Abstract
Whether osteogenesis is involved in the calcification process during atherosclerosis remains an important issue. In rabbits fed 0.5% cholesterol and 2% peanut oil for 3–4 months, mineral deposition initiates at the deeper zones of lesions adjacent to the smooth muscle layer and progresses along the interface after the intima is extensively thickened. In advanced human atherosclerotic aortas, calcification occurs both in the media and thickened intima. Contrary to the concept of osteogenesis as a major cause of vascular calcification, neither bone cells nor osteoids were observed in the mineralized areas in any of atherosclerotic rabbit and human aortas studied. Furthermore, tissue non-specific alkaline phosphatase (ALP), an essential biomarker of cartilage and bone was not detected in frozen sections of atherosclerotic rabbit and human aortas using a chromogenic ALP activity procedure. Unlike ALP-abundant matrix vesicles in bone or cartilage, calcifying vesicles from human or rabbit atherosclerotic aortas do not exhibit ALP activity. However, both types of vesicles are rich in ATPase and AMPase, which may play a role in providing Pi from nucleotides for calcification. These observations strongly suggest that aortic calcification induced by dietary cholesterol represents non-osseous dystrophic calcification, similar to the one frequently occurring in various diseased and injured tissues.
Published Version
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