ABSTRACT
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.
ABSTRACT
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.
