Dataset Information

Molecular response of the patellar tendon to fatigue loading explained in the context of the initial induced damage and number of fatigue loading cycles.

ABSTRACT: Accumulation of sub-rupture fatigue damage has been implicated in the development of tendinopathy. We previously developed an in vivo model of damage accumulation using the rat patellar tendon. Our model allows us to control the input loading parameters to induce fatigue damage in the tendon. Despite this precise control, the resulting induced damage could vary among animals because of differences in size or strength among their patellar tendons. In this study, we used number of applied cycles and initial (day-0) parameters that are indicative of induced damage to assess the molecular response 7 days after fatigue loading. We hypothesized that day-0 hysteresis, elongation, and stiffness of the loading and unloading load-displacement curves would be predictive of the 7-day molecular response. Results showed correlations between the 7-day molecular response and both day-0 elongation and unloading stiffness. Additionally, loading resulted in upregulation of several extracellular matrix genes that suggest adaptation; however, several of these genes (Col-I, -XII, MMP 2, and TIMP 3) shut down after a high level of damage was induced. We showed that evaluating the 7-day molecular profile in light of day-0 elongation provides important insight that is lost from comparing number of fatigue loading cycles only. Our data showed that loading generally results in an adaptive response. However, the tendon's ability to effectively respond deteriorates as greater damage is induced.

SUBMITTER: Andarawis-Puri N

PROVIDER: S-EPMC3763927 | biostudies-literature | 2012 Aug

REPOSITORIES: biostudies-literature

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Molecular response of the patellar tendon to fatigue loading explained in the context of the initial induced damage and number of fatigue loading cycles.

Andarawis-Puri Nelly N Sereysky Jedd B JB Sun Hui B HB Jepsen Karl J KJ Flatow Evan L EL

Journal of orthopaedic research : official publication of the Orthopaedic Research Society 20120106 8

Accumulation of sub-rupture fatigue damage has been implicated in the development of tendinopathy. We previously developed an in vivo model of damage accumulation using the rat patellar tendon. Our model allows us to control the input loading parameters to induce fatigue damage in the tendon. Despite this precise control, the resulting induced damage could vary among animals because of differences in size or strength among their patellar tendons. In this study, we used number of applied cycles a ...[more]

PMID: 22227881

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Project description:BackgroundMotion analysis is commonly used to evaluate joint kinetics in children with cerebral palsy who exhibit gait disorders. However, one cannot readily infer muscle-tendon forces from joint kinetics. This study investigates the use of shear wave tensiometry to characterize Achilles and patellar tendon forces during gait.Research questionHow do Achilles and patellar tendon wave speed and loading modulate with walking speed in typically developing children?MethodsTwelve typically developing children (9-16 years old) walked on an instrumented treadmill with shear wave tensiometers over their Achilles (n = 11) and patellar (n = 9) tendons. Wave speeds were recorded at five leg length-normalized walking speeds (very slow to very fast). Achilles and patellar tendon moment arms were measured with synchronized ultrasound and motion capture. The tendon wave speed-load relationship was calibrated at the typical walking speed and used to estimate tendon loading at other walking speeds.ResultsCharacteristic Achilles and patellar tendon wave speed trajectories exhibited two peaks over a gait cycle. Peak Achilles tendon force closely aligned with peak ankle plantarflexor moment during pushoff, though force exhibited less modulation with walking speed. A second peak in late swing Achilles loading, which was not evident from the ankle moment, increased significantly with walking speed (p < 0.001). The two peaks in patellar tendon loading occurred at 12 ± 1% and 68 ± 6% of the gait cycle, matching the timing of peak knee extension moment in early stance and early swing. Both patellar tendon load peaks increased significantly with walking speed (p < 0.05).SignificanceThis is the first study to use shear wave tensiometry to characterize Achilles and patellar tendon loading during gait in children. These data could serve as a normative comparison when using tensiometry to identify abnormal tendon loading patterns in individuals who exhibit equinus and/or crouch gait.

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

Molecular response of the patellar tendon to fatigue loading explained in the context of the initial induced damage and number of fatigue loading cycles.

Publications

Molecular response of the patellar tendon to fatigue loading explained in the context of the initial induced damage and number of fatigue loading cycles.

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