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Persistently high failure rates that are reported after rotator cuff repairs have encouraged greater understanding of the pathophysiology that underlies rotator cuff tears. Biologic changes that contribute to the pathogenesis of rotator cuff tears and tendinopathies, as well as adaptation after these changes, have been well described. A subset of patients with a genetic predisposition to early onset of rotator cuff tears and earlier symptom and disease progression have been identified. Many biologic changes occurring at the gene level have been identified. Pathways that are believed to contribute to rotator cuff tendinopathies include extracellular matrix remodeling, angiogenesis, changes in metabolism, apoptosis, and stress-related genes. Metaplasia of rotator cuff cells is contributed to by changes in gene expression. Modification of these gene changes may be possible through mechanical loading, drugs, or cellular manipulation. Gene changes may offer greater insight into why certain tears fail to heal and help to identify therapeutic targets.

Original publication




Journal article


Journal of shoulder and elbow surgery

Publication Date





191 - 199


Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Musculoskeletal Biomedical Research Unit, National Institute for Health Research, University of Oxford, Oxford, UK.


Rotator Cuff, Extracellular Matrix, Humans, Tendon Injuries, Genetic Predisposition to Disease, Risk Assessment, Wound Healing, Gene Expression Regulation, Needs Assessment, Tendinopathy, Rotator Cuff Injuries