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Vertebral compression fractures (VCFs) occur in 1 to 1.5 million patients in the US each year and are associated with pain, disability, altered pulmonary function, secondary vertebral fracture, and increased mortality risk. A better understanding of VCFs and their management requires preclinical models that are both biomechanically analogous and accessible. We conducted a study using twelve spinal vertebrae (T12-T14) from porcine specimens. We created mathematical simulations of vertebral compression fractures (VCFs) using CT scans for reconstructing native anatomy and validated the results by conducting physical axial compression experiments. The simulations accurately predicted the behavior of the physical compressions. The coefficient of determination for stiffness was 0.71, the strength correlation was 0.88, and the failure of the vertebral bodies included vertical splitting on the lateral sides or horizontal separation in the anterior wall. This finite element method has important implications for the preventative, prognostic, and therapeutic management of VCFs. This study also supports the use of porcine specimens in orthopedic biomechanical research.
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INTRODUCTION: Utilizing large animal model like male pig for biomechanical studies offers a cost-effective approach to understanding human joint and tissue mechanics. Our study explores the osteology and meniscus anatomy of the male porcine stifle joint and compares it to human knee joint parameters, aiming to provide a valuable reference for orthopaedic research and surgical training. METHODS: We examined 60 male porcine stifle joints and analyzed their menisci and bones. Dissections were meticulously performed, with measurements taken using digital Vernier calipers and ImageJ software. These dimensions included bone morphology and meniscal width, height, and volume, followed by statistical analysis using unpaired Student's t-tests. RESULTS: The various measurements of bones and menisci indicated a high degree of anatomical similarity to human knees. The anterior width of the medial meniscus was 12.545 ± 1.763 mm, while the lateral meniscus was 14.99 ± 1.720 mm. The middle width of the medial meniscus was 12.065 ± 1.691 mm, compared to the lateral meniscus at 14.375 ± 1.732 mm. The posterior width was 15.25 ± 1.741 mm for the medial meniscus and 16.39 ± 1.662 mm for the lateral meniscus. The femoral intercondylar notch dimensions widened and became shallower with age, resembling the maturation patterns seen in human knee development. The average volume of the medial meniscus was 4.30 ± 0.13 ml, while the lateral meniscus was 5.9 ± 0.29 ml. The aspect ratio of the femoral condyles was 1.04 ± 0.04 (0.95-1.11), while the aspect ratio of the tibial condyles was 0.65 ± 0.02 (0.61-0.70), measured via digital Vernier calipers. These findings were statistically significant, showcasing the male porcine model's relevance in replicating human knee mechanics (p < 0.05). CONCLUSION: Male porcine stifle joints present a valid and accessible model for knee anatomy research. Our study underscores the value of the male porcine model in understanding human knee joint biomechanics and supports its continued use in orthopaedic research and training. These findings have significant implications for advancing orthopaedic research methodologies and enhancing surgical training practices by providing a reliable and anatomically comparable model.
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Coronary artery disease caused by atherosclerosis is a major cause of morbidity and mortality around the world. Data from preclinical and clinical studies support the belief that atherosclerosis is an inflammatory disease that is mediated by innate and adaptive immune signaling mechanisms. This review sought to highlight the role of Rac-mediated inflammatory signaling in the mechanisms driving atherosclerotic calcification. In addition, current clinical treatment strategies that are related to targeting hypercholesterolemia as a critical risk factor for atherosclerotic vascular disease are addressed in relation to the effects on Rac immune signaling and the implications for the future of targeting immune responses in the treatment of calcific atherosclerosis.