Effect of supraspinatus tendon injury on supraspinatus and infraspinatus muscle passive tension and associated biochemistry

Silldorff MD, Choo AD, Choi AJ, Lin E, Carr JA, Lieber RL, Lane JG, Ward SR.
J Bone Joint Surg Am, 2014 96(20):e175.


Injury to the supraspinatus and infraspinatus tendons and the associated atrophic changes to the muscle remain a common clinical problem. Specifically, increased muscle stiffness has been implicated in failure of the repair and poor functional outcomes. We present a comparison of the passive mechanical properties and associated biochemical studies from patients with and without torn supraspinatus tendons.
Muscle biopsy samples (n = 40) were obtained from twenty patients undergoing arthroscopic shoulder surgery. Passive mechanical tests of both individual fibers and fiber bundles as well as analysis of titin molecular weight and collagen content were performed.
At the fiber-bundle level, a significant increase in passive modulus was observed between intact supraspinatus samples (mean [and standard error], 237.41 ± 59.78 kPa) and torn supraspinatus samples (515.74 ± 65.48 kPa) (p < 0.05), a finding that was not observed at the single fiber level. Within the torn samples, elastic moduli in the supraspinatus were greater than in the infraspinatus at both the single fiber and the fiber-bundle level. There was a significant positive correlation between bundle elastic modulus and collagen content (r(2) = 0.465) in the supraspinatus muscle as well as a significant positive correlation between tear size and bundle elastic modulus (r(2) = 0.702) in the torn supraspinatus samples.
Supraspinatus muscle passive tension increases in a tendon tear size-dependent manner after tendon injury. The increase in muscle stiffness appears to originate outside the muscle cell, in the extracellular matrix.

Muscle stiffness after rotator cuff tendon injury is more severe with large tears. This finding supports the concept of early intervention, when tendon tears are smaller, and interventions targeting the extracellular matrix.

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