Shoulder tendon injuries are frequently seen in the presence of abnormal scapular motion, termed scapular dyskinesis. The cause and effect relationship between scapular dyskinesis and shoulder injury has not been directly defined. We developed and used an animal model to examine the initiation and progression of pathological changes in the rotator cuff and biceps tendon. Sixty male Sprague-Dawley rats were randomized into two groups: nerve transection (to induce scapular dyskinesis, SD) or sham nerve transection (control). The animals were euthanized 4 and 8 weeks after surgery. Shoulder function and passive joint mechanics were evaluated over time. Tendon mechanical, histological, organizational, and compositional properties were evaluated at both time points. Gross observation demonstrated alterations in scapular motion, consistent with scapular "winging." Shoulder function, passive internal range of motion, and tendon mechanical properties were significantly altered. Histology results, consistent with tendon pathology (rounded cell shape and increased cell density), were observed, and protein expression of collagen III and decorin was altered. This study presents a new model of scapular dyskinesis that can rigorously evaluate cause and effect relationships in a controlled manner. Our results identify scapular dyskinesis as a causative mechanical mechanism for shoulder tendon pathology.
Keywords: animal model; rotator cuff; scapular dyskinesis.
© 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc.