A forty-four-year-old physically active man sustained a traumatic full-thickness supraspinatus tendon tear and a partial-thickness infraspinatus tendon tear. The medical history was negative, and he reported no current use of medications or any drug allergies. Physical examination demonstrated full passive motion of the left shoulder symmetric to the right shoulder. However, active forward flexion in the scapular plane was restricted to approximately 80°, and manual supraspinatus muscle strength testing revealed only antigravity strength (3/5) on the left side, compared with full strength (5/5) on the right side. Right shoulder active external rotation with the arm adducted was 80° on the right and 45° on the left. Lift-off and belly press examinations were normal. Radiographs demonstrated mild acromioclavicular joint degenerative changes, no glenohumeral degenerative changes, and no superior migration of the humeral head. An MR arthrogram (Fig. 1) revealed a massive full-thickness tear of the supraspinatus tendon and a partial-thickness tear of the infraspinatus tendon.
Given the traumatic rotator cuff injury as well as the impaired active motion and strength, the patient consented to an arthroscopic, double-row rotator cuff repair. Only the most anterior margin of the rotator cable just posterior to the biceps tendon was intact. There was a very large U-shaped tear extending through the entire supraspinatus tendon and the cephalad two-thirds of the infraspinatus tendon. The majority of the greater tuberosity footprint was clearly exposed. Adhesions on both the bursal side and the articular side of the rotator cuff were fully divided to restore normal mobility to this retracted tear. With use of a grasper, the mobilized rotator cuff tear was completely reducible with a posterior-to-anterior vector of pull. The medial and lateral margins of the footprint were defined and carefully prepared to expose a bleeding osseous surface. A double-row rotator cuff repair technique was subsequently performed with use of multiple 5.5-mm double-loaded suture anchors medially; horizontal mattress sutures were passed and secured into the supraspinatus and infraspinatus tendons. These sutures were subsequently secured in a crossed fashion on the bursal side of the tendon and secured to transosseous-equivalent anchors placed along the lateral margin of the footprint to achieve an anatomic, watertight repair. Following surgery, the patient underwent a supervised rehabilitation program7 and progressed through the program on schedule with minimal symptoms of pain or discomfort. Nine weeks following the repair, he sustained a traumatic retear as a result of shoulder trauma when he was struck by a vehicle while walking. The patient consented to a revision double-row repair that was performed by the same surgeon. A time line of events is presented in Figure 2.
Biopsy specimens of the muscle fibers and surrounding connective tissue of the supraspinatus muscle were carefully obtained with use of an arthroscopic biopsy punch at the time of the second surgery. These specimens were taken from the distal third of the supraspinatus muscle, and care was taken to ensure that these specimens came from the same region as those obtained during the first surgery. A portion of the specimens was prepared freshly for single muscle fiber contractility analysis, and the remaining portion was snap frozen in Tissue-Tek (Sakura Finetek USA) for immunohistochemistry analysis.
Permeabilized Fiber Contractility
The maximum isometric force production (Fo) and specific maximum isometric force production ([sFo], Fo normalized by muscle fiber cross-sectional area) of individual muscle fibers was measured with use of previously described techniques8 that were adjusted to an optimal sarcomere length of 2.7 μm for human muscle9.
Immunohistochemistry
Tissue was sectioned at 10 μm and labeled with primary antibodies or small fluorophore-tagged compounds that identify various biomolecules. These included c-Met antibodies (Santa Cruz Biotechnology, Santa Cruz, California) to identify muscle stem cells (satellite cells); wheat germ agglutinin lectin conjugated to Alexa Fluor 488 ([WGA lectin AF488]; Invitrogen, Carlsbad, California) and collagen I antibodies (AbCam, Cambridge, Massachusetts) to identify the extracellular matrix; BODIPY 493/503 (Invitrogen) to identify lipids; and DAPI (Sigma-Aldrich, Saint Louis, Missouri) to identify nuclei. Alexa Fluor-tagged secondary antibodies were used to detect primary antibodies.