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Background Deep infection after shoulder arthroplasty is a diagnostic and therapeutic challenge. The current literature on this topic is from single institutions or Medicare samples, lacking generalizability to the larger shoulder arthroplasty population. Questions/purposes We sought to identify (1) patientspecific risk factors for deep infection, and (2) the pathogen profile after primary shoulder arthroplasty in a large integrated healthcare system. Methods A retrospective cohort study was conducted. Of 4528 patients identified, 320 had died and 302 were lost to followup. The remaining 3906 patients had a mean followup of 2.7 years (1 day-7 years). The study endpoint was the diagnosis of deep infection, which was defined as revision surgery for infection supported clinically by more than one of the following criteria: purulent drainage from the deep incision, fever, localized pain or tenderness, a positive deep culture, and/or a diagnosis of deep infection made by the operating surgeon based on intraoperative findings. Risk factors evaluated included age, sex, race, BMI, diabetes status, American Society for Anesthesiologists (ASA) score, traumatic versus elective procedure, and type of surgical implant. For patients with deep infections, we reviewed the surgical notes and microbiology records for the pathogen profile. Multivariable Cox regression models were used to evaluate the association of risk factors and deep infection. Adjusted hazard ratios and 95% CI are presented. Results With every 1-year increase in age, a 5% (95% CI, 2%-8%) lower risk of infection was observed. Male patients had a risk of infection of 2.59 times (95% CI, 1.27-5.31) greater than female patients. Patients undergoing primary reverse total shoulder arthroplasty had a 6.11 times (95% CI, 2.65-14.07) greater risk of infection compared with patients having primary unconstrained total shoulder arthroplasty. Patients having traumatic arthroplasties were Each author certifies that he or she, or a member of his or her immediate family, has no funding or commercial associations (eg, consultancies, stock ownership, equity interest, patent/licensing arrangements, etc) that might pose a conflict of interest in connection with the submitted article. All ICMJE Conflict of Interest Forms for authors and Clinical Orthopaedics and Related Research editors and board members are on file with the publication and can be viewed on request. Each author certifies that his or her institution approved the human protocol for this investigation, that all investigations were conducted in conformity with ethical principles of research, and that informed consent for participation in the study was obtained.

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An in vivo animal model was used to evaluate overuse and overuse plus intrinsic tendon injury or extrinsic tendon compression in the development of rotator cuff injury. Forty-four male Sprague-Dawley rats were divided into groups of 22. Each left shoulder received an intrinsic or extrinsic injury plus overuse (treadmill running), and each right shoulder received only overuse. Eleven rats from each group were sacrificed at 4 and 8 weeks. Supraspinatus tendons were evaluated histologically or geometrically and biomechanically. Ten rats constituted a cage-activity control group. Both supraspinatus tendons of the experimental groups had increases in cellularity and collagen disorganization and changes in cell shape compared with control tendons. Tendons with injury plus overuse exhibited a worse histologic grade than those with overuse alone. The cross-sectional area of both supraspinatus tendons of the experimental rats was significantly more than in control tendons. The area of the injury plus overuse tendons was increased on average compared with overuse-alone tendons. Biomechanically, the tissue moduli of overuse/intrinsic injury tendons at 4 weeks and those of the overuse/extrinsic injury tendons at 8 weeks were significantly lower than in control tendons. Tissue moduli of the overuse/injury tendons were significantly lower than in the overuse-alone tendons at 8 weeks. This study demonstrated that damage to the supraspinatus tendon can be caused by overuse and intrinsic injury, overuse and extrinsic compression, and overuse alone.