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Maximizing Fluoride¹s Potential

Fluoride therapy is integral to dental caries management, however, its usefulness may be underestimated.

Widespread fluoride use is primarily responsible for the decline in the prevalence and severity of dental caries in the United States during the past 50 years.1 In fact, the US Centers for Disease Control and Prevention (CDC) recently named community water fluoridation, initiated in 1945, as one of the 10 most important public health measures of the 20th century.2

Early studies reported a 50% to 60% reduction in the prevalence of dental caries within just a few years following fluoridation.3 Fluoride dentifrices were introduced in 1955 and quickly dominated the market. By the early 1990s, they accounted for more than 90% of all toothpaste sold in the United States and Canada.4 Research reports a 20% to 45% reduction in caries experience that is attributable to fluoride dentifrice use.4-6 Although the benefits of fluoride are well-documented, recent studies suggest that dentists and dental hygienists alike may underestimate its effectiveness and, thus, underuse it as a preventive therapy.7-8

Mechanisms of Action

For many years, researchers believed the primary benefit of fluoride was gained by systemic exposure prior to tooth eruption. Fluoride ingested during pre-eruptive tooth development was thought to incorporate into the enamel, replacing hydroxyl groups in hydroxyapatite, to form fluorapatite. Compared to hydroxyapatite, fluorapatite is less soluble in acid in vitro. Therefore, increased fluorapatite content within the enamel crystalline structure was thought to convey increased resistance to caries formation with maximum benefit occurring when children drank fluoridated water from birth.6,9 However, even early studies showed that older children and adults also benefited from fluoridated water, suggesting a substantial posteruptive effect9 and later studies confirmed that fluoride’s benefits are derived predominantly through topical exposure following tooth eruption.6

Fluoride acts posteruptively through a combination of mechanisms to increase caries resistance. First, fluoride inhibits bacterial metabolism. Fluoride accumulates in dental plaque and when the plaque pH drops, eg, when the bacteria produce acids, it diffuses into the bacterial cell to disrupt cellular functions such as sugar transport and glycolysis. Fluoride also inhibits the ability of mutans streptococci to produce extracellular polysaccharide, which is necessary for plaque adherence to smooth enamel surfaces.10 These antibacterial effects appear to be enhanced at low pH, thus providing additional host protection during acidic challenges.11

Second, and more importantly, fluoride inhibits the demineralization of tooth structure. Silverstone identified the caries process as one of repeated cycles of demineralization and remineralization.12 A condition of health, ie, no net mineral loss from the tooth and, therefore, no clinical expression of dental caries, is maintained when the processes of demineralization and remineralization remain in equilibrium. Fluoride ingested during pre-eruptive tooth development is distributed fairly evenly, but at low levels (20 – 1000 ppm), throughout the forming enamel. Unfortunately, these levels do not significantly increase caries resistance. In contrast, frequent posteruptive exposure to low levels of fluoride, like that which occurs with the regular use of fluoridated water or fluoridated dentifrice, causes fluoride to adsorb, at much higher levels (~ 30,000 ppm) preferentially onto the outer surfaces of enamel crystals. This concentration of fluoride at the outer surface greatly increases the crystal’s resistance to acid dissolution.13-14

Third, and most importantly, fluoride enhances the remineralization of tooth structure. Fluoride has an affinity for porous or slightly demineralized enamel. Therefore, when mineral begins to dissolve during the caries process, fluoride adsorbs to the affected enamel crystals and attracts calcium and phosphate ions, accelerating the formation of new crystal surfaces. In addition, due to their increased fluoride content, these remineralized crystals are more resistant than sound, unremineralized enamel to subsequent acid challenges.13-15

Indications for Therapy

Fluoride therapies should be tailored to individual patient needs based on an assessment of caries risk status. In 1995, the American Dental Association (ADA) Council on Access, Prevention and Interprofessional Relations published guidelines for classification and treatment of low, moderate, and high caries risk patients based on caries history, fluoride exposure, diet, and other etiologic and behavioral factors.16 In 1999, the US Navy Dental Corps developed and implemented similar guidelines for use in the military public health environment (see Table 1).

Lack of fluoride exposure is considered a significant risk factor for future caries experience. The ADA recommends daily use of a fluoride dentifrice for all children and adults.16 However, parents must exercise caution, particularly with younger children, because children tend to swallow a substantial amount of dentifrice and ingestion of excess fluoride may result in fluorosis of the developing permanent teeth. The most critical period occurs during the development of the permanent incisors, between 15 and 30 months of age;17 the entire permanent dentition is at risk for fluorosis between 11 months and 7 years of age.18 Although the optimal level of daily fluoride intake has never been determined scientifically and is not known with certainty, daily ingestion in excess of 0.10 mg of fluoride (from all dietary and nondietary sources, including food and beverages, dentifrices, fluoride supplements, mouthrinses, and gels) per kilogram of body weight is generally accepted to cause dental fluorosis. A level of 0.05 – 0.07 mg per kilogram of body weight is often suggested as optimal. However, these are estimates only and daily intake of as little as 0.03 to 0.04 mg per kilogram of body weight has been associated with fluorosis.17,19

Based on these estimates, an upper limit of daily fluoride intake, ranging from 0.33 mg per day for 3-month-olds to 0.90 mg per day for 6-year-olds, has been suggested.20 A typical ribbon of dentifrice (covering the entire toothbrush head) weighs about 1 gram and contains approximately 1 mg of fluoride.18 Children 4 to 6 years of age may swallow up to 50% of the amount of dentifrice dispensed;19 younger children may swallow as much as 90%.17 Therefore, to reduce the risk of enamel fluorosis, young children should be supervised so that only a small, pea-sized quantity (covering no more than one fourth of the toothbrush head) is dispensed and inadvertent swallowing of the dentifrice is minimized.19

Patients who are caries-active and/or at increased caries risk require additional fluoride, as well as other preventive measures, such as diet modification, dental sealants, and antimicrobial therapy, to control the caries process. Both over-the-counter and prescription fluoride products are appropriate for these patients. Rinses, gels, foams, and varnishes are available in various compositions, most commonly sodium fluoride (NaF), stannous fluoride (SnF2), and acidulated phosphate fluoride (APF).1,6,21

Material Selection

The efficacy of topical fluoride agents depends primarily on the concentration of fluoride used, as well as the frequency and duration of application.22 In general, at equivalent fluoride concentrations, all topical fluoride compounds demonstrate very similar, if not equivalent, caries-preventive effects.6 Unfortunately, product labels often list compound concentrations, rather than actual fluoride concentrations. Therefore, to compare the strengths of two products, the concentration of fluoride in each compound must be estimated. This is a relatively simple calculation, based on molecular weights, using the following guidelines:

[sodium fluoride] ˜1/2 F (thus, 1.0% sodium fluoride contains approximately 0.50% F)

[stannous fluoride] ˜ 1/4 F (thus, 1.0% stannous fluoride contains approximately 0.25% F)

[sodium monofluorophosphate] ˜ 1/8 F (thus, 1.0% sodium monofluorophosphate contains approximately 0.125% F)

[acidulated phosphate fluoride] = [F] (thus, 1.0% acidulated phosphate fluoride contains exactly 1.0% F)

0.1% F = 1000 ppm F

Table 2 lists the concentrations of several commonly used topical fluoride agents.

All patients, regardless of caries risk status, benefit from frequent exposure to low doses of fluoride. This can be achieved by drinking water with an optimal fluoride content (1 ppm) and brushing twice daily with a dentifrice containing 1,000 to 1,100 ppm F. In placebo-controlled studies, brushing two or three times daily resulted in greater caries reductions than brushing once daily.20 Food and Drug Administration (FDA)/ADA-approved formulations include 0.243% sodium fluoride (NaF), 0.76% sodium monofluorophosphate (NaMFP), and 0.45% stannous fluoride (SnF2).1,21 For patients at low caries risk, this may be all that is needed to maintain an adequate balance between demineralization and remineralization.

Patients at moderate and high caries risk require more intensive therapies. In addition to daily use of an ADA-approved fluoride dentifrice, an appropriate regimen for moderate caries risk patients may include daily home use of a 0.05% neutral NaF rinse, along with semi-annual professional applications of 2.0% neutral NaF, 1.23% APF, or 5% NaF varnish. For high caries risk patients, providers may consider adding daily home use of a 1.1% neutral NaF brush-on gel/dentifrice or 1.1% neutral NaF gel in custom trays and increasing in-office applications of the above-mentioned agents to four times per year.22 In-office fluoride applications need not necessarily be accomplished at 3 month intervals. Evidence suggests that a series of multiple treatments over shorter intervals (three to four treatments over 4 to 6 weeks21 or three treatments over 1 week23) may provide equivalent anticaries benefit.

Combinations of fluoride therapies can be more beneficial than single therapies alone, although the effects of combined modalities may be only partially additive.1 A point of diminishing returns exists after which additional preventive therapy provides no further benefit to the patient.16 Therefore, it is important to remember that more fluoride is not always better. For those patients who fail to respond to multiple fluoride therapies, other etiologic factors that may be affecting the desired outcome must be explored.

Fluoride’s effects are derived predominantly from posteruptive topical, rather than pre-eruptive systemic exposure. Thus, patients of all ages benefit from fluoridated water, dentifrices, and other topical applications. Appropriate fluoride therapy is essential to the successful management of dental caries.


Disclaimer: The opinions expressed in this article are the private views of the author and should not be construed as reflecting official policies of the US Navy, Department of Defense, or US Government.


REFERENCES

  1. Recommendations for using fluoride to prevent and control dental caries in the United States. Centers for Disease Control and Prevention. MMWR Recomm Rep.2001;50(RR-14):1-42.
  2. Ten great public health achievements—United States, 1900-1999. MMWR Morb Mortal Wkly Rep.1999;48(12):241-243.
  3. Achievements in public health, 1900-1999: Fluoridation of drinking water to prevent dental caries. MMWR Morb Mortal Wkly Rep. 1999;48(41):933-940.
  4. Stamm JW. The value of dentifrices and mouthrinses in caries prevention. Int Dent J.1993;43(6 Suppl 1):517-527.
  5. Mellberg JR. Fluoride dentifrices: current status and prospects. Int Dent J.1991;41(1):9-16.
  6. Stookey GK. Caries prevention. J Dent Educ. 1998;62(10):803-811.
  7. Forrest JL, Horowitz AM, Shmuely Y. Caries preventive knowledge and practices among dental hygienists. J Dent Hyg. 2000;74(3):183-195.
  8. Bader JD, Shugars DA, Kennedy JE, Hayden WJ Jr, Baker S. A pilot study of risk-based prevention in private practice.J Am Dent Assoc. 2003;134:1195-1202.
  9. Beltran ED, Burt BA. The pre- and posteruptive effects of fluoride in the caries decline. J Pub Health Dent. 1988;48(4):233-240.
  10. HamiltonIR, BowdenGH. Effect of fluoride on oral microorganisms In: Ekstrand J, Fejerskov O, Silverstone LM, eds. Fluoride In Dentistry.Copenhagen,Denmark: Munksgaard; 1988:77-103.
  11. Marsh PD. Microbial ecology of dental plaque and its significance in health and disease. Adv Dent Res. 1994;8(2):263-271.
  12. Silverstone LM. Remineralization phenomena. Caries Res. 1977;11(Suppl 1):59-84.
  13. Featherstone JD. Prevention and reversal of dental caries: role of low level fluoride. Community Dent Oral Epidemiol. 1999;27(1):31-40.
  14. Featherstone JD. The science and practice of caries prevention. J Am Dent Assoc.2000;131(7):887-899.
  15. Koulourides T, Keller SE, Manson-Hing L, Lilly V. Enhancement of fluoride effectiveness by experimental cariogenic priming of human enamel. Caries Res. 1980;14(1):32-39.
  16. Caries diagnosis and risk assessment. A review of preventive strategies and management. J Am Dent Assoc. 1995;126(Suppl):1S-24S.
  17. Levy SM. An update on fluorides and fluorosis. J Can Dent Assoc. 2003;69(5):286-291.
  18. Stookey GK. Review of fluorosis risk of self-applied topical fluorides: dentifrices, mouthrinses and gels. Community Dent Oral Epidemiol. 1994;22(3):181-186.
  19. Levy SM, Kiritsy MC, Warren JJ. Sources of fluoride intake in children. J Public Health Dent. 1995;55(1):39-52.
  20. Levy SM. Review of fluoride exposures and ingestion. Community Dent Oral Epidemiol. 1994;22(3):173-180.
  21. Stookey GK. Current status of caries prevention. Compend Contin Educ Dent. 2000;21(10A):862-867.
  22. Newbrun E. Topical fluorides in caries prevention and management: a North American perspective. J Dent Educ. 2001;65(10):1078-1083.
  23. Anusavice KJ. Efficacy of nonsurgical management of the initial caries lesion. J Dent Educ.1997;61(11):895-905.

From Dimensions of Dental Hygiene. November / December 2003;1(7):26-28.

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