Flouride in small amounts unquestionably strengthens tooth defenses against dental caries. It cannot be listed literally as an element essential to life, but it is now established beyond reasonable doubt that optimal quantities of flourides are desirable and beneficial in improving tooth health. When flouride is naturally present in drinking water, is added mechanically, or more rarely, is ingested in more than minimal amounts in food, tooth decay diminishes.
Knowledge of flouride metabolism provides some understanding of the possible role of flouride in tooth health, as well as some reassurance as to the safety of fluoridated water.
Two aspects of the metabolic process will be discussed; absorption and excretion.
Approximately 90% of the flouride ingested each day is absorbed in the stomach and duodenum by passive diffusion. Presence of calcium , aluminium and magnesium reduce the absorption probably by formation of insoluble complexes with flouride. The half-time for absorption is approximately 30 minutes, hence peak plasma concentrations usually occur within 30-60 minutes. Absorption across the oral mucosa is limited and probably accounts for less than 1% of the daily intake. Absorption from the stomach occurs readily and is inversely related to the pH of the gastric contents, and most of the remaining flouride that enters the intestine will be absorbed rapidly. High concentrations of dietary calcium and other cations that form insoluble complexes with flouride can reduce flouride absorption from the gastrointestinal tract.
Most of the ingested flouride is absorbed in the digestive tract, and through the digestive tract it is absorbed into the blood.
Most of the flouride absorbed systemically that is not excreted via normal pathways (i.e through the kidneys, the colon or by sweating) is deposited in mineralizing tissues such as bone and developing teeth. Only small amounts remain unabsorbed which are excreted through the faeces. flouride is present in saliva at very low levels (0.01 ppm to 0.04 ppm) and in human milk at low levels (0.1 ppm). While the concentration of flouride in these body fluids is minimal, studies show it is enough to impact dental caries.
About 90% of flouride is absorbed in the gastrointestinal tract after consumption (up to 25% in the stomach and around 77% in proximal part of the small intestine). The remaining 10% is excreted in feces (15). After absorption, flouride is transported into the bloodstream and is distributed through the organism (4). The mean time of the peak concentration is 20-60 minutes after consumption (15). In the plasma, flouride ions are bound to plasma protein (15). Concentration rarely exceeds 0.06 ppm (parts per million). It is usually about 0.01 ppm and is not homeostatically regulated in the blood. Adults retain around 36% of flouride, whereas children retain approximately 50% of flouride; 99% of that is contained in mineralized tissues (bone and teeth) and 1% can be found in soft tissue (15). The remaining part of the absorbed flouride is excreted through the kidneys into the urine; excretion through saliva and sweat is negligible (4). The kidneys are therefore the only human organ that helps maintain the flouride concentration in our bodies. There are different factors that can influence flouride metabolism. The most important are: acid base disorders, hematocrit, altitude, physical activity, circadian rhythm, hormones, kidney function, genetic predispositions and diet (15). In pregnant women, uptake of flourides in the placenta is dependent on the flouride concentration in the mother`s bloodstream. When the concentration is low, flouride is transmitted into the placenta (16). On average, the concentration in the placenta is about 60% of the concentration in the mother`s bloodstream (17). If the flouride concentration increases over 0.4 ppm (17), the placenta works as a barrier, preventing the flouride from passing through and thus protecting the fetus from a high flouride concentration (16). flouride can also be transmitted through the plasma into the mother’s milk; however, the concentration is low (18).
Fluoride is identified as one of the elements present in dental hard tissues. Fluoride ion is "calcium seeking". Apatite is the principal mineral of skeletal tissues. It is a crystallized form of calcium phosphate.
It is present as two forms hydroxyapatite and fluorapatite.
The primary and most important action of fluoride is topical, when the fluoride ion is present in the saliva in the appropriate concentration.
Hydroxyapatite is the main mineral responsible for building the permanent tooth enamel after the development of the teeth is finished . During tooth growth, the enamel is constantly exposed to numerous demineralization processes, but also important remineralization processes, if the appropriate ions are present in the saliva. These processes can either weaken or strengthen the enamel. The presence of fluoride in an acidic environment reduces the dissolution of calcium hydroxyapatite. The main action is inhibition of demineralization of enamel, which is carried out through different mechanisms. There are different cariogenic bacteria in the plaque fluid the most important being S. mutans. When bacteria metabolize sugars, they produce lactic acid which decreases the pH in saliva.
When the pH falls below the critical level of hydroxyapatite (pH 5.5), the process of demineralization of enamel takes place and caries is formed. At the beginning, the process is reversible and it is possible to reduce the formation of new lesions with appropriate preventive measures. If fluoride is present in plaque fluid, it will reduce the demineralization, as it will adsorb into the crystal surface and protect crystals from dissolution. Because the fluoride ion coating is only partial, the uncoated parts of the crystal will undergo dissolution on certain parts of the tooth, if the pH falls below level 5.5. When the pH rises above the critical level of 5.5, the increased level of fluoride ion leads to remineralization, because it absorbs itself into the enamel and forms fluorhydroxyapatite (33). After repeated cycles of demineralization and remineralization, the outer parts of enamel may change and become more resistant to the acidic environment due to a lowered critical pH level of newly formed crystals (pH 4.5) (33). The most important effect of fluoride on caries progression is thus on demineralization and remineralization processes. It has also been proposed, that the fluoride ion can affect the physiology of microbial cells, which can indirectly affect demineralization. Fluoride ions affect bacterial cells through several mechanisms. One of them being a direct inhibition of cellular enzymes – glycolytic enzymes, H+ATPases). It affects cellular membrane permeability and also lowers cytoplasmic pH, resulting in a decrease in acid production from glycolysis (33).
Major part of fluoride which is retained on the teeth during topical application is Calcium Fluoride CaF2 or calcium fluoride like material. Calcium Fluoride is most likely source of free ions during carcinogenic challenges, which are subsequently incorporated into enamel as hydroxyfluorapatite or fluorapatite.
The Role of Fluoride in Caries
Prevention
There are three principle forms of fluoride
Ion reactivity with apatite:
1) Iso-ionic exchange of F– for OH– in apatite:
Ca10 (PO4)6 OH2 + 2F– ------- Ca10(PO4)6F2 + 2OH–
2) Crystal growth of fluorapatite from supersaturated solutions:
10 Ca2+ + 6 PO43– + 2 F– ------- Ca10(PO4)6F2
3) Apatite dissolution with CaF2 formation:
Ca10 (PO4)6 OH2 + 20F– -------10 CaF2
+6PO43– + 2OH–
The first two reactions may occur during long-term exposure to low fluoride levels in the solution (such as between 0.52 μmol and 0.52 mmol F/L) (0.01 and 10 ppm F) from either systemic or latent topical sources. These reactions result in fluoride incorporation that, in a traditional sense, would be defined as »firmly« bound fluoride, since it is part of the apatitic structure. With the increasing fluoride concentration an additional chemical reaction with the formation of significant calcium fluoride amounts begins to dominate. Fluoride concentrations ranging from 5.3 to 530 mmol/L (100–10,000 ppm F) are required to produce CaF2 as a reaction product. These concentrations are present in topicals, such as professional gels and varnishes or over the counter toothpastes and mouthrinses. The name » loosely«bound fluoride has served as an alternative description for calcium fluoride formation.
After fluoride is ingested, it is distributed from the plasma to all tissues and organs of the body, and gradually becomes incorporated into the crystal lattice structure of teeth in the form of fluorapatite. In teeth, the fluoride concentration is very high on surface enamel, but falls steeply within the first 100 µm. Then fluoride concentration remains constant up to the enamel–dentin junction. Fluoride concentration once again increases inside the dentin, increasing deeper into the tooth, with fluoride steadily accumulating over a lifetime at the dentin-pulp interface. It should be noted that there is no homeostatic mechanism that maintains fluoride concentration in the body. Therefore, regular exposure is required to maintain fluoride concentration in enamel, saliva, and in biofilm on dental surfaces.
Fluorapatite forms more compact and regular crystals than hydroxyapatite. It presents less surface area for the action of acids. Higher concentration of fluoride on outer enamel thus protecting against acid attack.
Calcium and fluoride ions released from the apatite during initial dissolution forms calcium fluoride (CaF2) on the surface of the fluorapatite hence reducing its solubility.
Fluoride ions replace carbonate ions in the paptite structure crystals with low carbonate contents are more stable and are less soluble compared to those with high carbonate ion content.
Plaque fluid contains fluoride. With decreased pH, fluoride level is increased. Thus enhancing remineralisation of enamel by facilitating the reprecipitation of calcium and phosphate ions into the enamel, thus leading to fluorapatite
Fluoride inhibits Enolase and ATPase acitivity (Embden Meyerhoff Parnas pathway in bacterial metabolism) in oral streptococci hence reduce acid production.
Fluoride administered during tooth formation may result in shallower and wider fissures and more rounded cusps, thus reducing the number and size of sites where food and plaque could accumulate.
Stannous ions in stannous fluoride may affect surface wetability and reduce plaque formation.
Flouride therapy is the delivery of fluoride to the teeth topically or systemically in order to prevent tooth decay. Most commonly, fluoride is applied topically to the teeth using gels, varnishes, toothpaste/dentifrices or mouth rinse. Systemic delivery involves flouride supplementation using water, salt, tablets or drops which are swallowed. Tablets or drops are rarely used where public water supplies are fluoridated.
Fluorides are incorporated pre-eruptively into enamel from tissue fluids during mineralization. Most of fluoride is incorporated into sound surface of enamel during the pre-eruptive maturation stage when enamel undergoes rapid and more complete mineralization. Primary teeth have a shorter period of enamel maturation and because acquires less fluoride than permanent teeth, different concentration of fluoride between permanent and primary term may be due to differences in maturation lines. Most Fluoride is acquired during pre- eruptive developed of term, but 10%, is acquired as a result of post eruptive nature.
The various types of systemic fluoridation are as follows:
The fluoridation of public water supplies represents one of the most successful public health measures ever undertaken. First added to public drinking water supplies at controlled concentrations in 1945, fluoride is now added to school water supplies, salt or milk in regions where the fluoridation of central water supplies is not possible. It is available in tablet form and in drops, which are designed as dietary supplements for children. Fluoride is present in a variety of dental products, which are intended for topical application to the teeth. The widespread use of these various vehicles for the systemic or topical delivery of fluoride is undoubtedly responsible in large part for the remarkable decline in the prevalence of dental caries that is currently being experienced in many countries of the Western world.
Water Fluoridation is defined as the controlled adjustment of concentration of fluoride in communal water supply so as to achieve maximum caries reduction and clinically insignificant level of fluorosis. Community water fluoridation (CWF) is safe and cost- effective and should be introduced and maintained wherever it is socially acceptable and feasible. The optimum water fluoride concentration is normally within the range of 0.5 ppm-1.0 ppm.
When communal water supplies are available, water fluoridation is the most effective, efficient and economical of all known measures for the prevention of dental caries. The greatest benefit is that fluoride is made available systemically during tooth development and topically after eruption. Lifetime protection against dental caries results from continuous use of low concentration of fluoride. Careful assessment of patient is necessary to decide the best method of administering fluoride.
Salt fluoridation was first initiated in Switzerland in 1955. As a dietary vehicle, domestic salt comes second to drinking water. It has been reported that 250 ppm F in salt or 250 mg F/Kg salt is effective. 90 mg Fluoride / kg salt was the ratio in Columbia Spain and Hungary. In Switzerland and Hungary, Fluoride is added to salt by spraying concentrated solutions of sodium fluoride and potassium fluoride to salt on conveyor belt. In USA , sodium fluoride and calcium fluoride are mixed with phosphate carrier salts, and these premixed granules are added to salt.
Milk is recommended as good food for infants and children, hence considered as suitable vehicle for children's fluoride intake.
2.5mg NaF
3.5 ppm
Not feasible in India
Fluorides tablets are commercially available as NaF tablets of 2.3mg, 1.1mg & 0.55mg yeidling 1mg,0.5mg, & 0.25mg fluoride respectively.
Not recommended for children < 2 years
The use of topical fluorides may result in a significant reduction in caries as the fluoride gets integrated into the enamel matrix, hardening the structure and making it more resistant to demineralization. Topical application of fluoride is available via:
The efficacy of fluoride treatment in reducing dental caries depends on the ability of Fluoride agents to increase the enamel Fluoride concentrations, to enhance remineralization, and to suppress bacterial growth.
When NaF is applied topically, it reacts with hydroxy apatite crystals to form CaF2, which is the main product of reaction.
Ca10 (PO4) 6 (OH) 2 + 2OF_________10CaF 2 + 6PO4 3- + 2OH-
(WHAT ?)This is due to high concentration of fluoride (9,000ppm) in 2% NaF due to which the solubility product of CaF2 gets excreted fast and the initial rapid reaction is followed by drastic reduction in its rate(Of what) and the phenomenon is called ‘choking off ’. This occurs because once a thick layer of CaF2 gets formed, it interferes with the further diffusion of fluoride from the topical fluoride solution to react with hydroxy apatite.
CaF2 + 2Ca3 (PO4) 5 OH________2Ca5(PO4) 3 + Ca (OH) 2.
It is because of this reason that, NaF if once applied and is left to dry for 4 minutes; Further CaF2 reacts with Hydroxy apatite to form Fluoridated hydroxy apatite.;which increases the concentration of surface fluoride thus making the tooth structure more stable, less susceptible to dissolution by acids, interferes with plaque metabolism through antienzymatic action and also helps in remineralization of the initial decalcified areas, thus showing its manifold anticaries effect.
The prolonged retention of reaction products, which form a coating on the enamel surface, may influence both initiation and progression of enamel caries.
It is applied at ages of 3, 7, 11 and 13 years in 4 appointments in a year.
Sodium Fluoride comes under brand names like Karidium, Karigel, Neutracare, Prevident.
MECHANISM OF ACTION OF SnF2: Muhler (1968) reported that when stannous fluoride reacts with Hydroxy apatite, in addition to fluoride, the tin? of stannous fluoride also reacts with enamel and a new crystalline product gets formed which is different from fluorapatite and this new compound which is stannous – tri - fluorophosphate which is more resistant to decay than enamel (Jorden etal, 1971). It is due to the reason that, (what reason)always a freshly prepared SnF2 solution should be used and the capsules of SnF2 should be kept in air tight containers otherwise the stannous form of tin gets oxidized to stannic form, thus making the SnF2 inactive for anti caries action.
Infra Red absorption and x-ray diffraction analysis of the reaction of stannous fluoride with hydroxy apatite shows that mainly four products get formed.
Tin hydroxy phosphate [Sn2 (OH) Po4] is formed. When SnF2 is applied in low concentration and the second and the main end product that gets formed is tin-tri-fluoro phosphate (Sn3F3Po4). At very high concentration of stannous fluoride, calcium- tri- fluoro stannate [Ca(SnF3)2] gets formed along with tin-tri-fluorophosphates. CaF2 in low quality is also the end product, both in low and high concentration.
The reaction at low concentration is
Ca5 (Po4) OH+ 2SnF2---------- 2CaF2+Sn2(OH)Po4+Ca3(PO4)2
At high concentration.
Ca5 (Po4) 3 OH+16SnF2_____
2Sn3F3PO4 +Sn2(OH)Po4+4CaF2(SnF3)2 +2CaF2
(Hydroxyphosphate)(Calciumtrifluorostannate)
CaF2 So formed further reacts with hydroxy apatite and small fraction of flor hydroxy apatite also gets formed.
2Ca5(Po4) 3 OH + CaF2________2Ca5(PO4) F +Ca (OH) 2
The other end product, tin hydroxy phosphate gets dissolved in oral fluid and is responsible for the metallic taste after topical application of stannous fluorides. The main end product, which is tin-tri- fluoride phosphate, is responsible for making the tooth structure more stable & less susceptible to decay.
However Babcock et al., (1978) reported that calcium tri-fluoro stannate has also get similar properties.
Method of preparation:
Stannous Fluoride is freshly prepared, by dissolving contents of gelation capsule filled with 0.8 gm powdered Stannous Fluoride in 10 ml distilled water.
Method of application:
Stannous fluoride is applied once a year.
Disadvantages of stannous fluoride:
Solutions of stannous fluoride (8%) are no longer used to any extent as professionally applied topical fluoride agents, because other products with less objectionable taste are now available.
Stannous fluoride gel is available with brand names of Flo-Gel, Gel-Kam etc
Acidulated phosphate fluoride emerged as a topical agent in prevention of dental caries with the investigation of Bibby in 1947, who reported that as the pH of NaF solution was lowered, fluoride was absorbed into enamel more effectively. This statement of Bibby had its inherent limitations, as indiscriminate lowering of pH of NaF solution will cause decalcification and demineralization of enamel thus obviating the fluoride effect.
MECHANISM OF ACTION OF APF: The main advantage of the APF is its ability to deposit fluoride in enamel to a deeper depth than neutral sodium fluoride or stannous fluoride.
When APF applied to the teeth, it initially leads to dehydration and shrinkage in the volume of hydroxy apatite crystals, which further on hydrolysis forms an intermediate product called Dicalcium phosphate dihydrate (DCPD). This DCPD is highly reactive with fluoride ion and starts forming immediately, when APF is applied fluoride penetrates more deeply through the openings produced by shrinkage and leads to formation of fluorapatite (FAp)
Ca5(PO4)3OH + 4H+ _________ 5Ca++
+3PO4+H2O
OH- Ca++ +HPO4- ______________2Ca.HPO4. 2H2O
(Dicalcium Phosphate dihydrate)
F-
5Ca.HPO.2H2O________Ca (PO4) 3 + 2HPO4-
The amount and depth of fluoride deposited, as fluorapatite is dependent on the amount and depth at which DCPD gets formed. Since for the conversion of whole of DCPD so formed into fluorapatite deeper penetration and continuous supply of fluoride is required because of this reason APF is applied every 30 seconds, then teeth has to be kept wet for 4 minutes.
Because high fluoride concentrations and low pH favour fluoride deposition, acidification of the fluoride solution with phosphoric acid was found to suppress the dissolution of enamel, as well as the formation of calcium fluoride and provide a more effective treatment, the intermediate product formed is the DCPD and CaF2 is the principal reaction product .L.C chow (1990) reported that the tooth enamel acquired larger amounts of fluoride with deeper penetration when pretreated with an acidic (pH 2-3) calcium phosphate solution before exposing to Fluoride solution.
Method of preparation:
Acidulated Phosphate Fluoride is prepared by dissolving 20 gms of Sodium Fluoride in 1 litre of distilled water and 0.1 M orthophosphoric acid. To this 50% Hydrofluoric acid is added to adjust the pH at 3.0.
To prepare a gel, methyl cellulose or hydroxyethyl cellulose is added and the pH is adjusted between 4 and 5.
It comes under trade names of Butler APF topical gel, APF Gel, Luride APF, Gel II APF Thixotrophic, Nuflor APF gel.
APF is applied semiannually.
SOLUTION:
GEL:
The cariostatic effect of topical fluoride agents has generally been related to their ability to deposit fluoride in the enamel and to their depth of penetration. However, the topical fluoride solutions (NaF, SnF2, APF in aqueous form) currently in use, have major disadvantage that they remain in contact with the teeth under in vivo conditions for a very short time i.e. 5 – 10 minutes before getting diluted by saliva & consequently exerting a relatively superficial effect on the dental enamel.
A second drawback with topical fluoride solutions is that soon after application, much of the acquired fluoride probably representing unreacted F & CaF2 leaves away.
To enhance the caries inhibitory property of topical fluoride experiments were carried out aiming at overcoming the two major draw backs, by developing methods to prolonging the contact of fluoride solutions with tooth enamel in vivo leading not only to deep penetration of Fluoride in enamel but also a more permanently bound form of Fluoride.
To achieve prolonged fluoride action in the mouth, Schmidt in 1964 developed a new method in which the teeth were coated with a lacquer containing fluoride, called Fluoride lacquer which released fluoride ions to the dental enamel in higher concentrations for several hours in the moist atmosphere of the mouth.
Types of varnish
Is a 5% sodium fluoride formulation in a viscous colophonium base. One milliliter of the varnish contains 50 mg of NaF (22.6 mg fluoride /ml). It is available as a 10ml tube. The resinous base is an alcoholic suspension which when applied to the tooth surface, evaporates, leaving a layer of fluoride rich varnish attached to the tooth surface.
Contains 1% difluorosilane in a polyurethane base. Each milliliter of varnish contains 1mg of fluoride ion (1000 ppm). Fluor protector has a lower pH than duraphat & is supplied in a box containing 20 vials. Each vial contains a 0.4ml (0.4 mg F) of the varnish solution. Fluor protector is less viscous than duraphat or Durafluor.
Is similar to duraphat in formulation & contains 5% NaF varnish in an alcoholic suspension of natural resins. The one additional ingredient in Durafluor (22.6 mg /ml) is the artificial sweetening agent Xylitol that as per manufacturer improves taste & patient acceptability. This varnish is less viscous in nature than duraphat & is supplied as 10 ml tube.
Is the most recent entrant in the fluoride varnish market.
It is a 5% NaF varnish in a resinous base. Each milliliter contains 50mg NaF. The difference between cavity shield & other varnishes is that it is a unit – dosed fluoride varnish. Each individual package contains either 0.25 ml (12.5 mg NaF) or 0.4 ml (20 mg NaF) depending on the number of teeth to be treated. This offers several advantages
Additionally, there is a tendency for the NaF in the varnishes to settle down to the particulate nature of NaF. This may be significant because in the tubes (Duraflor, Duraphat) there is no way to assess the amount of fluoride each child is getting. The cavity shield varnishes are supplied in individual pouches that are light resistant to avoid congealing of the varnish.
5.FluoritopSR: The first fluoride varnish manufactured in India with Fluorprotector. FluoritopSR is a new indigenously produced fluoride varnish produced by ICPA Health Products Ltd, Mumbai.
It contains 50 mg Sodium Fluoride per ml equivalent to 22.6 mg of fluoride in slow release form. Presentation is in the form of plastic bottle with 30 ml varnish.
Fluoritop SR may offer a better alternative to existing topical fluoride agents as a caries preventive agent in our country.
The caries preventive action of a topical fluoride varnish is probably a combination of mechanisms.
The fluoride reduces demineralization
The Reactions involved are:
10Ca5 (po4) 3 +10F-_______6Ca5 (PO4) 3 + 2CaF2 + 6Ca3(po4) 2 + 10 OH- …1
Fluoride keeps on slowly releasing & continuously reacting with the hydroxy apatite crystals of enamel over a long period of time leading to deeper penetration of Fluoride & formation of Fluorapatite
2Ca3(Po4) 3 OH + CaF2________2Ca5(PO4) 3 + Ca (OH) 2 … 2
A part of CaF2 so formed in low concentration further reacts with crystals of hydroxy apatite & form Fluoro apatite.
Fluoride varnish may offer an effective means of arresting early enamel lesions in the primary dentition. While detecting & monitoring these lesions in the study, the fluoride varnish applications may offer an effective non-surgical approach to the treatment of decay in children. 16
Fluoride dentifrices have been proven to be effective anticaries agents in over hundreds of clinical trials ever since 1955, when they were introduced for sale over-the-counter.
The most commonly evaluated fluoride dentifrices are ionic NaF and SnF, and more recently the covalent NaMFP and organic amine fluoride.
Sodium Fluoride Dentifrice
Stannous Fluoride Dentifrice
Amine Fluoride Dentifrice
Monofluorophosphate Dentifrice
There are two possible mode of action regarding caries inhibiting mechanism of monofluorophosphate (MFP). As per the first mode, it is essentially a fluoride effect (Erricsson, 1963, Gron et al 1971), but there appears to be a controversy, regarding the mechanisms of fluoride release.
Gron et al (1971) postulates that F- ion is released at the solution crystal interfere by means of hydrolysis.
PO3F2- + H2O -> H2PO4- + F- and this F- reacts with hydroxyapatite to form fluorapatite.
Below 4 years____Fluoride tooth paste not recommended
4-6 yrs_____Brushing once daily with fluoride toothpaste and 2 times without a paste
6-10 yrs____Brushing twice daily with Fluoride toothpaste and once without paste
Above 10 years___Brushing 3 times daily with fluoride toothpaste
Tooth Bound Fluoride
The cariostatic effect of ‘ambient fluoride ’ the fluoride present in plaque, saliva and other oral fluids have been well established.by Margolis, et al, (1986).
Unlike Ambient Fluoride which functions primarily through plaque, for the tooth bound Fluoride to effect its caries inhibition, it must be incorporated into those areas of teeth (fissures, a proximal surfaces etc) where caries occur.
The effectiveness of topical fluoride treatments may be significantly increased by
Fluoride Mouthrinses:
0.05% NaF mouthrinse
APF mouthrinse contains NaF in phosphate buffer at pH 4.
Practical applicability
Method of preparation
Home: dissolve 200 mg NaF tablet in 5 teaspoons of water. This provides 0.04% NaF. Monthly expenditure Rs.1.50 only
School: Dissolve 2 mg NaF powder in1000 ml of water to make 0.2% solution.
5-10 ml is used fortnightly.
In communities with fluoridated water supply 0.025% NaF mouthrinse is recommended fortnightly.
The individual's risk factor and the reason for treatment will determine which method of flouride delivery is used.
The indications for fluoride therapy are as follows:
Dental caries remains a major public health problem in most countries, affecting 60–90% of school children and the vast majority of adults, states a WHO report. The principal reasons for this increase are growing sugar consumption and inadequate exposure to fluorides.
A WHO expert committee report on fluorides and oral health published in 1994 is currently being updated. This commentary will seek, in the meantime, to provide an interim perspective on dental caries and dental fluorosis, diet and fluorides from a public health point of view.
The WHO oral health report noted that dental caries can be controlled by the joint action of communities, professionals and individuals aimed at reducing the impact of sugar consumption and emphasizing the beneficial impact of fluorides. In many developing countries however, access to oral health services is limited. Likewise, in developed countries significant numbers of population groups are underserved. For these reasons professionally applied fluorides were not considered relevant to this review.
Research on the oral health effects of fluoride started around 100 years ago. For the first 50 years or so it focused on the link between waterborne fluoride – both natural and artificial – and dental caries and fluorosis. In the second half of the 20th century this focus shifted to the development and evaluation of fluoride toothpastes and rinses and, to a lesser extent, alternatives to water fluoridation such as salt and milk fluoridation. Most recently, efforts have been made to summarize these extensive datasets through systematic reviews, such as those conducted on water fluoridation by the UK University of York Centre for Reviews and Dissemination on fluoride ingestion and bone fractures; and on fluoride toothpastes and rinses through the Cochrane Collaboration Oral Health Group.
These systematic reviews concluded that:
A recent WHO/FAO analysis of the evidence on the role of diet in chronic disease recommends that free (added) sugars should remain below 10% of energy intake and the consumption of foods/drinks containing free sugars should be limited to a maximum of four times per day. For countries with high consumption levels it is recommended that national health authorities and decision makers formulate country-specific and community-specific goals for reduction of consumption of free sugars. However, WHO also notes that many countries currently undergoing nutrition transition do not have adequate fluoride exposure. It is the responsibility of national health authorities to ensure implementation of feasible fluoride programmes.
First, it is clear that all countries and communities should advocate a diet low in sugars in accordance with the WHO/FAO recommendations. This has been emphasized most recently in May 2004 at the World Health Assembly by the confirmation of the WHO Global Strategy on Diet, Physical Activity and Health.
Secondly, countries with excessive levels of fluoride ingestion, particularly where there is a risk of severe dental fluorosis or of skeletal fluorosis, should maintain a maximum fluoride level of 1.5 mg/l as recommended by WHO Water Quality Guidelines, although this objective is admittedly not always technically easy to achieve.
Thirdly, where sugar consumption is high or increasing, the caries preventive effects of fluorides need to be enhanced. WHO recommends that every effort must be made to develop affordable fluoride toothpastes for use in developing countries. As a public health measure, it would be in the interest of countries to exempt these toothpastes from the duties and taxation imposed on cosmetics.
Water fluoridation, where technically feasible and culturally acceptable, has substantial advantages particularly for subgroups at high risk of caries. Alternatively, fluoridated salt, which retains consumer choice, can also be recommended. WHO is currently in the process of developing guidelines for milk fluoridation programs, based on experiences from community trials carried out in both developed and developing countries.
Finally it is essential to maintain and foster health services research, most importantly to:
Such a programme of health services research will help to maintain and develop the outstanding progress made over the past half century in emphasizing the beneficial effects of fluorides.
Use of fluoride complexers.
Use of fluoride containing polyelectrolytes.
Role of surface-active agents on fluoride- enamel interactions.
Self gelling liquid fluoride.
Additive protective effects of combination of fluoride and chlorhexidine.
Heifetz et al, 1983 and Horowitz, 1980 ® ???sustained release of fluoride from an intra oral device could be an effective approach.
Such an intra oral delivery system has now been developed (INTRA ORAL FLUORIDE RELEASING DEVICE; Cowsar et al„ 1976; Mirth et al„ 1980) to release fluoride at a predetermined rate when placed in an oral aqueous environment. It consists of a central depot of sodium fluoride intimately mixed with a plastic copolymer and surrounded by a rate controlling membrane. Fluoride diffuses out at a rate that is controlled by the thickness of the membrane and exposed area of the device. Short- term studies in humans revealed that individuals wearing this fluoride-releasing device had significantly elevated levels of fluoride in plaque and saliva (Adderly et al, 1981; Mirth, 1982).
In a subsequent caries trial in rats, with a fluoride releasing device rich released 0.15 mgF per day. Mirth et al„ (1983) reported that the incidences of total carious enamel surfaces were significantly reduced by 63 per cent over the untreated or placebo treated controls. The reductions achieved were 45 per cent on the sulcal and 75 to 77 percent on the smooth surfaces. In another group of rats that were given 10 ppm of fluoride in drinking water the caries reduction achieved was 25 per cent of the total carious enamel surfaces and 44% on the smooth surfaces over the untreated controls. This reduction achieved was significantly less as compared to those with fluoride releasing device.
An alternate approach to enhance the ability of enamel to retain fluoride was initially studied by McCann et al, (1969) who while analyzing enamel fluoride using ion specific electrode found that Aluminium ion caused major interference in the analysis suggesting the existence of Fluoride — Aluminium complexes in enamel and a directly proportionate concentration of the two. He hypothesized that it may be possible to retain fluoride in enamel to a greater concentration if Aluminium salt in solution is applied before fluoride or in conjunction with it, which was later confirmed. It was found that the fluoride was capable of forming strong fluoride complexes with any polyvalent metal while its retention in enamel was subjected to the metal being able to simultaneously bind to the apatite crystals.
The metals, which could perform both the functions simultaneously, were Aluminium and Titanium. Treatment of enamel for 1 min. with 0.5M aluminium nitrate, then 3 min. with APF solution and washed extensively retained 1800 ppm of fluoride in the outer 25 pm enamel layer as compared to 800 ppm fluoride with APF applications only. The mechanism by which fluoride deposition is enhanced is probably related to formation of fluoride-AI-Po4 complexes.
Another promising cation was found to be Titanium used in the form of 1 % Titanium tetrafluoride (TiF4) which in vitro to reduced enamel solubility (Shrestha et al, 1972) and produced significant uptake of fluoride in enamel (Wei et al, 1976). Further interest in this compound was spurred by the results of a clinical trial by Reed and Bibby (1976) in which 50 % caries reduction in DMFS was observed with 1% TiF4 applications as compared to 33% caries reduction with APF when both were compared to untreated controls.
Bartels et al, 1982 ® studied the enamel fluoride uptake at various depths from fluoride containing polyelectrolytes i.e. poly-(4-vinyl pyridine) using an acid etch technique. It was observed that there was a considerable deposition of 45000 ppm of fluoride 'on' and 'just below' the anatomical tooth surface which had a pronounced effect on acid solubility as compared to Acidulated phosphate fluoride solutions.
It has been postulated that these poly electrolytes (high molecular weight fluorides) are superior as compared to low molecular wt. fluorides viz. NaF, APF, SnF4 etc. due to the following reasons:
In an aqueous solution these polyelectrolyte fluoride ions have a low activity coefficient due to localised numerous positive charges within the polyelectrolyte sphere. Therefore initial adsorption of the macromolecules on the enamel surface is accompanied simultaneously by the adsorption of fluoride counter ions, which can be released from the polymer by phosphate exchange reactions.
Polyelectrolytes have an open randomly coiled confirmation and generally retain this diffuse character upon adsorption. This results in relative thick layer at the enamel interface and prevents the enamel from being expose the surrounding environment (Morrissey, 1977).
In addition polyamine fluorides are known to affect essential surface properties of hydroxyapatite/enamel e.g. as surface charge and wettability (Cartels et al., 1981).
Another area of current interest in the field of fluoride is prolonging the time of fluoride- enamel interactions in the process of topical applications leading to a high rate of penetration of fluoride into the body of enamel resulting in formation of a relatively more permanently bound form of fluoride (FAP). For this purpose a battery of Surface Active Agents (SAA) which can affect the wettability i.e. lowering the Surface tension of F-solution leading to its increased spread and penetration in the tooth surface, have been tested. (Caslavaska and Gron in 1981-83)
Thus these invitro investigations suggest that the SAAs do have a role to play in increasing the formation of firmly bound fluoride (fluorapatite), hence enhancing the clinical efficacy of enamel fluoride treatment.
Various investigators recently have focused their attention to prepare fluoride formulations which when applied as a solution initially can gel on the tooth surface, such a system might afford the advantage of being able to reduce the amount of fluoride used per treatment without sacrificing the efficacy of the fluoride agent. Caslavaska and Gron (1984) carried out research in this aspect and developed a system containing tetraethoxysilane (TES), Water, Surfactants and electrolytes for the purpose. This in vitro study suggested that TES can be used in combination with fluoride solutions and the total process of hydrolysis and gelation may be achieved in a period of a few minutes. Fluoride in a concentration of 0.2M (0.4%) to 1.0 M (1.9%) greatly facilitated the process. The system seems to have potential for eventual in-vivo application.
Have the potential to inhibit carbohydrate metabolism at several different sites including the PTS and PMF driven uptake of sugars and would, therefore, be expected to have additive inhibitory effect when used together. McDermid, Ann S et al. (1985) studied the effect of 0.07 and 0.15m M Chlorhexidine and 4.0 and 8.0m M Potassium fluoride individually and in combination, on acid production by Streptococcus mutans and Streptococcus sanguis.
Chlorhexidine was found to have a greater inhibitory action on Streptococcus mutans while Streptococcuss sanguis were more sensitive to Potassium Fluoride. Combinations of Fluoride and Chlorhexidine showed significant additive inhibitory effects on acid production, irrespective of the method of measurement.
Fluoride is a toxic substance and its acute ingestion in large quantities may be followed by rapidly developing signs and symptoms, which may result in death. Even when it is ingested in relatively small amounts during the period of tooth development, it changes in the quality and appearance of the enamel known as dental fluorosis. If larger amounts are ingested over years, changes in the quality and quantity of the skeleton may occur. The skeletal changes, however, may become severe enough to be classified as crippling skeletal fluorosis.
There are several variables that can affect the outcome of acute fluoride poisoning, but the exact fatal dose is uncertain. In cases of human poisonings, the exact lethal doses involved according to Dreisbach is 6-9 mg F /kg while the data of Lidbeck suggests that this is over 100 mg F /kg. The most frequently cited range for the lethal dose of sodium fluoride was offered by Hodge & Smith, who after reviewing case reports, concluded that 5-10 g of sodium fluoride would certainly be fatal for a person with a body weight of 70 kg. Because sodium fluoride is 45.2% fluoride by weight, the dose range for adults would be 32-64 mg F /kg. It should be noted that this range is equivalent to an LD lOO, i.e. any 70 kg adult who ingested that much fluoride would be expected to die. This is important information but values such as the LD lO, the LD 50 or the upper limit for the certainly safe dose would be of more utility from the public health and clinical perspectives.
Acute poisoning refers to rapid intake of an excess dose over a short time.
Certainly Lethal Dose (CLD):
Adults= 5-10 g NaF taken at one time or
= 32.4 mgF/Kg body weight
Children= 2.5 g of NaF
Saftely Tolerated Dose(1/4 CLD)
Adult=1.25 - 2.5 g NaF or
= 8 - 17 mg F/ Kg body weight
It is a powerful metabolic inhibitor. Death is thought to occur from blockage of cation dependent enzymes or transport system.
The compounds of fluoride differ widely with respect to fluoride bioavailability (absorbability) and, therefore, in their acute toxic potentials. The differences in toxic potential are related to the solubilities of the compounds and they are apparent even when they are given parenterally. In some cases, the cation of the compound may also exert a toxic effect. Thus, stannous fluoride is slightly more toxic than sodium fluoride apparently because high doses of the tin ion adversely affect the kidneys and other organs. A variety of other factors may also influence the toxicity of fluoride compounds, i.e. route of administration, age, rate of absorption and acid-base status.
After the ingestion of large amounts of fluoride, a toxic episode often develops with alarming rapidity.
In nearly all cases of fluoride poisoning, the victims experience nausea, vomiting and abdominal pain within minutes after ingestion. There may or may not be a variety of non- specific symptoms such as
As the episode progresses, a generalized weakness, carpopedal spasms or spasm of the extremities and tetany often develop. These myopathologic signs accompany declining plasma calcium concentrations, which may fall to extraordinarily low values (<5 mg%), and rising plasma potassium levels, which indicate a generalized toxic effect on cell membrane function.
Extreme disorientation or coma usually precedes death, which may occur within the first few hours after the fluoride exposure. Acute poisoning begins within 30 minutes of ingestion
The effects on various systems are as follows:
1) Gastro Intestinal Tract
Fluoride in the stomach is acted by hydrochloric acid to form hydrofluoric acid that is irritable to the stomach lining causing,
-Nausea, vomitting and diarrhoea
-Abdominal pain
-Increases salivation and thirst
2) Central Nervous System
-Hyperreflexia, convulsions and parasthesia
3) Cardiovascular System:
-Cardiac Failure
4) Respiratory System:
- Respiratory Paralysis
The immediate treatment should be aimed at reducing the amount of fluoride available for absorption from the gastrointestinal tract. Thus, vomiting should be induced by administering an emetic, such as ipecac, followed by the oral administration of 1% calcium chloride or calcium gluconate. If the calcium containing solutions are not available, then as much milk as can be ingested should be given.
The hospital emergency department should be informed that a case of fluoride poisoning is in progress while these procedures are being carried out. The patient should be transported to the hospital at the earliest possible time. Vomiting should not be induced if the victim has no gag reflex or while unconscious or convulsing because of the danger of aspiration. In these cases, a cuffed endotracheal tube should be inserted followed by gastric lavage with a solution containing calcium or activated charcoal.
In the hospital, the medical treatment will depend on the severity of the signs and symptoms. If vomiting has not occurred already, then it should be induced. If the patient is symptomatic, immediate attention should be given to establishing a patent airway, an intravenous line and to monitoring and maintaining the cardiovascular circulation. If gastric lavage has not been performed, it should be done as described above.
Chronic poisoning refers to long-term ingestion of fluoride in amounts that exceed the approved therapeutic levels. Continued ingestion of high doses of naturally occuring fluoride will be reflected in changes in the teeth. Flurosis of enamel is caused by defective matrix formation (hypoplasia) probably due to direct effect of fluoride on ameloblast metabolism. Lesion is usually confined to outer third of the enamel giving opaque white flecks appearance in mild fluorosis.
At the present time, the most common sources of fluoride intake are fluoridated drinking water or salt (e.g. in Switzerland and Hungary) and dental products. More rarely, fluoride exposure may come from fluorinated drugs such as certain steroids or analgesics, the fluorinated volatile anesthetics such as halothane, industrial exposure such as in phosphate fertilizer factories or aluminum processing plants, or the atmosphere downwind from such factories. There is no possibility of serious acute toxicity from the ingestion of drinking water or salt with controlled fluoride levels (ca. 1 mg/L and 300 mg/kg, respectively).
Due to inadvertent swallowing during and after the use of fluoride-containing rinses or dentifrices, or after the application of 1.23% APF gels, the cells of the gastric mucosa may be exposed to very high fluoride concentrations. It is not surprising that some patients occasionally complain of nausea and vomiting after APF gel treatments.
It is for these reasons that with products designed for topical application of the fluoride ion to the teeth, the systemic exposure to fluoride should be minimized. In the case of 1.23% APF gels, the following application technique should be used:
An important undesirable side effect associated with excessive fluoride intake is dental fluorosis. Several studies have identified the sources of the additional fluoride intake and have attempted to determine their relative importance. There are several possible ways to reduce the intake of non- dietary fluoride by young children. These include:
Clinical picture of endemic fluorosis:
1) Dental Fluorosis:
Diagnosis:
2) Skeletal Fluorosis:
Tests for Skeletal Fluorosis:
UNICEF's Clinical Test
Fluoride and health problems: Non- skeletal flurosis:
Excessive fluoride leads to flurosis of the microvilli present on the gastro-intestinal tract. Ultimately it leads to loss of micro-villi from the gastro-intestinal mucosa. Loss of micro-villi leads to non-absorption of nutrients resulting in anemia.
| FLUORIDE IN DRINKING WATER | EFFECTS | |
|---|---|---|
| 0.7 – 1.2 ppm | DEPENDING UPON THE TEMP OF THE AREA |
PREVENTS CARIES NO DENTAL / SKELETAL FLUOROSIS |
| 1.5 – 3 ppm | CONSUMED OVER A PERIOD OF 5-10 YRS. | MILD DENTAL FLUOROSIS |
| 4-8 ppm | CONSUMED OVER A PERIOD OF 15-20 YRS. |
SEVERE DENTAL FLUOROSIS MILD SKELETAL FLUOROSIS |
| 8 ppm OR MORE | CONSUMED OVER A PERIOD OF 15-20 YRS. |
SEVERE DENTAL FLUOROSIS SEVERE SKELETAL FLUOROSIS |
World Health Organization in 1963 has recommended a range of 0.7-1 .2 ppm F in drinking water as optimum limit for the prevention of dental caries. Dental fluorosis occurs in human beings consuming water containing 2.0 mg/litre or more of fluoride particularly during first eight years of life and skeletal fluorosis can result if the water contains F- above 4.0 ppm and is consumed regularly over a long period of time. Due to these reasons the drinking water in high F areas should be defluoridated to optimum levels before use.
Several methods have been suggested from time to time for defluoridation. These may be divided into two basic types –
In the first method the materials reported to have been used in the contact beds include processed bone, natural or synthetic tricalcium phosphate, hydroxyapatite, magnesia, activated alumina, activated carbons and ion exchangers.
Chemical treatment methods include the use of lime either alone or with magnesium salts; aluminium salts either alone or in combination with a coagulant aid. All these methods suffer from one or more of the drawbacks viz. high cost, lack of selectivity for fluorides, separation problem, complicated or expensive regeneration, etc.
Polystyrene anion exchange resins in general and strongly basic quarternary ammonium type resins in particular are known to remove fluorides from water along with other anions. It was found that these resins provide 20- 145 bed volume of deflouridated water per cycle but loose their fluoride removal capacity on prolonged use and a total replacement becomes necessary. The anion exchange resin treatment besides being costly, imparts an unacceptable taste to the treated water.
T.S. Bhakuni studied the defluoridating capacity of cation exchange resins viz. saw dust carbon, defluoron I, carbion etc. and reported that the defluoridating capacity of carbon gets reduced during Ist 18 cycles to remain constant at 160 mg F/l afterwards. The material had the problem of excessive attritional losses and appreciable head loss.
Defluoron -I, a sulphonated saw dust impregnated with 2% alum solution was developed by Bhakuni (1964, 1970). It was prepared by treating 20-40 mesh saw dust with sulphuric acid, washing the excess acid, soaking the sulphonated product in alum solution for 2 hours and finally washing it to remove excess alum. This medium was studied in great detail in the laboratory. A domestic defluoridator was also prepared with this medium for use by individuals. The medium was not tested on pilot plant scale, but experience of authors indicate that the medium had poor hydraulic properties and suffered from heavy attritional losses. F removal costs on the basis of laboratory studies were found to be Rs. 0. 60/m3 of water containing 4.3 mg/litre fluorides.
Carbion It is a cation exchange resin of good durability and can be used both on sodium and hydrogen cycles. It has a bulk density of 680 g/litre. Laboratory experiments using 50 ml aliquotos of 4.3 mg F /litre test water and regeneration using 200 ml of I % alum solution indicated all average fluoride removal capacity of 320 mg F/litre or 470 mg F/kg carbion.
Investigations were conducted by Thergaonkar to study usefulness of magnesia in fluoride removal.
A typical ground water containing 10 mg/litre fluorides, 500 mg/litre alkalinity and 7.6 pH was treated with magnesium oxide. The treated water showed pH above 9 and an average F concentration of 5.8 mgF/l. a dose of 1500 mg/litre magnesia and a contact period of 3 hours was required to reduce the F content of water to 1 mg/litre.
The study established that magnesia removed the excess fluorides but pH of treated water was beyond 10 and its correction by acidification or recarbonation was necessary. The acid requirement can be to an extent of 300 mg/litre as CaCo2.
The high initial cost of magnesia, large concentration required, complexity of preparation, alkaline pH of treated water are some of the salient inhibitive factors to render it acceptable in the field.
To overcome the problems faced with earlier methods, deflouron-2 was developed in 1968. Extensive trials with medium both in the laboratory and field showed that most of the problems encountered earlier could be overcome.
Defluoron-2 is a sulphonated coal and works on the aluminium cycles. It was found to give the best results with one bed vol of 4% (W/v) alum solution as regenerant. Life of medium was found to be 2-4 years.
To study the effect of prolonged use of this medium on fluoride removal capacity, work was carried out to an aggregate of 55 cycles of continuous operation of 100mm diameter and column charged with a total of litres of medium. Test water containing 5-6 mg F/litre and 140-168 mg/litre alkalinity was used throughout. The average fluoride removal capacity of medium was 484 mg F/litre of defluoron-2.
Two plants with a capacity to treat 91 m3 (20,000 gal) per regeration were installed at Municipal Corporation, Nalgonda and CTI, Hyderabad.
The plant included a pressure shell, regeneration tank and a storage reservoir of 4-6 hours capacity. The process in its simplest form consists of passing water through a bed of defluoron- 2 medium contained in a cylindrical steel shell to which are attached necessary pipe work and control valves.
Although defluron-2 was successful in removing fluorides; the regeneration and maintenance of plant required skilled operation which may not be readily available. In order to overcome this problem a method has been evolved, which is so simple and adaptable that even illiterate persons can make use of it. The cost of defluoridation has also been brought down considerably.
The new method named 'Nalgonda Technique' involves the addition of two readily available chemicals. The process comprises addition in sequence of sodium aluminate or lime, bleaching powder alld filter alum to the fluoride water followed by flocculation, sedimentation and filtration. Sodium aluminate or lime hastens settlement of precipitate and bleaching powder ensures disinfection. Lime is cheaper over aluminate and is preferred since its dose is only 1/20- 1/25th that of filter alum. The fluorides are reduced to about 1 mg and alkalinity of raw water does not become limiting. The technique can be used both for domestic as well as for community water supplies.
Any container of 20-50 lit capacity is suitable for this purpose. A tap 3-5 cm above the bottom of the container is useful to withdraw treated water but is not essential. Adequate amount of lime water and bleaching powder are sprinkled into water first and mixed well with it. Alum solution is then poured and the water is stirred for 10 mins. In a large size bucket of approx. 50 litres containing water with 8 mg F/litre and 5- 10 mg/litre alkalinity approx. 1 mg/litre of alum is added in 50 litres of bucket full of water. The contents are settled for 1 hour and the clear water is withdrawn either through the tap or decanted slowly without disturbing the sediment. The fluoride concentration in the settled water would be within the permissible limits. With domestic treatment, there is no capital investment and the cost of treatment is only that of the cost of chemicals.
For communities with a population ranging from 200 to 2000, a defluoridation plant of fill and draw type is recommended. The plant consist of a hopper- bottom cylindrical tank with a depth of 2 m. the diameter depends upon the quantity of water to be treated. It has a stirring mechanism which can be either hand operated or power driven.
Raw water is pumped to the unit and required quantity of bleaching powder, lime and alum are added.
The contents are stirred for 10 minutes and allowed to settle for 1-2 hour. The settled sludge is discarded and defluoridated supernatant is supplied through stand posts. The notable features of this process are:
A comprehensive plan for the defluoridation in areas of endemic fluorosis should be investigated and developed. Although several areas are known to be affected by endemic fluorosis, defluoridation has not received due attention. This was primarily due to non- availability of suitable defluoridation techniques, necessity to handle acids and alkalies for regeneration and high costs of operation. Now that a comparatively cheap process is available, most of the aforesaid constraints are greatly overcome and a beginning can be made to solve the fluorosis problem.
A few pre-requisites for preparation of comprehensive plan for defluoridation are:
(a) Consolidated information on fluoride levels in under- ground waters and incidence of fluorosis.
(b) Detailed maps showing levels of fluoride at village, district, state and National level for delineating the problem.
(c) State Governments should make it mandatory for the district administration authorities to take up the issue of defluoridation.
(d) A follow up action to study the benefits of defluoridation.
