Abstract

Large or massive tears of the rotator cuff can cause severe pain and substantially limit mobility, and thus negatively impact quality of life1. Following surgical repair, an estimated 50% of patients still have symptoms at six months and 40% have symptoms at one year2, demonstrating that surgical repair is often unable to fully restore the normal function and strength of the involved muscles. A common pathophysiological change that occurs in torn rotator cuff muscles is atrophy of muscle fibers and an accumulation of fat in the muscle extracellular matrix, collectively referred to as “fatty atrophy.” Despite improvements in surgical repair techniques to achieve biomechanically strong repairs to bone in a minimally invasive arthroscopic approach, studies of rotator cuff muscles with use of magnetic resonance imaging (MRI) or computed tomography (CT) scans often fail to demonstrate a reduction in fatty atrophy following surgical repair3,4. While these imaging modalities are commonly used as a benchmark of rotator cuff healing, there is little information regarding the cellular and molecular changes associated with fatty atrophy in patients who sustain rotator cuff tears. Several different animal models have been used to study the natural history of rotator cuff injuries and the impact of repair on tissue regeneration5,6. While the nature of these models allows for invasive analysis of the muscles before and after the repair, the ability to analyze the cellular and molecular changes at multiple time points is difficult in human subjects. We have been studying the physiology of torn rotator cuff muscles with use of biopsy specimens obtained at the time of surgical repair, but ethical and practical issues have limited our ability to study changes in rotator cuff contractility and morphology that occur subsequent to the repair. Our patient, who …

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