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OBJECTIVE This study examines the role of electronic learning platforms for medical knowledge acquisition in orthopedic surgery residency training. This study hypothesizes that all methods of medical knowledge acquisition will achieve similar levels of improvement in medical knowledge as measured by change in orthopedic in-training examination (OITE) percentile scores. Our secondary hypothesis is that residents will equally value all study resources for usefulness in acquisition of medical knowledge, preparation for the OITE, and preparation for surgical practice. DESIGN 9 ACGME accredited orthopedic surgery programs participated with 95% survey completion rate. Survey ranked sources of medical knowledge acquisition and study habits for OITE preparation. Survey results were compared to OITE percentile rank scores. PARTICIPANTS 386 orthopedic surgery residents SETTING 9 ACGME accredited orthopaedic surgery residency programs RESULTS 82% of participants were utilizing online learning resources (Orthobullets, ResStudy, or JBJS Clinical Classroom) as primary sources of learning. All primary resources showed a primary positive change in OITE score from 2018 to 2019. No specific primary source improved performance more than any other sources. JBJS clinical classroom rated highest for improved medical knowledge and becoming a better surgeon while journal reading was rated highest for OITE preparation. Orthopedic surgery residents’ expectation for OITE performance on the 2019 examination was a statistically significant predictor of their change (decrease, stay the same, improve) in OITE percentile scores (p CONCLUSIONS Our results showed that no specific preferred study source outperformed other sources. Significantly 82% of residents listed an online learning platform as their primary source which is a significant shift over the last decade. Further investigation into effectiveness of methodologies for electronic learning platforms in medical knowledge acquisition and in improving surgical competency is warranted.

BACKGROUND: Muscle atrophy and fatty infiltration (FI) are common occurrences following rotator cuff (RC) tears. Tears of all sizes are subject to muscle degeneration. The degree of muscle degeneration following RC tears is highly correlated with repair success and functional outcomes. We have recently discovered that muscle fibro-adipogenic progenitors (FAPs) can differentiate into uncoupling protein 1 (UCP-1)–expressing beige adipocytes and induce muscle regeneration. This study evaluated the potential of local cell transplantation of beige adipose FAPs (BAT-FAPs) to treat RC muscle degeneration in a murine model of RC repair. METHODS: BAT-FAPs were isolated from muscle in UCP-1 reporter mice by flow cytometry as UCP-1(+)/Sca1(+)/PDGFR(+)/CD31(−)/CD45(−)/integrin α7(−). C57/BL6J mice underwent supraspinatus tendon tear with suprascapular nerve transection followed by repair 2 or 6 weeks after the initial injury. At the time of repair, mice received either no additional treatment, phosphate-buffered saline injection, or BAT-FAP injection. Functional outcomes were assessed by gait analysis. Mice were humanely killed at 6 weeks after cell transplantation. Supraspinatus muscle FI, fibrosis, muscle fiber size, and vascularity were analyzed and quantified via ImageJ. Analysis of variance with post hoc Tukey test and P

This study stratifies complication risk in primary total joint arthroplasty (TJA) based on body mass index (BMI). Demographics, co-morbidities, perioperative variables, and complications were reviewed for 22,808 patients. Chi-squared, one-way ANOVA, univariate and multivariable regression analysis were performed. Increasing BMI led to an increase (P0.05) in combined complications, acute kidney injury (AKI), cardiac arrest (CA), reintubation, reoperation, and superficial infection (SI). Univariate analysis for BMI40 revealed an increase in combined complications (15.21-vs-17.40%), AKI (1.93-vs-3.87%), CA (0.22-vs-0.57%), reintubation (0.47-vs-0.95%), reoperation (2.36-vs-3.37%), and SI (0.82-vs-1.65%). Multivariable regression showed BMI40 as an independent predictor for combined complications (OR=1.18), AKI (OR=1.79), CA (OR=3.94), reintubation (OR=2.56), reoperation (OR=1.44), and SI (OR=2.11). Morbid obesity confers increased risk for complications in TJA.

Previous work has suggested that an extracellular matrix degrading enzyme-matrix metalloproteinase-2 (MMP-2) plays an important role in the development of muscle atrophy. However, the transcriptional regulation mechanism of MMP-2 in skeletal muscle atrophy remains largely unknown. Using transgenic MMP-2 promoter reporter mice, we have demonstrated that AP-1 and RE-1 binding sites in the MMP-2 promoter region, coupled with increased binding of Fra-1, Fra-2 and AP-2, play a critical role in MMP-2 transcriptional regulation in muscle atrophy. Novel information gained from this study has improved our understanding of in vivo transcriptional regulation of MMP-2 in skeletal muscle atrophy.

A retrospective outcomes study was performed on 25 consecutive acetabular reconstructions of major segmental defects by using an oblong-shaped cementless implant. All patients had combined acetabular defects (type III) as defined by the American Academy of Orthopaedic Surgeons classification of acetabular bone deficiency. Long-term follow-up was performed at an average of 11 years postoperatively. Clinical and radiographic outcomes were measured. Failures were defined by component revision or clear radiographic evidence of loosening. Six patients died before final evaluation, and 4 patients did not have complete radiographic data, leaving 14 patients (15 hips) for final analysis. At final follow-up, only 3 of the implants had failed and were revised. There was 1 case of a well-functioning implant with circumferential radiolucency; otherwise, there was no evidence of loosening among the remaining implants.

Cartilage repair technology is advancing at a rapid pace. However, all techniques share a common weakness—unintentional chondrocyte cell death resulting from cartilage injury that occurs during preparation of the defect site. The loss of chondrocytes at the edge of host cartilage is likely to contribute to failed integration of regenerated tissue or grafts to the surrounding cartilage. Recent studies have demonstrated that "apoptosis", or programmed cell death (PCD), may be responsible for much of the cell death caused by cartilage injury. Theoretically, inhibitors of key pathways responsible for PCD could rescue chondrocytes and improve the results of cartilage repair surgery. The purpose of this study was to test the hypothesis that short-term, intra-articular PCD inhibitor treatment can limit chondrocyte death in vivo following simulated preparation of host cartilage for a repair procedure. A microcurette was used to create full-thickness articular cartilage injuries to the femoral condyles of adult New Zealand White rabbits. Animals received daily intra-articular injections either with a potent PCD inhibitor or with vehicle alone. Treatment with the inhibitor resulted in a significant reduction in the percentage of chondrocytes undergoing PCD compared to controls [treated=10.1±2.4%; controls=26.5±3.6%; ( p =0.0013)]. These results provide proof of concept for the use of PCD inhibitors to enhance the results of cartilage repair surgeries.

Femoral component fracture is a rare but well-documented complication after total hip arthroplasty. Historically, most stem fractures have occurred at the middle third of the implant, where proximal stem loosening and solid distal stem fixation result in cantilever bending and eventual fatigue failure. In contrast, we report 2 early fatigue failures of well-positioned, well-fixed, cemented, forged, cobalt-chromium femoral components at the neck-shoulder junction. A contributing factor to the implant failures was heavy laser etching in a region of the implant subjected to high stresses, leading to decreased fatigue resistance and subsequent fracture.