Fluoridation: Misrepresenting the “saliva theory”

I sometimes wonder if anti-fluoridation propagandists are trying to extend their “freedom of choice” argument to the scientific facts themselves. Perhaps this is how they justify to themselves their frequent cherry-picking and misrepresentation of research.

A current example is Fluoride Free NZ’s (FFNZ) misrepresentation of the mode of action of fluoride in protecting existing teeth in Saliva Theory Critique. Nothing new here – it’s a rehash of an older article of theirs which I critiqued 2 years ago in Fluoridation – topical confusion. But it still contains the same misinformation.

Selective quoting

Again FFNZ  misrepresents the advice of the Center For Disease Control (CDC) by selective quoting. Here is the relevant section of the document (CDC, 2001. Recommendations for Using Fluoride to Prevent and Control Dental Caries in the United States). The FFNZ article quoted only the 2 sentences in red!:

“Saliva is a major carrier of topical fluoride. The concentration of fluoride in ductal saliva, as it is secreted from salivary glands, is low — approximately 0.016 parts per million (ppm) in areas where drinking water is fluoridated and 0.006 ppm in nonfluoridated areas (27 ). This concentration of fluoride is not likely to affect cariogenic activity. However, drinking fluoridated water, brushing with fluoride toothpaste, or using other fluoride dental products can raise the concentration of fluoride in saliva present in the mouth 100-to 1,000-fold. The concentration returns to previous levels within 1–2 hours but, during this time, saliva serves as an important source of fluoride for concentration in plaque and for tooth remineralization (28 ).”

Their misrepresentation claims (in their words) “The CDC acknowledges that fluoridated water has no cariostatic effect” because of the low concentration of fluoride in secreted saliva. However, the full quote shows that the CDC advised that “saliva is a major carrier of topical fluoride” and that “drinking fluoridated water” is one way of increasing saliva fluoride concentration sufficiently so that “saliva serves as an important source of fluoride for concentration in plaque and for tooth remineralization.”

FFNZ purposely confuses the issue by ignoring the direct transfer of fluoride from water and food to saliva, dental plaque and biological tissue in the oral cavity. These act as reservoirs which can top-up the fluoride concentration at the tooth surface and help prevent demineralisation (responsible for tooth decay in acid conditions) and remineralisation.

“Topical” role of fluoride at tooth surface

This figure from the CDC document cited above provides a simple illustration of the way that fluoride, from fluoridated water, helps prevent tooth decay with existing teeth.

Even this shows that the mechanism is far from simple as the process is influenced by the concentration of phosphate and calcium in saliva, as well as fluoride. I would add that organic material, such as proteins, will also influence the mechanism. Then there is a process of transfer of fluoride, and other ions, to saliva from reservoirs like plaque, the tongue and other biological tissues which are known to store fluoride. For example, Vogel (2011) states:

“Current models for increasing the anti-caries effects of fluoride (F) agents emphasize the importance of maintaining a cariostatic concentration of F in oral fluids. The concentration of F in oral fluids is maintained by the release of this ion from bioavailable reservoirs on the teeth, oral mucosa and – most importantly, because of its association with the caries process – dental plaque.
Oral F reservoirs appear to be of two types: (1) mineral reservoirs, in particular calcium fluoride or phosphate contaminated ‘calcium-fluoride-like’ deposits; (2) biological reservoirs, in particular (with regard to dental plaque) F held to bacteria or bacterial fragments via calcium-fluoride bonds.”

Confusing the concentration issue

The FFNZ article attempts to confuse the issue again by citing 5 studies they claim “show that fluoridated water is too low in fluoride to provide any topical benefit.” But, of course, a more honest approach to the scientific literature is to consider all studies (not just the ones confirming one’s bias) and check relevant experimental details.

The studies they cite were not aimed at determining a minimum concentration for the surface reaction at the tooth surface. They were laboratory studies, using bovine dental material, usually not taking into account the role of other ions like calcium and phosphate. Several were studying fluoride/sucrose solutions.

In contrast, the review by Buzalaf (2011), “Mechanisms of Action of Fluoride for
Caries Control“  found:

“very low fluoride concentrations (sub- ppm range) in solution are already able to substantially inhibit acid dissolution of tooth minerals [23, 27].”

This was confirmed in the review of Ten Cate & Featherstone (1991). They cited studies showing inhibition of demineralisation at fluoride concentrations as low as 0.2 ppm and 0.025 ppm (Margolis et al., 1986). They also mention the higher fluoride concentrations required when ions like calcium and phosphate are omitted.

Demonstrated inhibition of demineralisation at such low fluoride concentration when the other relevant minerals are present does raise the possibility that fluoride in secreted saliva may still play a role, despite the view expressed in the CDC document cited above. However, let’s stress here, one does not have to take sides on that particular debate to recognise that the saliva fluoride concentration resulting from transfer from food and fluoridated water in the oral cavity is high enough to play a protective role against tooth decay. Bruun & Thylstrup (1984), who reported the low concentrations cited by the CDC, concluded that:

“direct contact of the oral cavity with F in the drinking water is the most likely source of the elevated whole saliva fluoride and that the increased availability of fluoride in the oral fluids has an important relationship to the reduced caries progression observed in fluoridated areas.”

So, again, the real world is not as simple as suggested by those who seek only to confirm their biases.

References

Bruun, C., & Thylstrup, A. (1984). Fluoride in Whole Saliva and Dental Caries Experience in Areas with High or Low Concentrations of Fluoride in the Drinking Water. Caries Research, 18(5), 450–456.

Buzalaf M.A.R., · Pessan J.P., · Honório H.M., & ten Cate J.M, (2011). Mechanisms of Action of Fluoride for Caries Control. In Buzalaf MAR (ed): Fluoride and the Oral Environment. Monogr Oral Sci. Basel, Karger, 2011, vol 22, pp 97–114

Center for Disease Control, 2001. Recommendations for Using Fluoride to Prevent and Control Dental Caries in the United States).

Margolis, H. C., Moreno, E. C., & Murphy, B. J. (1986). Effect of Low Levels of Fluoride in Solution on Enamel Demineralization in vitro. Journal of Dental Research, 65(1), 23–29.

Ten Cate, J. M.; Featherstone, J. D. B. (1991). Mechanistic Aspects of the Interactions Between Fluoride and Dental Enamel. Critical Reviews in Oral Biology and Medicine, 2(2), :283–296.

Vogel, G. L., (2011). Oral Fluoride Reservoirs and the Prevention of
Dental Caries. In Buzalaf MAR (ed): Fluoride and the Oral Environment.
Monogr Oral Sci. Basel, Karger, 2011, vol 22, pp 146–157

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