Printer Friendly

Fluoride and the caries lesion: interactions and mechanism of action.

Introduction

Dental caries is defined as the destruction of tooth tissues by acid that is generated as a by-product of bacterial metabolism in dental plaque biofilms. The most exposed and most readily colonised tissue is dental enamel and caries prone sites are those stagnation areas where plaque microflora can colonise the tooth surface in a protected environment. Dental enamel is the most vulnerable and therefore the most studied of tooth tissues with respect to dental caries.

Structure and Chemistry of Dental Enamel.

Enamel comprises about 95% of substituted hydroxyapatite crystals, arranged in bundles of enamel prisms 2-5 microns in diameter extending from dentine to the enamel surface. Junctions between prisms are characterised by poor crystal packing providing a pathway for entry and exit of material from enamel. The crystal chemistry of apatite has been well documented [Kay et al., 1964] and a representation is shown in Figures 1a, b, 2a, b. Crystals can incorporate a wide range of extraneous ions from the surrounding environment substituting for calcium, phosphate and hydroxyl groups (Figures 1b, 2b) [Elliott, 1985]. Extraneous ion incorporation can occur as crystals form during tooth development or by interaction with the surrounding environment after tooth formation. Such substitutions can play a dramatic role in changing the way in which crystals form and the behaviour of crystals towards, for example, acid. With regard to caries some of the most important of these ions are carbonate, magnesium and fluoride (F).

Carbonate and Magnesium. Carbonate will substitute for phosphate and when large concentrations are present, also for hydroxyl ions (Figure 1b) [Elliott et al., 1985] and magnesium will replace calcium to a limited extent (Figure 1b) [LeGeros, 1984]. Both are disruptive in terms of crystal structure leading to less stable and therefore more soluble crystals. It is also more difficult to grow crystals or produce new ones when significant amounts of carbonate and magnesium are present. With these ions, demineralisation could be facilitated and remineralisation could be more difficult results in a more stable crystal that is less soluble in acid. Figure 2a illustrates the location of the hydroxyl group in the apatite crystal with hydrogen bonding between adjacent hydroxyls. Figure 2b shows the effect of replacing a hydroxyl by an F ion. Stronger hydrogen bonds occur between F and the hydroxyl hydrogen such that the sense of the hydroxyl column is reversed. More recently atomic force microscopy (AFM) studies have shown that at a stage preceding demineralisation, F uptake renders it more difficult to protonate the enamel surface [Robinson et al., 2006]. As a result, and in contrast with carbonate and magnesium, F would make demineralisation more difficult but remineralisation would be favoured. This is essentially the basis for the effect of F on dental tissues in reducing dental caries.

[FIGURE 1A OMITTED]

[FIGURE 1B OMITTED]

[FIGURE 2A OMITTED]

[FIGURE 2B OMITTED]

There have been many investigations into the effect of F on dental caries reduction. Almost all of these studies have, however, used bench investigations of the effects of F on de- and remineralisation of enamel or enamel-like mineral, in situ studies where enamel is placed in the mouth, or the clinical effects of F on caries experience.

These approaches do not take into account the chemistry of the enamel itself or the chemical changes which occur within the lesion. Studies of the chemistry of enamel and that of natural lesions have, however, been carried out which cast light on caries mechanisms and the role of F not available from other studies [Robinson et al., 1995, Robinson et al., 2000].

In enamel F occurs at high concentrations of 1,000 ppm and upwards in the extreme outer surface of the tissue (200-400 microns) [Weatherell et al., 1972, 1973], the surface to which pellicle and plaque adhere. However, even with the use of F toothpastes this F is lost with age presumably due to normal wear (Figure 3) [Weatherell et al., 1973].

[FIGURE 3 OMITTED]

Surfaces which are protected e.g. between teeth, in fissures and at the cervical margin, do not lose F and in fact its content may even increase. Such F uptake cannot simply be regarded as uptake by sound enamel as at such stagnation sites plaque always accumulates. Thus, F uptake is almost certainly facilitated by plaque F, early acidification of enamel crystals and subsequent demineralisation [Weatherell et al., 1979] (Figure 4).

[FIGURE 4 OMITTED]

This points strongly to the lesion, even at its earliest stage, as the site of action of F. A consideration of lesion structure and chemistry support this view.

Structure of the Caries Lesion

Long before cavitation occurs the enamel becomes porous. This begins at a subsurface level with pores increasing in size and number until cavitation occurs. Pore size and distribution are not haphazard but seem to follow a pattern that has provided some clues as to the way in which lesions may form [Darling, 1956]. The pores are considered to be very small as indicated by low diffusion constants for enamel [Burke and Moreno, 1975; Borggreven et al., 1981] the most important of which seem to be situated at prism boundaries [Boyde, 1989]. These changes are summarised in Figure 5.

[FIGURE 5 OMITTED]

The first visible change that can be viewed in polarised light, or using imbibition media, is a translucent zone that represents the loss of about one percent of mineral. It appears that the outer surfaces of crystals have been dissolved [Johnson, 1967; Boyde 1989]. Following the translucent zone the dark or positively birefringent zone appears [Silverstone, 1967]. Progressive loss of mineral has occurred resulting in the loss of about 5 per cent of mineral. Pore structure, however, is not simply more and larger pores. The dark zone is not just characterised by pore enlargement, intriguingly additional very small pores appear. This might be differential dissolution of crystals but has also been interpreted as some crystal regrowth or even new crystal formation (remineralisation). This was supported by increases in dark zone size when lesions were remineralised [Wefel et al., 1987a, b], see Figure 5.

The succeeding zone was termed the lesion body in which pore size and number increased further resulting in loss of 50% or more mineral. Continuance of this loss would lead to cavitation.

Chemistry of the Caries Lesion

In an effort to determine the mechanism behind these porosity changes and clarify the changes occurring during carious attack, efforts were made to dissect out each zone of a number of natural caries lesions and subject them to chemical analysis. Zones were visualised using imbibition media and polarised light. Dissection was achieved using hardened steel micro- dissecting needles [Hallsworth et al., 1972, 1973]. Alongside each piece of translucent zone, a piece of similarly sized adjacent sound enamel was removed for comparison. Mineral content was determined pycnometrically as well as by chemical analysis, carbonate was determined volumetrically, magnesium by atomic absorption and F by selective ion electrode analysis. Mineral content of each zone was similar to that determined by polarised light microscopy with the translucent zone losing about 1%, dark zone losing about 5% and the body of the lesion a minimum of about 20%.

Intriguingly, calculation revealed that early mineral lost in both translucent and dark zones contained a disproportionately high concentration of carbonate and magnesium [Robinson et al., 2000]. This could be explained simply by the fact that mineral rich in these components would be relatively unstable and prone to acid dissolution. Such high concentrations of carbonate and magnesium are likely to reside at crystal surfaces since during growth such disruptive ions would be recrystallised to the outer regions of growing apatite crystals. This was consistent with the dissolution of crystal surfaces seen in the translucent zone [Johnson, 1967].

[FIGURE 6 OMITTED]

F provided a completely different picture. Even in the translucent zone F content was elevated above that of the surrounding sound tissue (Figure 6). We have therefore in the translucent zone a loss of destabilising ions such as carbonate and magnesium and an increase in the stabilising effects of F. Both changes would tend to produce an environment favouring crystal deposition or growth. This is the most likely explanation for the production of the small pores of the dark zone, that is to say the occurrence of some new growth of mineral or regrowth of existing crystals (Figure 5). Whether this involves non-apatitic precursors is not clear at the moment but the effects of these chemical changes will certainly operate in the direction of remineralisation.

Subsequent dissolution of reprecipitated, more stable mineral in the ensuing lesion body can be explained by the pH gradient from the acid producing plaque at the tooth surface. The closer to the surface the lower the pH will be, [Vogel et al., 1988] thus dissolution even of the remineralised mineral will occur a lower pH values. See Figure 7.

[FIGURE 7 OMITTED]

Progress of the lesion, that is to say the balance between demineralisation and remineralisation, will depend on the pH gradient from the plaque/enamel surface i.e. the extent to which protons penetrate the lesion together with the extent to which fluoride penetrates the lesion. The source of this F has been reported as ranging from ill-defined F-phosphate complexes [Christoffersen et al., 1988] through calcium F (CaF) [Nelson et al., 1984; Rolla and Ogaard, 1986] to the extended CaF-hydrogen bonded complexes as described by Kreinbrink et al. [1990]. All, however, place high concentrations of F ion at the surface of the tooth where carious attack is initiated and could serve as a reservoir of F ion.

Fluoride and Dental Plaque

While much of the work on F and dental caries has concentrated on enamel, effects on plaque cannot be ignored especially if, to reach the caries lesion, F must be transported through the plaque layer. There is a considerable amount of data concerning average F concentrations in plaque but until recently there has been almost no information as to the distribution and uptake of F by natural plaque layers. This has been addressed to some extent by producing natural plaque on natural enamel; surfaces in the mouth. Such plaques produced over 7 days were recovered intact from the mouth and were sampled in 5 micron layers from saliva interface to enamel surface, F content was examined in each set of layers [Robinson et al., 1997].

Much of the F was located in the outer one third or one half of the plaque suggesting that the ion is taken up by plaque in the outer layers and diffusion to the enamel surface may be restricted [Robinson et al., 1997] (Figure 8). Subsequent experiments using such natural plaque layers exposed to 1,000 ppm F for 30 seconds up to 30 minutes confirmed this view [Watson et al., 2005]. Data suggested that the architecture of the plaque that was shown to be complex might be responsible in that surface area to mass ratios of plaque biomass mirrored the F distribution. Interaction with plaque biomass components would seem to restrict diffusion of F through the plaque layers [Robinson et al., 2005].

[FIGURE 8 OMITTED]

Conclusions

It is clear from the above considerations that F must continuously enter caries lesions to combat the effects of dissolution by plaque acid. If F is complexed, either in the plaque or at or in the enamel surface, then this will not be achieved. It seems likely then that the continuous supply apparently required may be a reflection of the necessity to saturate plaque and enamel surface binding sites so that penetration of some free F into lesions can occur. This may explain less than consistent relationships between plaque F and dental caries. If plaque cannot be satisfactorily removed then maintaining a thin plaque layer to permit access of fluoride to the enamel surface at risk would appear to be desirable.

References

Borggreven JM. Dijk JW van, Driessens FC. Effect of mono- and divalent ions in diffusion and binding in tooth enamel. Arch Oral Biol. 1981; 26: 663.

Boyde A. Enamel. In: Handbook of microscopic anatomy. Oksche A, Vollrath L, editors. Berlin: Springer Verlag, 1989 pp. 309-473.

Burke EJ, Moreno EC. Diffusion fluxes of tritiated water across human enamel membranes. Arch Oral Biol 1975; 20: 327- 332

Christoffersen J, Christoffersen MR, Kibalczyc W, Perdok Wg. Kinetics of dissolution and growth of calcium fluoride and effects of phosphate in solution and incorporated in the crystals on these processes. Acta Odont Scand, 1988; 36: 325-326.

Darling AI. Studies of the early lesion of enamel caries with transmitted light , polarised light and radiography. Br Dent J, 1956; 101: 289-297.

Elliott JC, Holcomb DW, Young RA. Infrared determination of the degree of substitution of hydroxyl by carbonate ions in human dental enamel. Calcif Tiss In., 1985; 7: 372-375.

Hallsworth AS, Robinson C, Weatherell JA. Mineral and magnesium distribution within the approximal carious lesion of dental enamel. Caries Res 1972; 6: 156-168.

Hallsworth AS, Robinson C, Weatherell JA. Loss of carbonate during the first stages of enamel caries Caries Res 1973; 7: 345-348.

Johnson NW. Some aspects of ultrastructure of early human enamel caries seen with the electron microscope. Archs Oral Biol 1967; 12: 1505-1521

Kay MI, Young RA, Posner AS, Crystal structure of hydroxyapatite. Nature 1964; 204: 1050- 1052.

Kreinbrink AT, Sazavsky CD, Pyrz JW, Nelson DGA, Honkonen RS. Fast magic angle spinning 19F NMR of inorganic fluorides and fluoridated apatitic surfaces. Magn Reson 1990; 88: 267-276.

LeGeros RZ. Incorporation of magnesium in synthetic and in biological apatites. In: Tooth Enamel IV, 1984; Fearnhead RW, Suga S, editors. Amsterdam: Elsevier, pp. 32-36.

Nelson DGA, Jongbloed WL, Arends J. Crystallographic structure of enamel surfaces treated with topical fluoride agents. TEM and XRD considerations. J Dent Res 1984; 63: 6-12.

Robinson C., Kirkham J., Shore R.C., et al. The Chemistry of Enamel Caries. Critical Reviews in Oral Biology & Medicine, 2000; 11, pp 481-495

Robinson C, Kirkham J, Brookes SJ, Shore RC. Chemistry of mature enamel. In: Dental enamel: formation to destruction. Robinson C, Kirkham J, Shore RC, editors. Boca Raton: CRC Press, 1995 pp. 167-191.

Robinson C., Kirkham J., Shore R.C., et al. A method for the quantitative site-specific study of the biochemistry within dental plaque biofilms formed in vivo. Caries Res 1997; 31, pp 194-200

Robinson C, Watson PS., Penetration of therapeutic agents through natural plaque biofilms. In Biofilms, Persistence and Ubiquity, 2005. The Biofilm, Club, Eds. Mcbain, A, Allison D, Pratten J; 343-353.

Robinson, C. Yamamoto, K. Connell, S.D. et al. The effects of fluoride on the nanostructure and surface pK of enamel crystals: an atomic force microscopy study of human and rat enamel. Eur. J. Oral Sci. 2006; 114, (Suppl 1): 99- 104

Rolla G, Ogaard B., How important is CaF2 in the cariostatic mechanism of fluoride in vivo. In: Factors relating to the demineralisation and remineralisation of teeth. Leach SA, editor. Oxford: IRL Press, 1986; pp. 45-50.

Silverstone LM. Observations on the dark zone in early enamel caries and in artificial caries-like lesions. Caries Res 1967; 1: 261-274.

Vogel GL, Cary CM, Chow LC, Gregory TM, Brown WE. Micro-analysis of mineral saturation within enamel during lactic acid demineralisation. J Dent Res 1988; 67: 1172-1180.

Watson PS, Pontefract HA, Devine DA, et al.. Penetration of fluoride into natural plaque biofilms. J Dent Res. 2005; 84:451-5.

Weatherell JA, Robinson C, Hallsworth AS. Changes in the fluoride concentration of the labial enamel surface with age. Caries Res 1972; 6: 312-324.

Weatherell, JA, Hallsworth AS, Robinson C, Effect of tooth wear on the distribution of fluoride in the enamel surface of humans teeth. Arch. Oral Biol. 1973; 18, 1175,

Weatherell, JA., Robinson, C. Patterson, C. The uptake and action of fluoride in dental enamel. J. Clin. Period, 1979; 6: 53-60

Wefel, JS, Maharry, GJ, Jensen ME, Harless JD. Development of an intraoral single section remineralisation model. J. Dent. Res. 1987a; 66: 14851489.

Wefel JS, Harless JD. The use of saturated DCPD in remineralisation of artificial caries lesions in vitro J Dent Res 1987b; 66: 1640-1643

Young RA. Biological apatite vs. hydroxyapatite at the atomic level. Clin Orthop 1975;113: 249- 262.

C. Robinson

Dept. Oral Biology, Leeds Dental Institute, University of Leeds, Leeds, Eng land.

Postal address: Prof. C. Robinson. Dept. Oral Biology, Leeds Dental Institute, Claredon Way, Leeds, England, LS2 9LU

Email: c.robinson@leeds.ac.uk
COPYRIGHT 2009 European Academy of Paediatric Dentistry
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2009 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Robinson, C.
Publication:European Archives of Paediatric Dentistry
Article Type:Report
Date:Sep 1, 2009
Words:2710
Previous Article:Guidelines on the use of fluoride in children: an EAPD policy document.
Next Article:Water fluoridation.
Topics:

Terms of use | Privacy policy | Copyright © 2019 Farlex, Inc. | Feedback | For webmasters