The major change involved with cardiovascular disease is development of atherosclerosis in critical arteries, which is partially characterized by vascular calcification. The level of coronary artery calcification is thought to be the most important indicator of future cardiovascular events.

Increased arterial calcifications have frequently been reported in those with skeletal fluorosis (Tuncel, 1984). Fluoride accumulation leads to cellular toxicity, likely causing the accumulation of calcium (Susheela and Kharb, 1990). The aorta has been shown to accumulate more fluoride than possibly any other soft tissue, with 8,400 ppm F reported in one case (Greever et al., 1971). Similarly, studies indicate that animals chronically exposed to fluoride have increased levels of both fluoride and calcium in the aorta (Susheela and Kharb, 1990) and heart (Stookey and Muhler, 1963).

Excerpts from the Scientific Literature:

“Given the assumption that fluoride uptake represents dynamic atherosclerotic calcification, we would expect that fluoride uptake occurs at the stage before the formation of detectable calcium deposition. Fluoride uptake either overlaps with calcification or locates adjacent to the detectable calcium deposits, suggesting that fluoride uptake and detectable calcification represent different stages of the atherosclerotic process.”
SOURCE: Li Y, et al. (2012). Association of vascular fluoride uptake with vascular calcification and coronary artery disease. Nuclear Med Comm 33:14-20.

“Results of this study suggest that endemic fluorosis might cause aortosclerosis, which greatly aggravate the course and range of sclerosis and calcification of the conducting arteries and which in turn make fluorosis severer.”
SOURCE: Song AH, et al. (1990). Observations on fluoric aortosclerosis by two-dimensional echocardiography. Endemic Diseases Bulletin 5(1):91-4.

“As with the liver tissue, the hearts from those animals which received the calcification-inducing diet and fluoride were found to contain nearly twice as much calcium and fluoride as those of comparable control animals.”
SOURCE: Stookey GK, Muhler JC. (1963). Relationship between fluoride deposition and metastatic calcification in soft tissues of rat and guinea pig. Proceed Soc Exp Biol Med 113:720-25.

“the fluoride contents of the serum and the aorta are significantly raised compared to normal, suggesting that prolonged administration of fluoride to rabbits results in the accumulation of fluoride in the aorta. It is evident that calcium levels are significantly increased in the aorta of animals administered fluoride, while phosphorus contents remain unaltered. The enhanced calcium content as well as the Ca/P ratio supports the view that the aorta is undergoing mineralization.”
SOURCE: Susheela AK, Kharb P. (1990). Aortic calcification in chronic fluoride poisoning: biochemical and electron microscope evidence. Exp Mol Path 53:72-80.

“A review of the literature indicates that, in skeletal fluorosis, arterial calcifications are common. Over age 60, patients in the high-fluoride group showed a significantly higher incidence of Moenckeberg [arterial] calcifications. A highly significant correlation (p<0.001) was observed between the severity of these calcifications and the severity of skeletal changes within this group.”
SOURCE: Tuncel E. (1984). The incidence of Moenckeberg calcifications in patients with endemic fluorosis. Fluoride 17(1):4-8.

“the decrease in elastic properties of the aorta in patients with chronic fluorosis might be due to calcification and degeneration of smooth muscle fibers in the tunica media of the aorta.”
SOURCE: Varol E, et al. (2010). Aortic elasticity is impaired in patients with endemic fluorosis. Biol Trace Elem Res 133:121-7.

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