Abstract
Introduction
Tendon disease and rupture are common in patients with diabetes and these are exacerbated by poor healing. although nanoscale changes in diabetic tendon are linked to increased strength and stiffness. The resistance to mechanical damage of a tissue may be measured using fatigue testing but this has not been carried out in diabetic tendon, although the toughness of diabetic bone is known to be reduced. The aim of this study was to measure the static fatigue behaviour of tendons from a streptozotocin (STZ)-induced rat model of diabetes, hypothesising that diabetes causes tendon to show lower resistance to mechanical damage than healthy tendon.
Materials and Methods
Diabetic (n=3, 12 weeks post-STZ) and age-matched control (n=3) adult male Sprague Dawley rats were culled, tails harvested and stored at −80ºC. Following defrosting, fascicles (5 per animal) were carefully dissected, mean diameter measured using an optical micrometer and mounted in a Bose Biodynamics test machine using custom grips in a PBS bath. Static fatigue testing at 30 MPa to failure enabled both elastic modulus (initial ramp) and steady state creep rate (gradient at creep curve inflexion) to be measured. Data are reported as median ± interquartile range and pw0.05 using a Mann-Whitney U test was taken as significant.
Results
Confirming previous reports, tendon from diabetic rats showed significantly higher elastic modulus (201 ± 68 MPa) than healthy (151 ± 62 MPa). Strain at failure showed no differences between groups. Tendon from diabetic rats showed significantly slower steady state creep (71 ± 44 μstrain s−1) than healthy (691 ± 1000 μstrain s−1).
Discussion
These preliminary data show an order of magnitude larger resistance to mechanical damage in diabetic tendons, possibly associated with the previously reported increased packing and decreased fibril diameters. Energy-storing flexor tendons, the most commonly affected in diabetics, and the positional tendons tested here show similar fatigue behaviour when tested at the same fraction of “stress-in-life”. Further investigation is required into the cell tissue repair response in diabetes in order to link reduced rates of mechanical damage with the clinically increased risk of disease and rupture in diabetic patients.
