Fluoride Arwa Owais. Fluoride: Human Health and Caries Prevention Fluoride ranks as a primary influence in better oral health because it demonstrated.

Fluoride

Arwa Owais

Fluoride: Human Health and Caries Prevention

Fluoride ranks as a primary influence in better oral health because it demonstrated that caries and subsequent tooth loss were not inevitable. Just as important, it helped dentists to reshape their attitudes toward tooth conservation and retention.

ENVIRONMENTAL FLUORIDE

Fluorine is one of the most reactive elements and therefore is never found naturally in its elemental form.

The F ion, however, is abundant in nature and occurs almost universally in soils and waters in varying, but generally low, concentrations. – Seawater contains 1.2 to 1.4 ppm F. – Fresh surface waters, 0.2 ppm F or less, – Deep well waters, 29.5 ppm F have been recorded

ENVIRONMENTAL FLUORIDE

– F's ubiquity in soil and water means that all plants and animals contain F to some extent.

– Given this environmental ubiquity, it seems likely that all forms of life must have evolved to thrive with continuous exposure to small amounts of F.

SOURCES AND AMOUNTS OF FLUORIDE INTAKE Humans absorb F from air, food, and

water.

Air intake is usually negligible, around 0.04 mg F/day. Exceptions can occur around some industrial plants that work with F-rich material, an issue that has nothing to do with the use of F to control caries.

SOURCES AND AMOUNTS OF FLUORIDE INTAKE

F's abundance in soils and plants means that everyone consumes some F.

Estimates for an adult North American male in a fluoridated area fall within the range of 1 to 3 mg F per day from food and beverages, decreasing to 1.0 mg F per day or less in a nonfluoridated area

Estimates from "market basket" analyses are that 6-month-old infants ingest 0.21 to 0.54 mg F/day in 4 American cities with different F concentrations in the drinking water.

For 2-year-olds in the same cities, the range was 0.41 to 0.61 mg F/day

For infants, The Iowa studies documented the F exposures of new­born infants at periodic intervals through extensive interviews about all likely sources of F exposure.

Total F intakes from drinking water alone during the first 9 months of life, either consumed directly or when added to formula and juice, averaged 0.29 to 0.38 mg F/day.

SOURCES AND AMOUNTS OF FLUORIDE INTAKE

SOURCES AND AMOUNTS OF FLUORIDE INTAKE Although similar to earlier market

basket surveys, there was considerable range of intake with 25% of 9-month old children ingesting 0.49 F/day.

Even without swallowing F toothpaste or taking F supplements, the risk of dental fluorosis is likely to be increased in these children because the upper limit of intake for 12-month-old children, beyond which the risk of detectable fluorosis is increased, has been estimated at 0.43 mg F/day.

SOURCES AND AMOUNTS OF FLUORIDE INTAKE For most people, water and other

beverages provide 75% of F intake, whether or not the drinking water is fluoridated.

This can occur because many soft drinks and fruit juices are processed in fluoridated cities.

FLUORIDE PHYSIOLOGY

Although the use of F is a contribution to the public's health of which dentistry can be proud, F compounds must be handled responsibly and with respect.

Everyone in dentistry should understand how the human body handles ingested F so that the material can be used safely and efficiently.

Absorption, Retention, and Excretion

Ingested F is absorbed mainly from the upper gastrointestinal tract.

About 80% of F in food is absorbed, as is 85% to 97% of F in water.

Absorbed F is transported in the plasma, and is either excreted or deposited in the calcified tissues.

Most absorbed F is excreted in the urine; F ingested on an empty stomach produces a

peak plasma level within 30 minutes. The time of the plasma peak is extended and

the level of the peak reduced, if F is taken with food. This is probably because of the binding of some F with calcium and other cations.

When F absorption is inhibited this way, fecal excretion of F increases.

The Body Burden of F

Studies on what is called the body burden of F, meaning how much can be safely absorbed and at what point F absorption becomes a health concern, have mostly relied on urinary volumes and plasma concentrations as the primary measures.

Samples of both are relatively simple to obtain, although both measures record only recent F intake (i.e., the previous 3 to 4 weeks) rather than lifetime intakes.

The Body Burden of F

Urinary concentrations can vary considerably with fluid intake during the period of F exposure and require a 24 ­hour sample to be accurate.

Accurate monitoring of plasma levels in individuals also requires frequent measures because of normal hour-to-hour fluctuations.

Plasma F concentrations are more closely correlated with urinary flow rates than with urinary F concentrations.

The Body Burden of F

Although there is no absolute measure of lifetime F intake, even theoretically, the nearest measure of long-term F intake would come from bone F content.

For research purposes, however, this is a theoretical concept only; people don't volunteer to give a bone sample!

Fluoride balance is the net result from the accumulated effects of F ingestion, degree of F deposition in bones and teeth, mobilization rate of F from bone, and the efficiency of the kidneys in clearing absorbed F.

Fluoride Balance

F has an affinity for calcified tissues (i.e., bone and developing teeth).

F that is not excreted is deposited in these hard tissues, al­though storage is dynamic rather than inert.

Bone F levels (from postmortem assays) range from 800 to 10,000 ppm, depending on many factors, including age and F intake.

F levels in the outer few microns of dental enamel range from 400 to 3000 ppm and decrease rapidly with greater enamel depth.

Fluoride Physiology

Fluoride Physiology

F concentrations in soft tissue rise or fall parallel to plasma F levels, but because healthy excretion and deposition mechanisms operate so rapidly there are negligible concentrations of F in the fluids of soft tissues other than the kidney.

A greater proportion of ingested F is excreted in older persons than in the young. It had been suggested that this was because children had lower renal clearance rates than adults, but is now attributed to greater adsorption of F by the young skeleton.

"Optimum Fluoride Intake"

Frank McClure, estimated in 1943 that the "average daily diet" contained 1.0 to 1.5 mg F, or about 0.05 mg F/kg body weight/ day in children up to 12 years of age.

Mc­Clure's estimate somehow came to be

interpreted as the lower limit of the range of "opti­mum" F intake.

A widely quoted 1974 reports suggested 0.06 mg F/kg body weight/day as "optimum,"

"Optimum Fluoride Intake" The range of 0.05 to 0.07 mg F/kg body

weight/day was suggested as "optimum" in 1980, and has even been accepted by opponents of water fluoridation.

The estimate of 0.05 to 0.07 mg F/kg/day converts to 3.5 to 4.9 mg F per day for a man weighing 70 kg

For a 10-kg infant , that is a 12- to 18-month-old child, this "optimum" intake converts to 0.45 to 0.64 mg F/day.

Fluoride was classified as beneficial and not essential nutrient

The discussions vague about what this intake is "optimum" for. "optimum" for caries resistance, but little of F's action in caries control can be attributed to ingested F.

There is no evidence to link this range of F ingestion with caries inhibition, so we suggest that the term "optimum intake" be dropped from common usage.

"Optimum Fluoride Intake“??

FLUORIDE and HUMAN HEALTH Early Studies The first study relating bone fracture experience to

the F concentration in home water supplies, a subject revisited in the 1990s, concluded that there was no relationship.

McClure then demonstrated the close relationship between urinary F and the F levels of domestic water. His balance studies during World War II, led to the conclusion that the elimination of absorbed F via urine and perspiration is almost complete when the quantity absorbed does not exceed 4 to 5 mg daily. McClure suggested that this may be the F limit that could be ingested without "appreciable hazard" of excessive F storage in the body.

There was sufficient research evidence to provide reasonable assurance that controlled fluoridation, with up to 1.2 ppm F in the drinking water, could be-instituted in North America without any public health hazard.

FLUORIDE and HUMAN HEALTH

Mortality

For the United States as a whole, no differences could be found in 1949-1950 death rates between 32 cities with 0.7 ppm F or more and 32 randomly selected nearby cities with 0.25 ppm F or less in the drinking water.

Mortality rates were similar for cancer, heart disease, intracranial lesions, nephritis, and cirrhosis of the liver.

Similar findings were reported later in 1979.

Cancer

A number of independent analyses of the same data, in both Britain and the United States, however, used more detailed age-sex-race adjustments; none could find a link between cancer incidence and consumption of fluoridated water.

A special committee appointed by the US Public Health Service, reached the follow­ing conclusion on cancer risk:

Optimal fluoridation of drinking water does not pose a detectable cancer risk to humans as evidenced by extensive human epidemiological data available to date.

No trends in cancer risk, including the risk of osteosarcoma, were attributed to the introduction of fluoride into drinking water in these new stud­ies.

Cancer

Down Syndrome

A claim that water fluoridation caused an increase in Down syndrome came mid-1950s.

The studies had errors in the research design. The most serious error was to assume that the city of birth was the place of residence of the mother, which is clearly not the case for hospitals serving a large rural population.

More rigorous independent studies failed to

show any correlation between fluoridation and Down syndrome.

Bone Density, Fracture Experience, and Osteoporosis

Bone fragility conditions (e.g., spontaneous vertebral fracture in the elderly as a result of osteoporosis) have been treated for years with high does of F combined with calcium, estrogen, and vitamin D.

Controlled clinical trials have shown that high doses of- F (30 to 60 mg/day), administered under medical supervision, can increase vertebral bone mass and reduce the vertebral fracture rate.

These favorable changes do not come without problems, however, for the new bone can be imperfectly mineralized and a good proportion of patients do not respond to treatment.

Recently, ecologic studies to assess the risk of bone fracture relative to fluoridated water have produced mixed results:– decreased risk no association, and – increased risk, with relative risks in the

range of 1.08 to 1.41.

Extensive reviews of literature have also reached the conclusion that no relationship can be discerned between bone fracture experience and water with 1.0 ppm F.

Bone Density, Fracture Experience, and Osteoporosis

In summary, although there does not appear to be any protective effect from fluoridated water, neither is there evidence that bone fracture experience is associated with drinking water containing 1.0 ppm F.

Bone Density, Fracture Experience, and Osteoporosis

Child Development

Newburgh-Kingston fluoridation project, No significant differences in general health or body processes

between children in the two cities were seen, No radiographic differences in bone density could be

demonstrated. Essential similarity in vision and hearing tests and in findings

for skeletal maturation, hemoglobin level, erythrocyte and leukocyte counts, and quantity of sugar, albumin, red blood cells, and casts in urine.

At the final examination, 19 of 476 children in Newburgh (4.0%) and 20 of 405 children in Kingston (4.9%) were referred to the family physician for conditions including such minor ailments as a plantar wart or ringworm.

Long-term downward trends in stillbirth and maternal and infant mortality rates continued in each of the cities. The overall conclusion was that no differences of medical signifi­cance could be found between the two groups of children.

FLUORIDE TOXICITY

There is difference between a single intake of 5.0 g F and constant intake of 1 to 3 mg F daily.

F is like many other nutrients: beneficial in small amounts, toxic in high amounts. This gradation in response with variations in dose is a common pharmaceutical phenomenon and is known as a dose­response relationship.

Ingestion of a single dose of 5 to 10 g of sodium fluoride by an adult male (32 to 64 mg F/kg body weight) results in a rather unpleasant death in 2 to 4 hours if first aid is not applied immediately.

From that lower limit of 32 mg F/kg body weight, the estimated equivalent dose for a 10-kg child (12 to 18 months old) is 320 mg F.

FLUORIDE TOXICITY

FLUORIDE TOXICITY

If an individual is known or suspected to have taken a potentially toxic amount of F, first aid is to– induce vomiting or – ingest a material to bind F. Milk is usually

the most readily available.

The ADA recommends, as a safety precaution, that F materials for home use contain no more than 264 mg F if packaged in a bulk container (tablets, mouthwash) or up to 300 mg F if the F material is individually packaged.

Dental Fluorosis

Dental fluorosis is a permanent hypomineralization of enamel, characterized by greater surface and subsurface porosity than in normal enamel. It results from excess F reaching the developing tooth during developmental stages.

FLUORIDE AND CARIES CONTROL: MECHANISMS OF ACTION

F works best to prevent caries when a constant, low ambient level of F is maintained in the oral cavity. Its most important caries-inhibitory action is posteruptive, though a pre-eruptive role continues to be suggested. F’s action in preventing caries is multifactorial; its effect comes from a com­bination of several mechanisms. Three major mechanisms of action have been identified, although some possible addi­tional mechanisms have been hypothesized.

FLUORIDE AND CARIES CONTROL: MECHANISMS OF ACTION

Earlier assumptions: Pre-eruptive F is thought to act by being incorporated into the developing enamel hydroxyapatite crystal and thus reducing enamel sol­ubility.

It has been argued that pre-eruptive benefits are especially important for reducing pit-and-fissure lesions.

This is the "pre-eruptive" model for which the actual supportive evidence is thin. The evidence for posteruptive F action is much stronger.

Fluoride and Plaque

F introduced into the mouth is partly taken up by dental plaque, where 95% of it is held in bound form rather than as ionic F.

Plaque contains 5 to 10 mg F/kg wet weight in low F areas and 10 to 20 mg F/kg wet weight in fluoridated areas.

The bound F can be released in response to lowered pH, and F is taken up more readily by demineralized enamel than by sound enamel. The availability of plaque F to respond to the acid challenge leads to the gradual establishment of a well-crystallized and more acid-resistant apatite in the enamel surface during demin-remin.

F in plaque also inhibits glycolysis, the process by which fermentable carbohydrate is metabolized by cariogenic bacteria to produce acid. F from drinking water and toothpaste concentrates in plaque, which contains higher levels of F than does saliva.

There is also some evidence that plaque F can inhibit the production of extracellular polysaccharide by cariogenic bacteria, a necessary process for plaque adherence to smooth enamel surfaces.

Fluoride and Plaque

Fluoride and Plaque

High ­concentration F gels may have a specific bactericidal action on cariogenic bacteria in plaque.

These gels also leave a temporary layer of CaF2 on the enamel surface, which is available for release when the pH drops at the enamel surface.

At lower concentrations, Streptococcus mutans has been shown, to become less acidogenic through adaptation to an environment where F is constantly present. It is not yet known whether this ecologic adaptation reduces the cariogenicity of acidogenic bacteria in humans.

Fluoride and Enamel

It became evident to researchers as early as the mid-1970s that a higher concentration of enamel F could not by itself explain the extensive reductions in caries that F produced.

The theoretical concentration of F in pure fluorapatite that would reduce its acid solubility is 38,000 ppm, a concentration not even approached in human dental enamel.

Perhaps the most revealing study on the action of F in inhibiting dental caries came from the Tiel-Culemborg fluoridation study in the Netherlands.

Although there were considerably fewer dentinal lesions in fluoridated Tiel than in nonfluoridated Culemborg after 15 years of fluoridation.

There was no difference between the two communities in initial enamel lesions.

This finding means that fewer enamel lesions progress to dentinal caries in a fluoridated area than in a nonfluoridated area.

F, therefore, does not prevent the initial carious at­tack, which would be expected if its presence in the enamel crystal increased enamel resis­tance to acid dissolution.

The Tiel-Culemborg findings mean than F in the oral cavity inhib­its further demineralization of the lesion and promotes its remineralization.

Fluoride and Plaque

Fluoride and Saliva

Salivary F concentrations are low, although they are 3 times higher in fluoridated than in nonfluoridated areas.

In a fluoridated area, salivary F levels have averaged 0.016 ppm; in a nonfluoridated area, they were 0.006 ppm.

After toothbrushing with an F toothpaste or mouthrinsing with an F solution, salivary F levels can rise 100- to 1000-fold.

Effects on Different Tooth Surfaces

Although F reduces caries on both types of surface, the greatest relative effect is on smooth and proximal surfaces.

EFFECTIVE USE OF FLUORIDE

Categorizing F compounds into systemic fluorides and topical fluorides is not easy .

The most cost-effective way of reaching an entire community with regular, low-concentration F is through water fluoridation.