Development of overuse tendinopathy: A new descriptive model for the initiation of tendon damage during cyclic loading

Abstract

Tendinopathic tissue has long been characterized by changes to collagen microstructure. However, initial tendon damage from excessive mechanical loading-a hallmark of tendinopathy development-could occur at the nanoscale level of collagen fibrils. Indeed, it is on this scale that tenocytes interact directly with tendon matrix, and excessive collagen fibril damage not visible at the microscale could trigger a degenerative cascade. In this study, we explored whether initiation of tendon damage during cyclic loading occurs via a longitudinal compression-induced buckling mechanism of collagen fibrils leading to nanoscale kinkband development. Two groups of tendons were cyclically loaded to equivalent peak stresses. In each loading cycle, tendons in one group were unloaded to the zero displacement mark, while those in the other group were unloaded to a nominal level of tension, minimizing the potential for fibril buckling. Tendons that were unloaded to the zero displacement mark ruptured significantly sooner during cyclic loading (1,446 ± 737 vs. 4,069 ± 1,129 cycles), indicating that significant fatigue damage is accrued in the low stress, toe region of the load-deformation response. Ultrastructural analysis using scanning electron microscopy of tendons stopped after 1,000 cycles showed that maintaining a nominal tension slowed the accumulation of kinkbands, supporting a longitudinal compression-induced buckling mechanism as the basis for kinkband development. Based on our results, we present a new descriptive model for the initiation of tendon damage during cyclic loading. The so-called Compression of Unrecovered Elongation or CUE Model may provide useful insight into the development of tendinopathy. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:467-476, 2018.

In Vitro Innovation of Tendon Tissue Engineering Strategies

“…Mechanical forces are translated, by means of mechanotransduction processes, into biochemical signals that are able to activate and control key signaling pathways into tendon cells [94,95]. However, if on the one hand normal mechanical loads are essential for appropriate tendon development/maintenance and to induce anabolic responses in tendon cells [95], on the other, abnormal mechanical forces cause pathological conditions (such as tendinopathy), determining the cellular catabolic adaption of the tendon [1,96].…”

Mechanical and Material Tendon Properties in Patients With Proximal Patellar Tendinopathy

“…Furthermore, although tensile stiffness has received all the attention of studies assessing the impact of tendinopathy on tendon mechanical properties, there is to date no information regarding tendon elastic hysteresis. The energy dissipation (∼9% in healthy tendons; Bennett et al, 1986) occurring during recoil affects the amount of energy recovered from tendon stretch and, importantly, may be linked to the tissue susceptibility to fatigue damage (Maganaris et al, 2008;Farris et al, 2011;Lichtwark et al, 2013;Herod and Veres, 2017). The current lack of information about tendon hysteresis seems mainly due to the methodological difficulty to test this parameter in vivo (Finni et al, 2013).…”

Fatigue loading of tendon results in collagen kinking and denaturation but does not change local tissue mechanics

“…Currently, limited data exist regarding the specific changes in local tissue structure and mechanics that result from tendon fatigue damage. Clear changes in collagen organization (Fung et al, 2010; Sereysky et al, 2012; Herod and Veres, 2017) and molecular damage in the form of denaturation (Veres et al, 2014) have been identified. Surprisingly, these structural changes do not seem to alter tissue strains at the cellular level (Shepherd et al, 2014).…”