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Multiscale mechanisms of tendon fatigue damage progression and severity are strain and cycle dependent.

ABSTRACT: Tendinopathies are common chronic injuries that occur when damage accumulation caused by sub-rupture fatigue loading outpaces repair. Studies have linked fatigue loading with various mechanical, structural, and biological changes associated with pathology. However, the multiscale progression of damage accumulation with respect to area, severity and the distinct contributions of strain level and number of cycles has not been fully elucidated. The objective of this study was to investigate multiscale mechanisms underlying fatigue damage accumulation and their effect on the cellular environment. Using an in situ model in rat tail tendon (RTT), fatigue loading was applied at various strains and cycle numbers to induce fatigue damage. Pre- and post- fatigue diagnostic mechanical testing, second harmonic generation (SHG) imaging, and transmission electron microscope (TEM) imaging were used to investigate extracellular and cellular damage modes at multiple scales. Fatigue loading at strains at or below 1.0% resulted in no significant changes in SHG damage area or severity and no changes in collagen fibril or cell morphology compared with controls. Fatigue loading at strains above 1.5% resulted in greater mechanical changes correlated with increased damage area measured by SHG and collagenous damage observed by TEM. Increased cycles at high strain further altered mechanical properties, increased structural damage severity (but not area), and altered TEM collagen rupture patterns. Cell morphology was similarly progressively affected with increased strain and cycle number. These damage mechanisms that may trigger degenerative changes characteristic of tendinopathy could be targeted as a part of prevention or therapy.

SUBMITTER: Ros SJ

PROVIDER: S-EPMC6608713 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature

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Multiscale mechanisms of tendon fatigue damage progression and severity are strain and cycle dependent.

Ros Stephen J SJ Muljadi Patrick M PM Flatow Evan L EL Andarawis-Puri Nelly N

Journal of biomechanics 20190119

Tendinopathies are common chronic injuries that occur when damage accumulation caused by sub-rupture fatigue loading outpaces repair. Studies have linked fatigue loading with various mechanical, structural, and biological changes associated with pathology. However, the multiscale progression of damage accumulation with respect to area, severity and the distinct contributions of strain level and number of cycles has not been fully elucidated. The objective of this study was to investigate multisc ...[more]

PMID: 30732906

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Project description:Tendon pathology is associated with damage. While tendon damage is likely initiated by mechanical loading, little is known about the specific etiology. Damage is defined as an irreversible change in the microstructure that alters the macroscopic mechanical parameters. In tendon, the link between mechanical loading and microstructural damage, resulting in macroscopic changes, is not fully elucidated. In addition, tendon damage at the macroscale has been proposed to initiate when tendon is loaded beyond a strain threshold, yet the metrics to define the damage threshold are not determined. We conducted multi-scale mechanical testing to investigate the mechanism of tendon damage by simultaneously quantifying macroscale mechanical and microstructural changes. At the microscale, we observe full recovery of the fibril strain and only partial recovery of the interfibrillar sliding, indicating that the damage initiates at the interfibrillar structures. We show that non-recoverable sliding is a mechanism for tendon damage and is responsible for the macroscale decreased linear modulus and elongated toe-region observed at the fascicle-level, and these macroscale properties are appropriate metrics that reflect tendon damage. We concluded that the inflection point of the stress-strain curve represents the damage threshold and, therefore, may be a useful parameter for future studies. Establishing the mechanism of damage at multiple length scales can improve prevention and rehabilitation strategies for tendon pathology.Statement of significanceTendon pathology is associated with mechanically induced damage. Damage, as defined in engineering, is an irreversible change in microstructure that alters the macroscopic mechanical properties. Although microstructural damage and changes to macroscale mechanics are likely, this link to microstructural change was not yet established. We conducted multiscale mechanical testing to investigate the mechanism of tendon damage by simultaneously quantifying macroscale mechanical and microstructural changes. We showed that non-recoverable sliding between collagen fibrils is a mechanism for tendon damage. Establishing the mechanism of damage at multiple length scales can improve prevention and rehabilitation strategies for tendon pathology.

Dataset Information

Multiscale mechanisms of tendon fatigue damage progression and severity are strain and cycle dependent.

Publications

Multiscale mechanisms of tendon fatigue damage progression and severity are strain and cycle dependent.

Similar Datasets

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