthia Vezina, Communications Manager, COA, 4150-360 Ste. Catherine St. West, Westmount, QC H3Z 2Y5, Canada
