Abstract
Background:
Patellar tendinopathy (jumper's knee) is characterized by localized tenderness of the patellar tendon at its origin on the inferior pole of the patella and a characteristic increase in signal intensity on magnetic resonance imaging at this location. However, it is unclear why the lesion typically occurs in this area of the patellar tendon as surface strain gauge studies of the patellar tendon through the range of motion have produced conflicting results.
Hypothesis:
The predicted patellar tendon strains that occur as a result of the tendon loads and patella-patellar tendon angles (PPTAs) experienced during a jump landing will be significantly increased in the area of the patellar tendon associated with patellar tendinopathy.
Study Design:
Descriptive laboratory study.
Methods:
A 2-dimensional, computational, finite element model of the patella-patellar tendon complex was developed using anatomic measurements taken from lateral radiographs of a normal knee. The patella was modeled with plane strain rigid elements, and the patellar tendon was modeled with 8-node plane strain elements with neo-Hookean material properties. A tie constraint was used to join the patellar tendon and patella. Patella-patellar tendon angles corresponding to knee flexion angles between 0° and 60° and patellar tendon strains ranging from 5% to 15% were used as input variables into the computational model. To determine if the location of increased strain predicted by the computational model could produce isolated tendon fascicle damage in that same area, 5 human cadaveric patella-patellar tendon-tibia specimens were loaded under conditions predicted by the model to significantly increase localized tendon strain. Pre- and posttesting ultrasound images of the patella–patellar tendon specimens were obtained to document the location of any injured fascicles.
Results:
Localized tendon strain at the classic location of the jumper's knee lesion was found to increase in association with an increase in the magnitude of applied patellar tendon strain and a decrease in the PPTA. The principal stresses and strains predicted by the model for this localized area were tensile and not compressive in nature. Applying the tendon strain conditions and PPTA predicted by the model to significantly increase localized strain resulted in disruption of tendon fascicles in 3 of the 5 cadaveric specimens at the classic location of the patellar tendinopathy lesion.
Conclusion:
The localized increase in patellar tendon strain that occurs in response to the application of tendon loads and decreased PPTA could induce microdamage at the classic location of the jumper's knee lesion.
Clinical Relevance:
The association of decreasing PPTA with increasing localized tendon strain would implicate the role of knee-joint angle as well as tendon force in the etiopathogenesis of jumper's knee.
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