Elsevier

Journal of Dentistry

Volume 33, Issue 3, March 2005, Pages 187-191
Journal of Dentistry

Caries and fluoride processes

https://doi.org/10.1016/j.jdent.2004.10.004Get rights and content

Summary

Objectives

The purpose of the work was to establish the level and source of salivary fluoride, whether it could interact with tooth mineral and whether it was able to effect calcium re-acquisition and remineralisation.

Methods

Fluoride in saliva and in solution was measured by electrode, calcium by complexometric titration and phosphate colourimetrically—to measure salivary fluoride, its uptake by mineral and the effects of such low levels on calcium and phosphate levels in solution in contact with suspensions of mineral hydroxyapatite.

Results

Fluoride levels in saliva were low but could interact with hydroxyapatite. Such levels caused apatite crystallite growth and preferential acquisition of calcium by calcium-deficient apatite.

Conclusions

Salivary fluoride contents rose with increasing water fluoride levels. It was acquired by hydroxyapatite mineral. Topical fluoride was stored on oral tissues. Even these low fluoride contents could cause mineral crystallite growth with preferential calcium uptake. On a mineral area basis these effects were caused by quite low fluoride uptakes. These findings do not support reliance upon large fluoride uptakes by tooth enamel as evidence for commensurate caries reductions.

Introduction

Prior to the careful studies of Miller1 there were many folk theories of the cause of dental caries and probably as many folk remedies. It was not until 19162 and 19293 that firm clues emerged of a possible route to protect populations against dental caries when the dental health of persons in areas of fluoride mottled teeth was assessed. No information as to the mechanisms of this protection was available until the findings by Volker4 that fluoride treatment reduced the acid solubility of enamel and dentine.

The connection was at once made between the desirability of reducing enamel solubility and protection against caries. This depended upon the belief that dental caries was a relatively simple dissolutive process without considering that other, more subtle processes were at work. Another phenomenon was the presentation of early enamel caries as the well-known ‘white-spot’ subsurface lesion.

A major advance was the ability to produce histologically-realistic enamel lesions in acidified gelatin gels. However, this chemically impure system was not able to identify those processes happening during early caries-like attack. The use of pure methyl cellulose gels5 resulted in the formation of white-spot lesions and revealed the preferential removal of calcium compared to phosphate, especially during the earliest stages of the attack6 also noted by ten Cate and Duijsters7, 8, 9 and by Featherstone et al.10 A possible fault in these observations was that part of the outward flux of calcium could be balanced by carbonate dissolution.11 However, the preferential removal of calcium was confirmed using a pure, already calcium-deficient hydroxyapatite.12

These findings gave an insight into chemical changes during early formation of lesions but did not elucidate the existence of the apparently-intact surface zone over the white-spot lesion. Thus, it remained until the elegant work by von Bartheld,13 using time-lapse polarised light micrography of the development of lesions in enamel slices in vitro. The slices were mounted, in contact with acidified gel, on microscope slides then photographed at intervals on cine film. The first changes appeared at the surface of the enamel where a translucent zone developed. This proceeded deeper into the specimen until, behind this advancing from, a negatively-birefringent surface zone appeared thus giving an apparently-intact surface zone over the white-spot.

This observation is consistent with later studies in vitro6 where the enamel surface was the first area of attack and measurements14, 15 of larger enamel crystallite dimensions in the surface layer compared with sound enamel, changes which could occur during crystallite accretion as this surface layer reformed. Thus, the apparently sound surface, regarded as a proof of probity of lesion structure, is reformed during the caries process, rather than being preserved throughout it.

So, we have a volume of mineral where calcium has been depleted with higher contents of acid phosphate groups.16 The resulting mineral falls within the compositions described by Berry17 where a whole range of apatites can exist where a lack of calcium ions is balanced in terms of charge by protonating the phosphate and hydroxyl groups. The lack of mutually-attractant ions in the lattice results in an expanded a-axis in enamel and apatite as the calcium deficiency increases.18 Such a less tightly bound lattice is less stable than a stoichiometric one.

The question now arises as to the action of fluoride, often at low levels in affecting clinical caries incidence. A number of experiments have shown that the fluoride ion, often at higher concentrations than those encountered, as with water fluoridation, can influence plaque behaviour. However, the avidity with which the ion is acquired by the mineral phase has been widely shown. Also, although Volker4 showed that this treatment reduced enamel solubility, high resident contents of fluoride in enamel did not correlate with reduced caries incidence.19, 20, 21 Further, high fluoride uptakes did not necessarily show such a correlation, either.21, 22, 23

Moreno et al.24 studied the solubility behaviour of hydroxyapatite at various levels of fluoride substitution. The maximum effect was obtained when only 50% of the hydroxyl groups had been replaced corresponding to the greatest lattice stability and reflecting a low lattice free energy (G). In those circumstances, there would be a reduced tendency for lattice ions to dissolve and, conversely a greater tendency for such ions to join or rejoin the lattice. This underlies the role of fluoride in observations of remineralisation.25

Consider the behaviour of the now calcium-deficient enamel crystallites in an area of recent acid attack. Ambient fluoride will be readily acquired by such crystallites, which will gain in stability. This only has to affect the outermost unit cells of the crystallites since, so far as the outside solution is concerned that is the physico-chemical nature of those crystallites. The next question which arises, is whether the now more stable crystallite unit cells will offer a thermodynamically more receptive location for the dissolved calcium ions to re-enter the vacancies created by the earlier acid attack. This effect should be in addition to the crystallite regrowth made evident in remineralisation.

This hypothesis was tested by Ingram and Nash26 using three calcium-deficient hydroxyapatites with Ca:P (M) ratios of 1:60, 1:60 and 1:61 but with different surface areas. It was found that, in the presence of 5, 2.5 or 1 ppm F, the Ca:P (M) ratios of mineral acquired by the apatites were well in excess of the 1.67 dictated by crystallite growth as in remineralisation. Thus, these findings were consistent with the physico-chemically based hypothesis.

The experimental values of 5, 2.5 and 1 ppm F seemed low and reasonable in 1980. However, techniques of fluoride measurement have advanced and interest has moved to levels of fluoride found in saliva. The present piece of work examined the concentrations of fluoride present in salivas from different areas, whether the fluoride was of systemic origin or was stored locally in the mouth. The answer was also sought as to whether such low levels were capable of interacting with apatite mineral in the presence of other salivary components. Although, the work of Ingram and Nash26 supported the hypothesis that 1 ppm F and upwards caused the preferential re-acquisition of calcium the current work extended this to test whether low salivary levels of fluoride could exert a similar action.

Section snippets

Materials and methods

Three synthetic hydroxyapatites, all calcium-deficient, were used in the work. These and their specific surface areas (ssa) were:

0 (old)Ca:P (M)=1.60ssa=18 m2/g
N (new)Ca:P (M)=1.60ssa=8 m2/g
76 (1976)Ca:P (M)=1.61ssa=26 m2/g

These were suspended at a solid:solution ration of 0.2 g in 200 ml in 0.04 M/l tris buffer in the presence of 0.035 M/l potassium chloride and equilibrated overnight at 25 and 37 °C. Baseline levels of dissolved calcium and phosphate were measured after Millipore filtration prior to

Results

Table 1 shows how the levels of F differed in salivas from districts with water fluoride concentrations of 0.026, 0.16 and 1.0 ppm.

Table 2 shows how a low surface area hydroxyapatite acquired this fluoride from saliva.

To establish whether the fluoride in saliva was locally or systemically derived Table 3 shows how, without a fluoride rinse, some 80% of the total salivary fluoride could be accounted for by analysis of parotid saliva. This dropped to a little over 40% 18 h after saliva F levels

Discussion

It has previously been shown that fluoride in drinking water raises the fluoride level in saliva.28, 29, 30, 31 The results in Table 1 show how over the range of fluoride concentrations up to those in fluoridated water areas there are discernible differences in salivary fluoride levels. This may be of no consequence if such levels do not interact with the mouth (with the tooth mineral). Despite the presence of other salivary components the low surface area hydroxyapatite acquired much of the

Conclusions

Salivary fluoride levels although low, become elevated in areas with increasing water fluoride contents. This fluoride is available to interact with hydroxyapatite mineral.

Further, although some salivary fluoride is systemic in origin and is secreted in parotiduct saliva, fluoride from topical treatment may be stored locally in the mouth and slowly eluted in the whole saliva.

Levels of fluoride typical of those in saliva cause growth of apatite crystallites and are thus capable of favourably

Acknowledgements

We wish to thank the Editor of the Oxford University Press for permission to reproduce data in Table 1, Table 2, Table 3 previously printed in ‘Clinical and Biological Aspects of Dentifrices’ edited by Embery and Rolla and published by the Oxford University Press, 1992.

References (31)

  • J.M. ten Cate et al.

    Demineralisation of enamel in the presence of fluoride

    Journal of Dental Research

    (1981)
  • J.M. ten Cate et al.

    Alternating de- and remineralisation of artificial enamel lesions

    Caries Research

    (1982)
  • J.M. ten Cate et al.

    Influence of fluoride in solution on tooth demineralisation

    Caries Research

    (1983)
  • J.D.B. Featherstone et al.

    Chemical and histological changes during development of artificial caries

    Caries Research

    (1985)
  • A.S. Hallsworth et al.

    Loss of carbonate during the first stages of enamel caries

    Caries Research

    (1973)
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