Tendons function to transfer load, maintain alignment and permit motion in joints. To perform these functions, tendons have complex mechanical behavior which is modulated by the tissue’s structure and composition, such as the collagen fibers and surrounding extracellular matrix. When these matrix proteins are altered, the mechanical properties are also altered, which could potentially lead to reduced loading and healing capacity. Diabetes is a metabolic disease which, among other co-morbidities, has been associated with Achilles tendon disorganization and tendinopathy, as well as increased overall joint stiffness in humans . We have recently reported that the skin from the Db/Db diabetic mouse, a model of Type II Diabetes, as well as the skin from human diabetics, have impaired biomechanical properties compared to non-diabetic skin as the result of altered extracellular matrix composition. . However, the mechanical properties of tendons from these animals have never been studied and could serve as a unique model of altered collagen structure as well as provide further understanding to the cause of tendinous injuries in the diabetic population. Therefore, the objective of this study is to measure the tensile mechanical properties and collagen fiber re-alignment in the db/db mouse model compared to non-diabetic controls. We hypothesize that tendon stiffness and modulus will be increased in the db/db group in the insertion site and midsubstance, and that db/db tendons will re-align earlier and faster during the testing protocol.
- Bioengineering Division
Altered Mechanical Properties and Fiber Re-Alignment in Diabetic Mouse Supraspinatus and Achilles Tendons
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Connizzo, BK, Liechty, KW, & Soslowsky, LJ. "Altered Mechanical Properties and Fiber Re-Alignment in Diabetic Mouse Supraspinatus and Achilles Tendons." Proceedings of the ASME 2012 Summer Bioengineering Conference. ASME 2012 Summer Bioengineering Conference, Parts A and B. Fajardo, Puerto Rico, USA. June 20–23, 2012. pp. 857-858. ASME. https://doi.org/10.1115/SBC2012-80129
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