Comparative Study of Pathologic Cardiovascular Biomineralization
One of the most severe consequences of atherosclerosis is the irreversible formation of calcific deposits in different sites of the cardiovascular system. The pathogenesis appears to be related to the initial damage of the endothelium (Ross and Glomset, 1976), which increases endothelial permeability. When a lesion forms, the natural vasodilation/vasoconstriction performance of endothelium and underlying cellular layers is impaired. This condition can result in progressive atherogenesis, leading to pathologic mineralization. Dystrophic calcification is a major problem associated with prolonged use of bioprosthetic heart valves (Schoen,1989). The biomineralization and deterioration of bioprostheses appears to be a fast process, compared to degeneration of natural heart valves. This may be due to the absence of the vital protective endothelium layer, which in healthy tissues prevents active transport of atherosclerotic plaque ingredients. Wickham et al. (1988) documented an increase of intracellular calcium in infected endothelial cells. This increase may be a valid messenger of inorganic ion diffusion from extracellular fluid into intracellular calcification sites.
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