Abstract
The skeletal system exhibits functional adaptation. For bone the mechanotransduction mechanisms have been well elucidated; in contrast, the response of tendon to its mechanical environment is much more poorly understood despite tendon disorders being commonly encountered in clinical practice. This study presents a novel approach to developing an isolated tendon system in vivo. This model is used to test the hypothesis that stress-shielding, and subsequent restressing, causes significant biomechanical changes. We propose a control mechanism that governs this process.
A custom-built external fixator was used to functionally isolate the ovine patellar tendon(PT). In group 1 animals(n=5) the right PT was stress-shielded for 6 weeks. This was achieved by drawing the patella towards the tibial tubercle, thus slackening the PT. In group 2 (n=5) the PT was stress-shielded for 6 weeks. The external fixator was then removed and the PT physiologically loaded for a further 6 weeks. In each case, the PT subsequently underwent tensile testing and measurement of length(L) and cross-sectional area(CSA). The untreated left PTs acted as controls (n=10).
6 weeks of stress-shielding significantly decreased material and structural properties of tendon compared to controls (elastic modulus(E) 76.2%, ultimate tensile strength(UTS) 69.3%, stiffness(S) 79.2%, ultimate load(UL) 68.5%, strain energy(SE) 60.7%; p< 0.05). Ultimate strain(US), L and CSA were not significantly changed. 6 weeks of subsequent functional loading (Group 2) caused some improvement in material properties, but greater recovery in structural properties (E 79.8%, UTS 91.8%, S 96.7%, UL 92.7%, SE 96.5%). CSA was significantly greater than Group 1 tendons at 114% of control value.
Previous models of tendon remodelling have relied on either joint immobilization or direct surgical procedures. This model allows close control of the tendon’s mechanical environment whilst allowing normal joint movement and avoiding surgical insult to the tendon itself. The hypothesis that stress-shielding, and subsequent restressing, causes significant biomechanical changes has been upheld. We propose that the biomechanical changes observed are governed by a strain homeostasis feedback mechanism.
Correspondence should be addressed to Mr Carlos Wigderowitz, Senior Lecturer, University Department of Orthopaedic and Trauma Surgery, Ninewells Hospital and Medical School, Dundee DD1 9SY.
