Structural damage to the heart resulting from fluoride toxicity has been observed in numerous human and animal studies. The general features of this damage include cloudy swelling, vacuolization or vacuolar degeneration, hemorrhages, interstitial edema, fibrous necrosis, dissolution of nuclei, and thickening of the vessel walls in the heart muscle (Basha and Sujitha, 2011; Cicek et al., 2005; Shashi and thapar, 2001; Pribilla, 1968; Takamori et al., 1956).
Fluoride-induced oxidative stress and inflammatory response have been demonstrated in humans and experimental animals (Barbier et al., 2010), and are likely responsible for this myocardial cell damage (Varol and Varol, 2012). In studies of the cardiovascular system, rats treated chronically with high levels of fluoride have reduced activity of antioxidant enzymes in the heart (Basha and Sujitha, 2011; Cicek et al., 2005), and toxic concentrations of fluoride have been shown to increase gene expression of inflammatory-related molecules in rabbit aorta (Ma et al., 2012).
Excerpts from the Scientific Literature:
“In conclusion, fluoride and arsenic induce the expression of key molecules involved in cell adhesion molecules, chemokines, and proinflammatory cytokines both at mRNA and protein levels. Our data contribute to the concept that induction of inflammatory responses, but not lipid metabolic disorder, may play an important role in the mechanism of the cardiovascular toxicity of arsenic and fluoride.”
SOURCE: Ma Y, et al. (2012). Inflammatory responses induced by fluoride and arsenic at toxic concentration in rabbit aorta. Arch Toxicol 86:849-56.
“In the present investigation, pathological changes, viz. extensive interstitial oedema, fibrous necrosis, and cloudy swellings were significant in the myocardium of all fluoridated rabbits of each group. The degree of myocardial damage seemed to be directly proportional to the dosage of fluoride administered. Since there are degenerative changes in myocardial fibres in acute poisoning due to massive doses of fluoride, the effect of persistent minute doses of fluoride cannot be ignored.”
SOURCE: Shashi A, Thapar SP. (2001). Histopathology of myocardial damage in experimental fluorosis in rabbits. Fluoride 34(1):43-50.
“The results of histological sections in the present study showed signs of severe cloudy swelling, sarcoplasmic vacuolization, small hemorrhages, interstitial edema, fibrous necrosis, dissolution of nuclei, fibrillolysis, edematous fluid in the interstitial spaces and extensive vacuolization of both auricle and ventricle regions on exposure to chronic fluoride.”
SOURCE: Basha MP, Sujitha NS. (2011). Chronic fluoride toxicity and myocardial damage: antioxidant offered protection in second generation rats. Toxicol Int 18(2):99-104.
“In soft tissues, [fluoride] interferes by inhibiting numerous enzymes, finally leading to the production of free radicals. Its accumulation in soft tissues causes injury by reducing the potential of scavenging free radicals, which critically injure the biological membranes. Intensified free radical production or disturbed antioxidant level leads to oxidative stress, which is known to be a key etiopathological factor in a variety of cardiac diseases such as heart failure and ischemic heart disease.”
SOURCE: Basha MP, Sujitha NS. (2011). Chronic fluoride toxicity and myocardial damage: antioxidant offered protection in second generation rats. Toxicol Int 18(2):99-104.
“The sialic acid/glycosaminoglycan ratio [diagnostic test to assess chronic exposure to fluoride] in patients with coronary artery ectasia [abnormal dilation of arteries surrounding the heart] was significantly lower than in controls…We demonstrated that chronic fluoride exposure has an important role in pathogenesis of coronary artery ectasia.”
SOURCE: Dede O, et al. (2011). Chronic fluoride exposure has a role in etiology of coronary artery ectasia: sialic acid/glycosaminoglycan ratio. Biol Trace Elem Res 143:695-701.
“prolonged ingestion of fluoride through drinking water, particularly with high doses, induced significant histopathological and biochemical changes leading to myocardial tissue damage. …fluoride probably increases the production of reactive oxygen species. It is believed that fluoride toxicity is brought about by oxidative stress and, thus, the probably interaction between fluoride and the myocardial metabolism can be responsible for histopathological and biochemical changes in myocardial tissue.”
SOURCE: Cicek E, et al. (2005). Effects of chronic ingestion of sodium fluoride on myocardium in a second generation of rats. Human Exper Toxicol 24:79-87.
“In the experiments described here the fluoride concentration required for significant or maximal effect [cAMP accumulation in rat aorta and diaphragm] was near or below the normal plasma fluoride concentrations of 0.5-2.0 µM (Taves, 1968). Thus it could be speculated that normal function of both smooth and skeletal muscle might be influenced by small changes in plasma fluoride levels.”
SOURCE: Allmann DW, et al. (1986). Stimulation of cAMP accumulation in rat aorta and diaphragm by fluorine containing compounds. Res Comm Chem Pathol Pharmacol 52(3):275-84.
“Our observations showed that the myocardial damage was proportional to the fluoride content of drinking water and to the extent of mottled enamel [i.e. dental fluorosis].”
SOURCE: Okushi I. (1954a). Changes in the heart muscle due to chronic fluorosis. Part I: Electrocardiogram and cardiac x-rays in inhabitants of a high fluoride zone. (Abstracted from) Shikoku Acta Medica 5:159-165.
“Histologically, regressive degeneration, cellular infiltration, hyperemia, hemorrhages and thickening of vessel wall were noted in the heart muscle [of rabbits given sodium fluoride orally]. The degree of myocardial damage was proportionate to the dosage of sodium fluoride and the length of time of its administration.”
SOURCE: Okushi I. (1954b). Changes in the heart muscle due to chronic fluorosis. Part II: Experimental studies on the effects of sodium fluoride upon the heart muscle of rabbits. (Abstracted from) Shikoku Acta Medica 5:238-45.
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