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PubMed1976

Activation and inhibition of fat cell adenylate cyclase by fluoride.

Incubation (30 degrees) of fat cell particulate fractions with fluoride before assay in the effective absence of fluoride results in activation of adenylate cyclase. Whereas the effect of fluoride (1.3 to 7 mM) when added to the assay was maximal in less than 2 min, 10 or 15 min of incubation before assay was usually required to produce maximal activation with any given concentration of fluoride. Under both conditions 3 to 5 mM fluoride produced maximal activation. After incubation with fluoride for 5 to 20 min cyclase activity was constant for at least 15 min of assay without fluoride; maximal activity was greater than that produced by fluoride added to the assay system and the concentration required to produce significant activation was lower. Fluoride activation in the assay or during prior incubation could be prevented by pyrophosphate. When added during the early minutes of assays with fluoride, 1.5 mM pyrophosphate, which had little effect on the activity of enzyme previously incubated with fluoride, rapidly reduced activity to essentially basal levels; when added after 10 min its effect was equally rapid but much smaller. It appears that activation is initially reversible by removal of fluoride as it is by addition of pyrophosphate, but becomes largely irreversible by these means with continued exposure to fluoride. Fluoride in the assay system inhibited cyclase activated by isoproterenol or choleragen or by incubation with fluoride prior to assay; inhibition, dependent on fluoride concentration, was maximal at 5.3 mM. Since maximal activity produced by incubation with fluoride before assay exceeded that of nonincubated preparations assayed with fluoride, and was reduced to the latter level when assayed in the presence of fluoride, we infer that inhibition is reversible at a time when fluoride activation is relatively irreversible. Pyrophosphate (1.5 mM), which prevented fluoride activation, did not reduce fluoride inhibition of isoproterenol-, fluoride-, or choleragen-activated cyclase. When 3 mM MnCl2 was present in the assay, inhibition by fluoride was not observed. In descriptive terms, MnCl2 appeared to cause rapid reversal of fluoride inhibition. Thus, fluoride inhibits, in an apparently similar manner, fat cell adenylate cyclase whether it is activated by isoproterenol, fluoride, or choleragen. Although fluoride activation and inhibition can apparently be dissociated or modified differentially, until the mechanism(s) of action of fluoride is elucidated it cannot be concluded that these are totally independent processes.

Adenylyl Cyclase Inhibitors↗
PubMed1990

NTP Toxicology and Carcinogenesis Studies of Sodium Fluoride (CAS No. 7681-49-4)in F344/N Rats and B6C3F1 Mice (Drinking Water Studies).

Sodium fluoride is a white, crystalline, water-soluble powder used in municipal water fluoridation systems, in various dental products, and in a variety of industrial applications. Toxicology and carcinogenesis studies were conducted with F344/N rats and B6C3F1 mice of each sex by incorporating sodium fluoride into the drinking water in studies lasting 14 days, 6 months, and 2 years. In addition, genetic toxicology studies were performed with Salmonella typhimurium, with mouse L5178Y cells, and with Chinese hamster ovary cells. 14-Day Studies: Rats and mice received sodium fluoride in drinking water at concentrations as high as 800 ppm. (Concentrations are expressed as sodium fluoride; fluoride ion is 45% of the sodium salt by weight.) In the high-dose groups, 5/5 male and 5/5 female rats and 2/5 male mice died; one female rat was given 400 ppm in the drinking water also died before the end of the studies. No gross lesions were attributed to sodium fluoride administration. 6-Month Studies: Rats received concentrations of sodium fluoride in drinking water as high as 300 ppm, and mice as high as 600 ppm. No rats died during the studies; however, among the mice, 4/9 high-dose males, 9/11 high-dose females, and 1/8 males in the 300 ppm group died before the end of the studies. Weight gains were less than those of controls for rats receiving 300 ppm and mice receiving 200 to 600 ppm. The teeth of rats and mice receiving the higher doses of sodium fluoride were chalky white and chipped or showed unusual wear patterns. Mice and male rats given the higher concentrations had microscopic focal degeneration of the enamel organ. Rats receiving 100 or 300 ppm sodium fluoride had minimal hyperplasia of the gastric mucosa of the stomach, and one high-dose rat of each sex had an ulcer. Acute nephrosis and/or lesions in the liver and myocardium were observed in mice that died early, and minimal alterations in bone growth/remodeling were observed in the long bones of mice receiving sodium fluoride at concentrations of 50 to 600 ppm. The sodium fluoride concentrations selected for the 2-year studies in both rats and mice were 0, 25, 100, and 175 ppm in the drinking water. These concentrations were selected based on the decreased weight gain of rats at 300 ppm and of mice at 200 ppm and above, on the incidence of gastric lesions in rats at 300 ppm in the 6-month studies, and on the absence of significant toxic effects at sodium fluoride concentrations as high as 100 ppm in an earlier 2-year study. Body Weights and Survival in the 2-Year Studies: Mean body weights of dosed and control groups of rats and mice were similar throughout the 2-year studies. Survival of rats and mice was not affected by sodium fluoride administration. Survival rates after 2 years were: male rats-control, 42/80; 25 ppm, 25/51; 100 ppm, 23/50; 175 ppm, 42/80; female rats-59/80; 31/50; 34/50; 54/81; male mice-58/79; 39/50; 37/51; 65/80; female mice-53/80; 38/52; 34/50; 52/80. Neoplastic and Nonneoplastic Effects in the 2-Year Studies: The teeth of rats and mice has a dose-dependent whitish discoloration, and male rats had an increased incidence of tooth deformities and attrition leading on occasion to malocclusion. The teeth of male and, to a lesser degree, female rats had areas of microscopic dentine dysplasia and degeneration of ameloblasts. Dentine dysplasia occurred in both dosed and control groups of male and female mice; the incidence of this lesion was significantly greater in high-dose than in control male mice. Osteosclerosis of long bones was increased in female rats given drinking water containing 175 ppm sodium fluoride. No other significant nonneoplastic lesions in rats or mice appeared related to sodium fluoride administration. Osteosarcomas of bone were observed in 1/50 male rats in the 100 ppm group and in 3/80 male rats in the 175 ppm group. None were seen in the control or 25 ppm dose groups. One other 175 ppm male rat had an extraskeletal osteosarcoma arising in the subcutaneous tissue. Osteosarcomas occur in historical control male rats at an incian incidence of 0.5% (range 0-6%). The historical incidence is not directly comparable with the incidences observed in this study because examination of bone was more comprehensive in the sodium fluoride studies than in previous NTP studies of other chemicals, and the diet used in previous studies was not controlled for fluoride content. In the current study, although the pairwise comparison of the incidence in the 175 ppm group versus that in the controls was not statistically significant, osteosarcomas occurred with a statistically significant dose-response trend, leading to the conclusion that a weak association may exist between the occurrence of these neoplasms and the administration of sodium fluoride. No other neoplastic lesions in rats or mice were considered possibly related to chemical administration. Genetic Toxicology: Sodium fluoride was negative for gene mutation induction in Salmonella typhimurium strains TA100, TA1535, TA1537, and TA98 with and without S9. In two laboratories, sodium fluoride was tested for induction of trifluorothymidine resistance in mouse L5178Y lymphoma cells; results were positive both with and without S9. Sodium fluoride was tested for cytogenetic effects in Chinese hamster ovary (CHO) cells in two laboratories. In the first laboratory, the sister chromatid exchange (SCE) test was negative with and without S9, and the chromosomal aberration (Abs) test was positive in the absence of S9; in the second laboratory, the SCE test was positive with and without S9, but no induction of Abs was observed. The laboratory that reported a negative result for Abs tested at doses below that shown to be positive at the other laboratory. Similarly, the positive SCE result was obtained at a higher dose and longer harvest time than used by the laboratory reporting the negative SCE response. Conclusions: Under the conditions of these 2-year dosed water studies, there was equivocal evidence of carcinogenic activity of sodium fluoride in male F344/N rats, based on the occurrence of a small number of osteosarcomas in dosed animals. "Equivocal evidence" is a category for uncertain findings defined as studies that are interpreted as showing a marginal increase of neoplasms that may be related to chemical administration. There was no evidence of carcinogenic activity in female F344/N rats receiving sodium fluoride at concentrations of 25, 100, or 175 ppm (11, 45, or 79 ppm fluoride) in drinking water for 2 years. There was no evidence of carcinogenic activity of sodium fluoride in male or female mice receiving sodium fluoride at concentrations of 25, 100, or 175 ppm in drinking water for 2 years. Dosed rats had lesions typical of fluorosis of the teeth and female rats receiving drinking water containing 175 ppm sodium fluoride had increased osteosclerosis of long bones.

Journal Article↗
PubMed2001

Topical fluorides in caries prevention and management: a North American perspective.

A review of evidence-based literature indicates incomplete evidence for the efficacy of most measures currently used for caries prevention, with the exception of fluoride varnishes and the use of fluoride-based interventions for patients with hyposalivation. Not all fluoride agents and treatments are equal. Different fluoride compounds, different vehicles, and vastly different concentrations have been used with different frequencies and durations of application. These variables can influence the clinical outcome with respect to caries prevention and management. The efficacy of topical fluoride in caries prevention depends on a) the concentration of fluoride used, b) the frequency and duration of application, and to a certain extent, c) the specific fluoride compound used. The more concentrated the fluoride and the greater the frequency of application, the greater the caries reduction. Factors besides efficacy, such as practicality, cost, and compliance, influence the clinician's choice of preventive therapy. For noncavitated smooth surface carious lesions in a moderate caries-risk patient, the appropriate fluoride regimen would be semiannual professional topical application of a fluoride varnish containing 5 percent NaF (22,600 ppm of fluoride). In addition, the patient should use twice or thrice daily for at least one minute a fluoridated dentifrice containing NaF, MFP, or SnF2 (1,000-1,500 ppm of fluoride), and once daily for one minute a fluoride mouthrinse containing .05 percent NaF (230 ppm of fluoride). If the noncavitated carious lesion involves a pit or fissure, the application of an occlusal sealant would be the most appropriate preventive therapy. The management of the high caries-risk patient requires the use of several preventive interventions and behavioral modification, besides the use of topical fluorides. For children over six years of age and adults, both office and self-applied topical fluoride treatments are recommended. For office fluoride therapy at the initial visit, a high-concentration agent, either a 1.23 percent F APF gel (12,300 ppm of fluoride) for four minutes in a tray or a 5 percent NaF varnish (22,600 ppm of fluoride), should be applied directly to the teeth four times per year. Self-applied fluoride therapy should consist of the daily five-minute application of 1.1 percent NaF or APF gel (5,000 ppm of fluoride) in a custom-fitted tray. For those who cannot tolerate a tray delivery owing to gagging or nausea, a daily 0.05 percent NaF rinse (230 ppm of fluoride) for 1 minute is a less effective alternative. In addition, the patient should use twice or thrice daily for at least 1 minute a fluoridated dentifrice as described above for treatment of noncavitated carious lesions. In order to avoid unintentional ingestion and the risk of fluorosis in children under six years of age, fluoride rinses and gels should not be used at home. Furthermore, when using a fluoride dentifrice, such children should apply only a pea-size portion on the brush, should be instructed not to eat or swallow the paste, and should expectorate thoroughly after brushing. Toothbrushing should be done under parental supervision. To avoid etching of porcelain crowns and facings, neutral NaF is indicated in preference to APF gels for those patients who have such restorations and are applying the gel daily. The rationale for these recommendations is discussed. Important deficiencies in our knowledge that require further research on topical fluoride therapy in populations with specific needs are identified.

Adult↗
PubMed1996

Total fluoride intake in children aged 3 to 4 years--a longitudinal study.

Several previous studies using food consumption tables or diet records have estimated that children aged 1 to 12 years resident in fluoridated (1 ppm) areas receive, on average, between 0.05 and 0.07 mg fluoride/kg body weight from foods and drinks alone. In this study, the duplicate-diet approach, which is a more accurate method of determining nutrient intake, was used to determine if levels of fluoride intake from foods and drinks are similar to those estimated from food consumption tables or diet records. Duplicate portions of all foods and drinks consumed over 24 hours by 66 children aged 3 to 4 years resident in fluoridated and low-fluoride areas of New Zealand were collected on three separate days over a period of 12 months and analyzed for fluoride. Fluoride intake from the use and ingestion of toothpastes and fluoride supplements was also determined for each child. It was hypothesized that the total amount of fluoride received by children in low-fluoride areas from diet, toothpastes, and fluoride supplements was similar to that received by children in fluoridated areas from diet and toothpastes. The mean fluoride intake from foods and drinks alone in the low-fluoride areas was 0.008 +/- 0.003 mg/kg body weight (0.15 +/- 0.06 mg/day; n = 34) and in the fluoridated areas was 0.019 +/- 0.009 mg/kg body weight (0.36 +/- 0.17 mg/day; n = 32). The mean fluoride intake from foods and drinks and toothpastes in the low-fluoride areas was 0.027 +/- 0.012 mg/kg body weight (0.49 +/- 0.25 mg/day) and in the fluoridated areas was 0.036 +/- 0.015 mg/kg body weight (0.68 +/- 0.27 mg/day). Fluoride intake from diet alone did not exceed 0.04 mg/kg body weight (0.74 mg/day), and fluoride intake from diet and toothpaste did not exceed 0.07 mg/kg body weight (1.31 mg/day). The results suggest that levels of fluoride intake from foods and drinks alone as estimated by the duplicate-diet approach are much lower than previously estimated from food consumption tables or diet records. It was calculated that if all children in the low-fluoride areas were to take currently recommended dosages of fluoride tablets, which have been based on dietary surveys and diet records, then the total fluoride intake of some children in the low-fluoride areas would exceed that of their counterparts in the fluoridated areas. The results suggest that currently recommended dosages of fluoride tablets need to be further reduced if dental fluorosis in children is to be avoided.

Child, Preschool↗
PubMed1996

Fluoride content of infant formulae in Australia.

The prevalence of dental fluorosis in Australia and the United States of America has increased in both optimally fluoridated and non-fluoridated areas. This has been attributed to an increase in the fluoride level of food and beverages through processing with fluoridated water, inadvertent ingestion of fluoride toothpaste, and the inappropriate use of dietary supplements. A major source of fluoride in infancy is considered to be infant formula which has been implicated as a risk factor for fluorosis in a number of studies. In this study the fluoride content of the infant formulae commonly used in Australia was determined. The acid diffusible fluoride of each powdered formula was isolated by microdiffusion and measured using a fluoride ion-specific electrode. The fluoride content of milk-based formulae ranged from 0.23 to 3.71 micrograms F/g and for soy-based formulae from 1.08 to 2.86 micrograms F/g. When reconstituted, according to the manufacturer's directions, with water not containing fluoride, the formulae ranged in fluoride content from 0.031 to 0.532 ppm, with the average fluoride content 0.240 ppm. Using average infant body masses and suggested volumes of formula consumption for infants 1-12 months of age, possible fluoride ingestion per kg body mass was estimated. None of the formulae, if reconstituted using water containing up to 0.1 ppm F, should provide a daily fluoride intake above the suggested threshold for fluorosis of 0.1 mg F/kg body mass. However, if reconstituted with water containing 1.0 ppm F they should all provide a daily fluoride intake of above the suggested threshold for fluorosis with intakes up to 2-3 times the recommended upper 'optimal' limit of 0.07 mg/kg body mass. Under these conditions the water used to reconstitute the formulae would provide 65-97 percent of the fluoride ingested. These figures are likely to be overestimates due to the intake of nutrients from other sources reducing formulae consumption and also due to the lower bioavailability of fluoride from milk-based formulae. Further, it is generally believed that the maturation stage of enamel formation is the critical period for fluorosis development by chronic, above-threshold fluoride exposure. The maturation stage for the anterior permanent teeth, however, is after the first twelve months of life where fluoride intake from infant formula consumption per kg body mass is highest. The level of fluoride in the commonly used Australian formulae would suggest that infant formula consumption alone is unlikely to be a risk factor for dental fluorosis in a non-fluoridated community, but could make a major contribution to an infant's daily fluoride intake. However, prolonged consumption (beyond 12 months of age) of infant formula reconstituted with optimally-fluoridated water could result in excessive amounts of fluoride being ingested during enamel development of the anterior permanent teeth and therefore may be a risk factor for fluorosis of these teeth.

Acids↗
PubMed1996

Water fluoridation and osteoporotic fracture.

Osteoporotic fractures constitute a major public health problem. These fractures typically occur at the hip, spine and distal forearm. Their pathogenesis is heterogeneous, with contributions from both bone strength and trauma. Water fluoridation has been widely proposed for its dental health benefits, but concerns have been raised about the balance of skeletal risks and benefits of this measure. Fluoride has potent effects on bone cell function, bone structure and bone strength. These effects are mediated by the incorporation of fluoride ions in bone crystals to form fluoroapatite, and through an increase in osteoblast activity. It is believed that a minimum serum fluoride level of 100 ng/ml must be achieved before osteoblasts will be stimulated. Serum levels associated with drinking water fluoridated to 1 ppm are usually several times lower than this value, but may reach this threshold at concentrations of 4 ppm in the drinking water. Animal studies suggest no effect of low-level (0-3 ppm) fluoride intake on bone strength, but a possible decrease at higher levels. Sodium fluoride has been used to treat established osteoporosis for nearly 30 years. Recent trials of this agent, prescribed at high doses, have suggested that despite a marked increase in bone mineral density, there is no concomitant reduction in vertebral fracture incidence. Furthermore, the increase in bone density at the lumbar spine may be achieved at the expense of bone mineral in the peripheral cortical skeleton. As a consequence, high dose sodium fluoride (80 mg daily) is not currently used to treat osteoporosis. At lower doses, recent trials have suggested a beneficial effect on both bone density and fracture. The majority of epidemiological evidence regarding the effect of fluoridated drinking water on hip fracture incidence is based on ecological comparisons. Although one Finnish study suggested that hip fracture rates in a town with fluoridated water were lower than those in a matching town without fluoride, a later study failed to show differences. Ecological studies from the United States and Great Britain have, if anything, revealed a weak positive association between water fluoride concentration and hip fracture incidence. Two studies examining hip fracture rates before and after fluoridation yielded discordant results, and are complicated by underlying time trends in hip fracture incidence. Only two studies have attempted to examine the relation between water fluoride concentration and fracture risk at an individual level. In one of these, women in a high fluoride community had double the fracture risk of women in a low fluoride community. In the other, there was no relationship between years of fluoride exposure and incidence of spine or non-spine fractures. In conclusion, the epidemiological evidence relating water fluoridation to hip fracture is based upon ecological comparisons and is inconclusive. However, several studies suggest the possibility of a weak adverse effect, which warrants further exploration. Data on the relationship between fluoride intake and hip fracture risk at the individual level, and data relating fluoridation to bone mineral density are required. Until these become available, the burden of evidence suggesting that fluoridation might be a risk factor for hip fracture is weak and not sufficient to retard the progress of the water fluoridation programme.

Aged↗
PubMed1984

Effects of cortisol and fluoride on ion-transporting ATPase activities in cultured osteoblastlike cells.

Na+,K+-ATPase, HCO3(-)-ATPase, Ca2+,Mg2+,-ATPase, Ca2+-ATPase, and alkaline phosphatase activities were measured in cultures of osteoblastlike cells treated with fluoride and cortisol separately and in combinations. Low concentrations of cortisol increased HCO3- -ATPase (10(-11) to 10(-18) M cortisol) and alkaline phosphatase (10(-11) to 10(-9) M cortisol) activities, but higher cortisol concentrations reduced these activities. Na+,K+-ATPase, Ca2+,Mg2+-ATPase, and Ca2+-ATPase activities tended only to be reduced by cortisol. Fluoride (10(-6) and 5 X 10(-6) M) increased HCO3(-)-ATPase and alkaline phosphatase activities, but these activities were similar to controls in the presence of 10(-5) M fluoride. Ca2+,Mg2+-ATPase activity was decreased and Na+,K+-ATPase activity was increased as the concentration of fluoride increased (10(-6) to 10(-5) M). Preliminary experiments with fluoride indicated that lower concentrations (10(-7) M) were without effect. Cortisol concentrations of 10(-9) and 10(-8) M were chosen for studies with combinations of cortisol and fluoride because the effects of these concentrations on alkaline phosphatase activity were opposite, i.e. 10(-9) M increased whereas 10(-8) M decreased activity. Fluoride concentrations of 10(-6), 5 X 10(-6), and 10(-5) M were chosen because a peak of alkaline phosphatase activity occurred at 5 X 10(-6) M fluoride. Higher (10(-4) M) and lower (10(-7) M) fluoride concentrations were without effect. The effects of combinations of cortisol and fluoride depend on the enzyme activity measured. Fluoride (10(-6) M) combined with cortisol (10(-9) M) produced a peak of Na+,K+-ATPase activity. The increased activity obtained with all concentrations of fluoride alone was preserved when fluoride was combined with 10(-8) M cortisol, although the activity tended to be reduced at 5 X 10(-6) and 10(-5) M fluoride. HCO3(-)-ATPase activity was increased by fluoride combined with 10(-8) M cortisol and decreased by fluoride combined with 10(-9) M cortisol compared to the activities obtained with fluoride alone. The decrease in Ca2+,Mg2+-ATPase activity caused by fluoride alone was prevented by 10(-9) and enhanced by 10(-8) M cortisol, although all treatments produced the same activity at 10(-5) M fluoride. Ca2+-ATPase activity tended to be increased by combinations of fluoride and cortisol, but significantly so only at 10(-5) M fluoride in combinations with 10(-8) and 10(-9) M cortisol.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphatases↗
PubMed1994

Water fluoridation: current effectiveness and dental fluorosis.

This paper reviewed the literature on the evidence for water fluoridation's effectiveness under current conditions of multiple fluoride use at recommended and at reduced concentrations, the extent of dental fluorosis at different fluoride concentrations, and the "halo" effect of water fluoridation. Using the relative difference in dental caries between communities with low and optimal water fluoride as an indicator, the effectiveness of water fluoridation has decreased over time as the use of other fluorides has increased. Thus the effectiveness of water fluoridation alone cannot now be determined. Compared to the early fluoridation studies, the differences in dental caries and fluorosis prevalence between fluoridated and non-fluoridated areas have markedly narrowed. Both the prevalence and severity of dental fluorosis have increased since 1945; however, the portion of fluorosis due to water fluoridation is now less (40%) than that attributed to other fluoride sources (60%). Research also suggests that the "halo" effect of community water fluoridation may result in a significantly greater intake of fluoride for people in non-fluoridated communities. This review recognized that since water fluoridation has unique advantages from the perspectives of distribution, equity, compliance and cost-effectiveness over other fluoride technologies, it remains as the fundamental base for caries prevention. The increasingly greater contribution that other sources of fluoride make to dental fluorosis suggests that these sources of fluoride, many of which are used on an elective basis, should be more closely examined for needed changes.

Adolescent↗
PubMed1996

High fluoride intakes cause osteomalacia and diminished bone strength in rats with renal deficiency.

Renal insufficiency is known to increase plasma fluoride levels, which may increase the risk of fluorosis and osteomalacia. The purpose of this study was to determine the effects of fluoride on skeletal fragility and mineralization in renal-deficient animals. We evaluated the skeleton of rats with surgically induced renal deficiency (4/5 nephrectomy) that were chronically exposed to fluoridated water at concentrations of 0, 5, 15, and 50 ppm for a period of 6 months. The chosen fluoride doses caused plasma fluoride levels equivalent to those in humans consuming fluoridated water levels of 0, 1, 3, and 10 ppm, respectively. Animals with renal deficiency drank about 60% more water and excreted 85% more urine than control animals. Glomerular filtration rate (GFR) was decreased 68% and plasma BUN was increased fourfold in rats with renal deficiency. Plasma fluoride was strongly correlated with 1/GFR and was greatly increased by renal deficiency in all animals consuming fluoridated water. There was a strong positive, nonlinear relationship between plasma fluoride and bone fluoride levels, suggesting nonlinear binding characteristics of fluoride to bone. The amount of unmineralized osteoid in the vertebral bone was related to the plasma fluoride levels. Vertebral osteoid volume was increased over 20-fold in animals with renal deficiency that received 15 or 50 ppm fluoride, suggesting osteomalacia. Should osteomalacia be defined as a tenfold increase in osteoid volume, there appeared to be a threshold plasma fluoride level of about 20 micromol/L, above which osteomalacia was observed consistently. This plasma fluoride level was not achieved in control rats regardless of fluoride intake, nor was it achieved in renal-deficient rats receiving 0 or 5 ppm fluoride. A fluoride concentration of 50 ppm reduced femoral bone strength by 11% in control rats and by 31% in renal-deficient rats. Vertebral strength also was decreased significantly in renal-deficient rats given 50 ppm fluoride. In conclusion, fluoridated water in concentrations equivalent to 3 and 10 ppm in humans, caused osteomalacia and reduced bone strength in rats with surgically-induced renal deficiency.

Alkaline Phosphatase↗
PubMed2004

[Study on the application of benchmark dose and biological monitoring indexes of fluorides in drinking water].

OBJECTIVE: By using Benchmark Dose (BMD) approach to explore the relations among drinking water fluoride, urine fluoride, serum fluoride and dental fluorosis; and to evaluate the significance of urine fluoride and serum fluoride in control and prevention of endemic fluorosis. METHODS: 512 children (290 in Xinhuai Village, 222 in Wamiao Village) aged 8-13 years were recruited in the study. Epidemiological methods were used to investigate the prevalence of dental fluorosis, and the levels of urine fluoride, serum fluoride, and drinking water fluoride in superficial well. The children were divided into six subgroups by the concentration of fluoride in drinking water: < 0.5 mg/L, 0.5-mg/L, 1.0-mg/L, 2.0-mg/L, 3.0-mg/L and > or = 4.0 mg/L. RESULTS: There was significant dose-response relationship between the drinking water fluoride and the prevalence of dental fluorosis or the prevalence of defect dental fluorosis. The BMDLs (Benchmark Dose Lower Bound) were 1.01 and 1.30 mg/L, respectively. Urine fluoride and serum fluoride also had significant dose-response relationship to the prevalence of dental fluorosis or defect dental fluorosis. The correlation coefficient between drinking water fluoride and urine fluoride was 0.717, and it was 0.855 between drinking water fluoride and serum fluoride, and 0.617 between urine fluoride and serum fluoride. CONCLUSIONS: The currently national standard of fluoride in drinking water in China is safe and reasonable. As a biological monitoring index, the levels of fluoride in serum may be more useful than that in urine in the control and prevention of endemic fluorosis.

Adolescent↗
PubMed1989

Kinetics of acquisition and loss of calcium fluoride by enamel in vivo.

Two in vivo experiments were performed, concerning (1) the kinetics of the acquisition of calcium fluoride on enamel during daily rinses with a solution of 0.023% F as sodium fluoride, and (2) the loss of calcium fluoride from enamel slabs which had been topically treated with a neutral solution containing 0.9% F as sodium fluoride. Enamel slabs were carried in the mouth by 6 volunteers for 8 days in both experiments. Sound and etched enamel were included. (1) During mouthrinses moderate amounts of fluoride were acquired by sound enamel, and more as calcium fluoride than as fluoridated apatite, whereas on etched enamel, more fluoride was deposited as fluoridated apatite. On etched enamel there was also a tendency that the deposition of calcium fluoride levelled out whereas the incorporation of firmly bound fluoride continued. This may indicate that calcium fluoride was transformed into fluoridated apatite, probably through remineralization during pH cycling in plaque covering the etched enamel. (2) After single topical application, it was found that etched enamel initially took up more calcium fluoride than sound enamel, but also lost more during the 1st day of in vivo exposure. The loss of calcium fluoride was arrested after 1-2 days, on sound enamel at 70% and on etched enamel at 40% of the original level. It is suggested that the increased amounts of firmly incorporated fluoride in enamel originated from calcium fluoride on enamel, and that calcium fluoride is an important and clinically significant source of fluoride ions on enamel.

Acid Etching, Dental↗