CARIES PREVENTION—FLUORIDE B.H. CLARKSON

Department of Pediatric Dentistry, School of Dental Medicine, University of Connecticut Health Center, Farmington, Connecticut 06030 Adv Dent Res 5:41-45, December, 1991

Abstract—A clear understanding of the mechanism of action of fluoride and its pharmacokinetics would ensure appropriate clinical use of fluoride and fluoride-containing modalities. Convincing evidence exists that fluoride has a major effect on the demineralization and remineralization of dental hard tissues, and that it interferes with the acid production from "cariogenic" bacteria. However, it has also been shown to be physiologically harmful if fluoride concentrations and/or exposure periods are inappropriate. In order to establish appropriate clinical concentrations and exposure periods for fluoride administration, this review is concentrated on the theme that fluoride controls but does not prevent caries. The review is organized along classical lines, with a discussion of the role of systemic vs. topical fluoride. Discussion of the systemic effects of fluoride includes ingestion through water fluoridation, fluoride supplements, topical fluoride applications, and dentifrices. The benefits and problems associated with the systemic route of fluoride administration are discussed with special reference to caries control and fluoride's mechanism of action and its toxic effect. The same discussions are focused on the role of the topical effects of fluoride, with particular emphasis placed upon: low vs. high fluoride concentrations; calcium fluoride vs. fluorhydroxyapatite; and fluoride distribution, in both the mouth and in the teeth.

Presented during "Prevention Revisited", a Symposium at Eastman Dental Center's 75th Anniversary Celebration, Rochester, NY, September 13-14, 1990

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ver the past two to three years, senior dental administrators, scientists, and professional dental organizations have been extolling the fact that 60% of children between the ages of five and 11 are caries-free. Such caries reductions are not peculiar to the USA, for even in the United Kingdom, where much of the population does not receive the benefit of fluoridated water, cares reduction is apparent. This is certainly something of which the dental profession can be proud, considering that, as late as the 1960' s, only 5% of such children would have been caries-free. The reason for the high proportion of caries-free children in this group has been attributed to fluoride. To ascribe this cariespreventive property to fluoride, rather than fluoride's ability to control the progression of the disease, is, however, misunderstanding its mechanism of action. The epidemiologist's definition of dental caries is based upon the cavitation of the tooth surface, or at least access through the outer surface of the tooth by a dental probe, and resistance upon its removal, which may be accompanied by stickiness at the base of the lesion (Radike, 1968). This definition does not take into account the presence of white spot lesions. Groeneveld et al. (1990) recently re-examined the Culemborg and Tiel fluoridation study data (a study that compared the prevalence of caries in two cities—one fluoridated and one non-fluoridated—in The Netherlands) and showed that if white spots were incorporated into both sets of prevalence data, then there was no difference in caries activity between the fluoridated town of Tiel and the non-fluoridated town of Culemborg. However, if the classic epidemiological diagnosis of caries was used, the fluoridated town of Tiel showed a 50% decline in caries activity compared with the non-fluoridated town of Culemborg. Thus, the re-interpretation of these data suggests that fluoride does not prevent the initiation of the disease but, in fact, controls its progression. Does this distinction between control and prevention really matter, or is it purely a pedantic argument? The consequences of the general public's inability to distinguish between control and prevention (eradication) of disease have been evident in other public health measures used to control disease. For example, public apathy toward vaccination programs has become widespread, perhaps because of the human syndrome of "out of sight, out of mind". However, the sudden and disastrous outbreaks of measles reinforce the fact that the disease was only controlled and not eradicated. Fluoride is not, of course, a vaccine, since fluoride interferes with the active, on-going disease process by controlling its progression, while a vaccine acts by preventing the establishment of the disease process in the host. It must also be remembered that public apathy toward vaccination occurs despite the lack of a vocal anti-vaccine lobby. On the other hand, anti-fluoride lobbyists are quite vocal and have long sought to remove fluoride from municipal water supplies; some have even advocated the removal of fluoride from dental

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CLARKSON

products. A recent fluoride toxicology study (reporting a link between high fluoride doses and osteosarcoma of the long bones of rats) and other studies (suggesting that enamel fluorosis may be increasing in certain population groups) have provided new support for the anti-fluoridation lobby. Thus, senior dental administrators, scientists, and dental professional organizations should make it clear to the public that fluoride controls the progression of caries rather than prevents its initiation. Therefore, there is a life-time need for fluoride to be continually available in the oral environment. Removal of fluoride from water supplies and/or dental products would ultimately result in overt cavitation of teeth occurring at the prevalence and severity observed years ago. Even within the confines of teaching and clinical practice, a clear understanding of the mechanism of action of fluoride and its pharmacokinetics would help ensure appropriate clinical use of fluoride and fluoride-containing modalities. Convincing evidence exists that fluoride has a major effect at low concentrations on the demineralization and remineralization kinetics of dental hard tissues and, at relatively high concentrations, on acid production of cariogenic bacteria. However, it has also been shown that fluoride can be physiologically harmful if fluoride concentrations and/or exposure periods are inappropriate. What is, therefore, the most effective way of using fluoride to control the caries process without precipitating any unnecessary physiologically harmful effects? There have been much research, empirical clinical observations, discussions, and even dogma in attempts to distinguish whether topical or systemic fluoride administration is the optimum route. The arguments used for the systemic administration of fluoride through water fluoridation or fluoride supplements are that this method works either by making the tooth resistant to the disease (a pre-emptive effect) or, as stated less often, by increasing the level of fluoride in the saliva. The Groeneveld et al (1990) paper quoted a 1987 study by Van Eck, which suggests "that when water fluoridation coincided with eruption, the caries reduction was half the greatest reduction; with respect to free smooth and occlusal surfaces the topical effect was calculated to be 70% and 27% of the highest reduction, respectively." Thus, the major systemic effect of fluoride appears to be on reducing fissure caries. Other studies, reviewed by Thylstrup (1990), have suggested that exposure to fluoride around the time of tooth eruption provided caries reduction equal to that achieved by people receiving fluoridated water in utero and from birth onward. Furthermore, fluoride levels in primary teeth from fluoridated areas are below those for permanent teeth from non-fluoridated areas, but caries reductions in primary teeth are at the 50% level, i.e., similar to that seen in permanent teeth from fluoridated districts. Another major systemic route of administration to children is via fluoride supplements. Thylstrup (1990) and Hargreaves (1990) summarized many of the reviews and clinical trial papers on the use of fluoride supplements, and concluded that such supplementation could be effective in reducing the overt signs (cavitation) of dental decay. It is again difficult to discriminate between pre-emptive and post-emptive effects, because many trials were not set up to do so. In fact, the controlled clinical

ADV DENT RES DECEMBER

1991

trials, reviewed by both Thylstmp (1990) and Hargreaves (1990), which were initiated to examine the effects of fluoride supplements from birth (and showed a caries reduction of 60% or more), continued fluoride supplementation using either chewable tablets or drops during the post-emptive period, thus combining a topical and a systemic effect. Systemic administration of fluoride mns the risk of causing untoward physiological events which may manifest themselves in the form of fluorosis. In studies summarized by Ekstrand and Whitford(1988)andEkstrand^ra/.(1990),itwas postulated that transient elevated blood fluoride levels, after the ingestion of fluoride tablets, may result in undue fluorosis. AngmarMansson et al. (1976) and Angmar-Mansson and Whitford (1982) demonstrated that peak fluoride levels of 10 |imol/L or more are needed to produce fluorosis in rats. These workers suggested that such levels would not be reached in man unless 5 to 10 mg of fluoride were taken each day. However, Spak and Ekstrand (1988) demonstrated that, in young adults, plasma fluoride peaks of >7 and

Caries prevention--fluoride.

A clear understanding of the mechanism of action of fluoride and its pharmacokinetics would ensure appropriate clinical use of fluoride and fluoride-c...
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