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Morphometrical and histochemical techniques were used to demonstrate changes to the cartilage layer of the rat temporomandibular joint condyle following chronic exposure to fluoride. An increase in thickness of the cartilage layer was noted in rats given 100 parts per million sodium fluoride in drinking water. No significant changes were observed with either control or low dose (10 parts per million) groups. The observed thickening was attributable to an increase in number and size of cells of the lower hypertrophic zone. Accumulations of glycogen were observed in these cells, which reflects the inhibitory effect of fluoride on glycolysis. Stimulation of chondrocytes by fluoride may have delayed the normal processes of capillary invasion, resulting in thickening of the cartilage layer. No changes to staining patterns of immature or mature types of collagen were observed, nor did the staining pattern of detectable glycosaminoglycans change due to fluoride.

Female Wistar rats, 3 weeks old, were given sodium fluoride in saline solution (isotonic) by intraperitoneal injection at a dose of either 0, 10 or 20 mg per kg body weight. This treatment was given 9 times over 4.5 days. After fixation by perfusion and demineralization in neutral EDTA, hemi-mandibles were sectioned in a cryostat. Sections were stained for dipeptidyl peptidase II activity, using the specific substrate Lys-Ala-MNA and the coupler Fast Blue B for histochemical localization. Staining indicative of dipeptidyl peptidase II was found in the enamel organ of the incisor, particularly in cells of the stratum intermedium and in both secretory and maturation ameloblasts. This staining was markedly reduced in ameloblasts of rats given either 10 or 20 mg sodium fluoride per kg body weight.

Fluoride in high concentrations is known to have an adverse effect on the formation of enamel. The effect of a single injection of two concentrations of sodium fluoride on inner enamel secretory ameloblasts was investigated morphologically by electron microscopy and functionally by assessing the location and relative amount of available calcium, using the potassium pyroantimonate method. The results showed that acute doses of fluoride interfere with the normal function of secretory ameloblasts. The increase in the population of lysosome-like structures observed after fluoride administration is suggestive of defects in the synthetic pathway. Concomitant with the effect of fluoride on secretory ameloblasts is an inhibition of enamel formation, resulting in incomplete enamel rods and leaving large remnants of Tomes' processes buried in the enamel. The distribution of the calcium pyroantimonate deposits found tends to support the concept of calcium traveling between the cells to the enamel. Acute doses of fluoride also reduce the amount of calcium available for complexing with pyroantimonate in the intercellular region.

Various doses of sodium fluoride (NaF), salmon calcitonin (CT) and NaF combined with CT were given intravenously to rats (236 +/- 2 g). Blood plasma samples were collected at various times up to 24 hours and measured for total calcium (adjusted for variation in plasma albumin), inorganic phosphate, ionic fluoride, urea, and creatinine. Following injection of NaF alone, significant hypocalcemia and hyperphosphatemia was observed. In contrast, CT injections resulted in hypocalcemia and hypophosphatemia. NaF and CT given in combination generally resulted in the hypocalcemia being equal to or greater than that calculated from the simple addition of their individual effects. Significant increases in both plasma creatinine and plasma urea were observed following treatment with NaF alone or with CT and NaF together, whereas CT alone had negligible effect. These results suggest that NaF does not mimic the effects of CT; rather that NaF and CT interact to modify their individual effects. The influence of NaF probably occurs via an effect on kidney function.

This study assessed the effect of a single intravenous dose of sodium fluoride (20 mg/kg body wt.) on plasma ionic fluoride and on some other plasma electrolytes and metabolites in rats, rabbits, and cockerels. At any given time following sodium fluoride administration, the plasma ionic fluoride was highest in rabbits and lowest in cockerels. The rate of removal of fluoride from plasma was slower in rabbits as compared with that in the other two species. Plasma sodium, chloride, total protein, albumin, total globulins, and osmolality were not significantly altered by sodium fluoride in any of these three species. However, plasma phosphate (inorganic), urea, creatinine, and glucose were elevated, and plasma calcium was reduced in the rats and the rabbits, but none was significantly altered in the cockerels. The analyses indicated that species variability does exist in fluoride toxicity.

Between 1978 and 1983, at least 20 children with fluoride poisoning were admitted to two major children's hospitals in Brisbane. Data on telephone calls received by Poisons Information Centres in Australia about fluoride toxicity show that Brisbane, the water supply of which is not fluoridated, received approximately twice as many calls per head of population as were received in Sydney and Melbourne. Concern is also expressed at the standard of packaging of fluoride tablets currently marketed in Australia. A treatment plan for cases of acute fluoride poisoning after oral ingestion is presented.