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Coll. Antropol. 25 (2001) 2: 703712UDC 616.314-002:615.242

Review

Current Concept on the AnticariesFluoride Mechanism of the Action

K. Ro{in-Grget and I. Lin~ir

Department of Pharmacology, School of Dental Medicine, University of Zagreb, Zagreb, Croatia

A B S T R A C T

The paper discusses a possible new concept of the role of fluoride and its mechanismof action in caries prevention. In the past fluoride inhibition of caries was ascribed to re-duced solubility due to incorporation of fluoride (F) into the enamel minerals (firmlybound fluoride or fluorapatite). Based on the new findings, it appears that fluoride, eitherreleased into or present in the fluid phase bathing the hard tissue, is more important forthe reduction of caries development and progression. There is convincing evidence thatfluoride has a major effect on demineralization and remineralization of dental hard tis-sue and that it interferes with acid production from cariogenic bacteria. The provisionof dissolved fluoride is the key to successful therapy. The source of this fluoride could ei-ther be fluorapatite or calcium fluoride (CaF2) (like) precipitates, which are formed on

the enamel and in the plaque after application of topical fluoride. The precipitates ofcalcium fluoride do not dissolve quickly as was initially believed. Calcium fluoride coat-ing at neutral pH by pellicle proteins and phosphate is the main reason for this. The dis-solution of the fluoride from calcium fluoride is pH dependent. At lower pH, the coatingis lost and an increased dissolution rate of calcium fluoride occurs. The CaF2, therefore,act as an efficient source of free fluoride ions during the cariogenic challenge. These aresubsequently incorporated into the enamel as hydroxyfluorapatite or fluorapatite.

Introduction

The mechanism of the cariostatic ef-fect of fluoride (F) is still not clearly un-derstood. In the past caries inhibitionwith fluorides was ascribed to the re-duced solubility of the enamel due to in-corporation of F into the enamel miner-als during tooth formation1. However,recent studies have shown that the pres-ence of fluoride in the enamel, even at

very high levels, is not directly responsi-ble for the caries preventive effect of

fluoride. Recently, it was found that evenshark enamel containing nearly purefluorapatite had a limited resistance tocaries attack in an oral human cariesmodel2. Consequently, fluoridation of theenamel and production of high levels ofincorporated fluoride would not be suffi-cient to inhibit tooth decay. Some investi-gators have shown that fluoride in the so-

703Received for publication December 5, 2000.

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lution surrounding the apatite crystalsinhibits demineralization much more ef-fectively than fluoride incorporated in thecrystals35.

There is now much evidence which in-dicates that the caries preventive action offluoride is primarily post eruptive throughthe topical effect, which includes:

inhibition of demineralization enhancement of remineralization inhibition of bacterial activity in the

plaque

Research indicates that topicals whichare used frequently, such as daily use ofdentifrices and mouthrinses can enhanceremineralization and retard demineral-ization of enamel. The marked caries re-duction in many countries over the lastthree decades is thought to be mainly theresult of the widespread and frequent useof low concentrations of fluorides mainlyvia toothpastes6,7.

There is evidence that a major part ofthe fluoride which is retained on the teeth

during topical application is calcium fluo-ride (CaF2) or calcium fluoride-like mate-rial. Calcium fluoride is the most likelysource of free ions during cariogenic chal-lenges, which are subsequently incorpo-rated into enamel as hydroxyfluorapatiteor fluorapatite8. Thus, in the last fewyears understanding of the cariostaticmechanism of fluorides has changed fun-damentally.

The aim of the present paper is to de-

scribe the current concept on the mecha-nism of the fluoride cariostatic effect andpropose recommendations for future useof fluoride.

The Chemical Properties of Enamel

Highly calcified enamel has approxi-mately 96% mineral by weight, 1% or-ganic matter and 3% water9. The solidphase of enamel consists mainly of crys-tallized calcium phosphate, that persist

in different forms. X-ray diffraction anal-yses have shown that enamel mineralscome mainly as hydroxyapatite and someless stable forms such as dicalciumphos-

phathydrat (DCPD), brushit or octacal-ciumphosphat (OCP). The mineral com-ponent of human dental enamel is basi-cally an impure calcium hydroxyapatite.Carbonate is the most abundant impu-rity. Carbonated calcium hydroxyapatiteis more soluble than calcium hydroxy-apatite, especially in acidic media1012.The pure hydroxyapatite [Ca10 (PO4)6 (OH)2]allows the incorporation of many ionsthat fit in the crystallite structure and af-

fect its solubility. The substitution in thehydroxyapatite crystal occurs during de-velopment with carbonate, magnesium,fluoride, etc. Fluoride improves the qual-ity of mineralized tooth tissues in generalby reducing the relative amounts of car-bonated apatite.The reaction betweenhydroxyapatite and low concentrations offluoride has been postulated to be anionic exchange in which fluoride replacesand assumes the positions of the hydroxylions in the crystal lattice structure. The

replacement of hydroxyl groups with thesmaller fluoride ions should result in amore stable apatitic structure. If the OH

ion in pure hydroxyapatite is completelyreplaced by a fluoride ion (F) the result-ing mineral is fluorapatite [Ca10 (PO4)6 F2]9. However, even in severely fluorosedhuman enamel such complete substitu-tion is never achieved. The pure fluor-apatite practically can never be found13.Only 10% of the hydroxyl groups can be

substituted by fluoride in the surfaceenamel. The compound hydroxyapatite--fluorapatite is formed when the hydroxylpositions are only partially replaced byfluoride ion.

Dental Caries

Dental caries is localized, progressivedestruction of the tooth initiated by aciddissolution of the outer tooth surface. Inthe presence of the fermentable carbohy-

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drate, organic acids are produced by pla-que microorganisms which colonize thetooth surface. Some of the dental plaquebacteria, such as Streptococcus mutansand Lactobacillus are acidogenic. The ac-ids (i.e. lactic, pyruvic, acetic, propionic,butyric) can dissolve the calcium phos-phate mineral of the enamel or dentine(demineralization)14,15. The acids diffusethrough the plaque into the pores of thesound enamel surface, releasing hydro-gen ions, which can dissolve the underly-ing enamel. The dissolved mineral ions,calcium and phosphate will then back--diffuse into the surface layer and induce

the precipitation of the mineral phases inthis region. At the same time, some of thedissolved mineral ions will diffuse out ofthe enamel surface to the oral environ-ment. It is known that incipient or smallcarious lesions (white spot lesion) inhuman enamel consist of a subsurfacearea of demineralization with an overly-ing, apparently intact, surface zone. It isconsidered that the enamel surface layeris a result of reprecipitation of minerals

(remineralization) dissolved from thesubsurface16. The leaching calcium andphosphate from enamel can cause col-lapse of the tooth structure and formationof a cavity. Demineralization and remi-neralization can be considered a dynamicprocess, characterized by the flow of cal-cium and phosphate out of and back intothe enamel.

The saliva plays an important role, in-cluding buffering (neutralizing) the acidand providing minerals that replace tho-se dissolved from the tooth during demin-eralization challenge. The enamel surfaceis in constant contact with saliva which isconsidered to be saturated with certaincalcium phosphate salts, thereby main-taining the integrity of the enamel sur-face. It was found that within physiologi-cal pH limits the salivary content ofcalcium and inorganic phosphate wassufficient to supersaturate the saliva with

respect to hydroxyapatite. The protectivefactors, which include salivary calcium,phosphate and proteins, salivary flow,and fluoride in saliva can balance, pre-vent or reverse dental caries14.

The Role of Fluoride in CariesPrevention

There are three principle forms of flu-oride ion reactivity with apatite:1) Iso-ionic exchange of F for OH in apa-tite:

Ca10 (PO4)6 OH2 + 2F Ca10(PO4)6F2 + 2OH

2) Crystal growth of fluorapatite from su-persaturated solutions:

10 Ca2+ + 6 PO43 + 2 F Ca10(PO4)6F2

3) Apatite dissolution with CaF2 formation:

Ca10 (PO4)6 OH2 + 20F 10 CaF2+6PO43 + 2OH

The first two reactions may occur dur-ing long-term exposure to low fluoridelevels in the solution (such as between0.52 mol and 0.52 mmol F/L) (0.01 and10 ppm F) from either systemic or latenttopical sources. These reactions result influoride incorporation that, in a tradi-tional sense, would be defined as firmlybound fluoride, since it is part of theapatitic structure. With the increasingfluoride concentration an additional che-

mical reaction with the formation signifi-cant calcium fluoride amounts begins todominate. Fluoride concentrations rang-ing from 5.3 to 530 mmol/L (10010,000ppm F) are required to produce CaF2 as areaction product. These concentrations arepresent in topicals, such as professionalgels and varnishes or over the countertoothpastes and mouthrinses17. The na-me loosely bound fluoride has served asan alternative description for calcium flu-oride formation.

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Firmly-bound fluoride

It has been suggested that firmlybound fluoride is most beneficial for

anticaries efficacy due to its lower solu-bility. Numerous studies have investi-gated the effects of fluoride on tooth min-eral solubility. In all studies, fluorapatitewas found to dissolve appreciably moreslowly than hydroxyapatite18. Moreno etal.19 has calculated the solubility productconstants for various degrees of substitu-tion of fluoride for hydroxyl in hydro-xyapatite. The results showed that therewas a steady decrease in the solubility of

fluoridated hydroxyapatites, with increa-sing values of the degree of substitutionup to a level of about 60%. However, a rel-atively high concentration of fluoridewithin the enamel is required for signifi-cant reduction in enamel solubility. Sub-surface enamel generally contains fluo-ride at levels of about 20100 ppm,depending on fluoride ingestion duringtooth development. Only the outer fewmicrometers of enamel can have F levels

of 1,0002,000 ppm in teeth which de-velop in a fluoridated water area. Even atthis level there is no measurable protec-tion against acid induced dissolution14.Based on solubility data the thermody-namic solubility product constant (Ksp)of fluorapatite is only slightly less thanthat of hydroxyapatite20. Brown et al.21

pointed out that this difference alone isnot sufficient to account for the dramaticeffects of fluoride on the acidic resistance

of enamel and apatite.The formation of lesions in shark

enamel in both in vitro22 and intraoral2

models suggests that fully fluoridated ap-atite can also dissolve. This observationhas indicated that structurally bound flu-oride are not very effective in inhibitingenamel demineralization.

However, Chow23 suggested that F

rich mineral is still considerably more re-sistant to demineralization than F poor

mineral. He reported that tooth bound Fin the lesion area can produce the follow-ing effects:

a) reduction of tooth mineral solubilityb) reduction of mineral diffusion fromlesion

c) interactions between tooth -boundand ambient fluoride

The apatitically bound F can affect theconcentration of calcium and phosphateand/or pH of the lesion fluid. When weakacids are present in the plaque the driv-ing forces for diffusion of calcium andphosphate ions of the lesion fluid are de-

creased due to the action of tooth boundfluoride. This should lead to a reducedrate of demineralization. When onlystrong acids (e.g. lactic acid) are presentin the cariogenic plaque, the calcium andphosphate concentrations are not lower-ed by tooth bound F effect, but the pH ofthe lesion fluid is significantly reduced.This would decrease the rate of H+ ion dif-fusion into the lesion. Since H+ ions arethe major driving forces for demineraliza-

tion, this would also decrease the rate ofdemineralization24. Another importantfunction of tooth bound F is the reducedability of the tooth mineral to scavengethe F in the fluids within the tooth. Fluo-ride rich mineral, under severe challenge,will release F into the solution which,when the challenge becomes less severe,may promote remineralization. Takagi etal.25 showed that enamel resistance to le-sion formation increased with increasing

tooth bound fluoride content.The caries process occurs at the ena-

mel-plaque interference and therefore, theextracellular aqueous phase of plaque,i.e. plaque fluid, is the most relevant tothe caries process. Saliva, and also pla-que fluid, are supersaturated with re-spect to both hydroxyapatite and fluor-apatite, which explains the permanentpresence and stability of these apatite inthe oral cavity26. However, when the oral

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fluids become unsaturated with respectto the apatites e.g., caused by a pH drop,a change in apatite composition may oc-cur. In the pH range below about 5.5, theoral fluids are unsaturated with respectto hydroxyapatite, which therefore maydissolve. The low fluoride concentrationsprevailing in oral fluids under physiologi-cal conditions will ensure a concurrentsupersaturation with respect to fluor-apatite, theoretically in the pH range ofabout 5.54.5, so that dissolution of hy-droxyapatite competes with simultane-ous fluorapatite or mixed fluorohydro-xyapatite formation27. This mechanismprevents the loss of minerals and pro-vides additional protection of the mineralcrystallites by laying fluoride rich outerlayers onto the apatite crystallites28.Crommelin et al.29 observed that fluor-apatite-coated hydroxyapatite dissolvedlargely the same as fluorapatite, but thehydroxyapatite in a hydroxyapatite andfluorapatite mixture dissolved the sameas hydroxyapatite. Therefore, significantprotection could be obtained if all crystalsalong the acid ions diffusion pathway arecoated with fluorapatite. At low pH, pre-sumably below 4.5, the liquid phase of theplaque will be undersaturated with re-spect to both hydroxyapatite and fluor-apatite, and no re-deposition of lost min-eral (remineralization) will occur. It isreported that sound human enamel, at apH of around 7 in the oral fluids, does nottake up fluoride to a significant extent iffluoride concentrations are below 50 ppm.Living in an artificially water-fluoridatedarea or regularly rinsing with neutral flu-oride solution does not affect the fluorideconcentrations in sound enamel. Incorpo-ration of fluoride into sound enamel ispossible only as a result of concomitantenamel dissolution (caries lesion develop-ment)30. Therefore, these authors con-cluded that posteruptive maturation oferupting sound enamel, during which theenamel may be particularly susceptible to

fluoride uptake, is a misnomer and mostlikely reflects de- and remineralizationprocesses at a subclinical level.

Recently, it has been observed thatlow concentrations (up to 1 ppm) of fluo-ride in solution can reduce and even in-hibit enamel demineralization31. TenCate and Duijsters32 showed that theamount of mineral loss during demineral-ization is a function of both pH and fluo-ride concentration. When the fluorideconcentration in solution is elevated thefluorapatite is correspondingly increasedand it appears sufficient to prevent a car-ies lesion from developing. It was shownthat inhibition of demineralization is alogarithmic function of the fluoride con-centration in solution11. The clinical im-plications of this would be that simply in-creasing fluoride concentrations mightnot necessarily give increased cariostaticbenefit. The delivery of relatively low flu-oride concentrations for longer periodsshould be more appropriate for enhanc-ing clinical efficacy. Some clinical trialsshowed that lower fluoride concentra-tions than usually used in topical fluoridepreparations could provide similar cariesreduction. It is possible that a lower fluo-ride solution provides a sufficient reser-voir of calcium fluoride, so that no differ-ence in the efficacy between the twofluoride concentrations can be detec-ted33,34. It is conceivable that ambient flu-orides provided by various F regimensmay have overwhelmed the effect oftooth-bound F. Thus, efforts to increase

the fluoride content of dental hard tissuesby systemic or topical fluoride are not alogical approach to caries prevention35.Tooth-bound fluoride can only be a sup-plement to ambient fluorides for greaterprotection.

In older studies it was claimed thatthe morphology of molars is affected bysystemic fluoride to such an extent as torender the occlusal surfaces more resis-tant to bacterial invasion and demineral-

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ization. More recent studies have not pro-vided any reliable evidence to suggestpre-eruptive influence on the tooth mor-phology36.

Loosely bound fluoride

In the last few years the general viewis that loosely bound fluoride (CaF2) actsas a potential reservoir of fluoride, en-hancing remineralization and retardingdemineralization processes28,3740. Topicaltreatments with high fluoride concentra-tions result in the formation of calciumfluoride-like material on the surface ofteeth. As early as 1945 Gerould41 repor-

ted that calcium fluoride was a majorproduct on enamel when teeth were ex-posed to high concentrations of fluoride.It is visible by scanning electron micro-scope (SEM) as small globules on the sur-face of fluoridated teeth (Figure 1). Theglobular precipitates on the enamel aremore homogeneous when the fluorideconcentration of an applied solution ishigher42. The globular structure of thecalcium fluoride is thought to be due to

incorporation of phosphate during its for-mation on the tooth surface43, since purecalcium fluoride is cubical rather thanspherical. The material is described ascalcium fluoride-like. For a long periodthe general view was that formation of

calcium fluoride on enamel is unfavor-able, because calcium fluoride is solublein saliva to the same extent as in water26.The oral fluids are unsaturated with re-spect to calcium fluoride, thus this saltdissolves whenever it is exposed to sali-va30. However, several studies have shownthat calcium fluoride is quite insoluble insaliva at the neutral pH, and that it canpersist on the tooth surface for weeks andmonths after topical application of fluo-ride4446. The resistance of calcium fluo-ride is presumably caused by adsorptionof secondary phosphate (HPO 42) to cal-cium sites in the surface of calcium fluo-ride crystal and by pellicle proteins atneutral pH. At lower pH, as during a car-ies attack, primary phosphate will be thedominant phosphate ion species (HPO4)which is unable to inhibit the dissolutionof calcium fluoride. Thus fluoride ions re-leased during cariogenic challenges aredue to reduced concentration of second-ary phosphate ions at acid pH. The re-leased fluoride is subsequently built intohydroxyapatite through dissolution/re--precipitation reactions8,38. After cariesattack, the calcium fluoride globules areagain stabilized by adsorption of proteinsand secondary phosphate47. Calcium fluo-ride thus constitutes a pH-controlled res-ervoir of fluoride on enamel. Calcium flu-oride is contaminated with phosphate,not only on the surface, but also insidethe crystal. This phosphate-contaminedcalcium fluoride is more soluble thanpure calcium fluoride and may thus re-lease fluoride at a higher rate than purecalcium fluoride43. The calcium fluorideformation, its resistance in the oral envi-ronment and release of fluoride ions atlow pH, explain the long-term effect oftopically applied fluoride. It is suggestedthat the potential for formation of cal-cium fluoride should probably be increa-sed in topical fluoride agents48. Increasedtime of exposure, increased concentrati-on, lowered pH and calcium pre-treat-

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Fig. 1. Scanning electron micrographs of ena-mel surface treated for 3 min. with an amine

fluoride solution with 1% F.

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ment have proved to be effective means ofincreasing calcium fluoride deposition onenamel in vitro49.

CaF2 can be formed on intact enameland be covered with plaque, on and in de-mineralized enamel, or in plaque. The re-activity of fluoride on sound enamel andcarious enamel differs significantly50.Carious enamel is more reactive with flu-oride than sound enamel. Carious enamelacquires more fluoride, acquires it faster,and acts as a source of retained fluoridein comparison with the more limited re-activity of sound enamel17. Ten Cate andLoveren51 hypothesized that differentmorphology of a calcium fluoride depositin the lesion pores may result in more ef-fective inhibition than the fluorapatitegrowing on the existing hydroxyapatitecrystallites. However, no data describedthe dissolution kinetics of calcium fluo-ride formed in inaccessible pores of natu-ral lesions. It could be expected that thedissolution period is much longer30. An-other interesting observation is that acontinuos layer of small particles of cal-

cium fluoride may cover the enamel com-pletely and protect it to a higher degreethan fluorapatite, because the solubilityof calcium fluoride is less pH dependentthan fluorapatite8. Thus the preparationsof fluoride with low pH produce pure oralmost pure calcium fluoride which mayprotect the enamel surfaces38. Koulou-rides52 demonstrated that acid-softenedenamel, rehardened by fluoridation, ac-quired significant secondary resistance toacid attack, developing so-called acqui-red resistance. The acquired fluoride en-hances both remineralization and demin-eralization resistance.

Overall, it is clear that both fluor-apatite and calcium fluoride can provideF to the solution phase and enhanceremineralization and retard demineral-ization of enamel hydroxyapatite crystal-lites. The fluorapatite provides most F

under low pH conditions, while CaF2 pro-vides F at neutral or lower pH. The fluo-

ride, present in the solution from topicalsources, enhances remineralization byspeeding up the growth of a new surfaceon the partially demineralized subsur-

face crystals in the caries lesion. Thus,the fluorapatite probably has limitedvalue in caries prevention, whereas theremineralization process as such may becrucial. This supports the hypothesis thatpermanent fluoride ion activity during acaries process is more important than ahigh content of fluoride in the enamel35.

The Antimicrobial Action of

FluorideIn spite of extensive literature on the

antimicrobial effects of fluoride on oralmicroflora, today there is very little con-sensus that the anticaries effect of fluorideis related to inhibition of oral bacteria.

Early studies showed the inhibitoryeffect of fluoride on pH fall or acid pro-duction in plaque after a sucrose or glu-cose challenge53. Initially, it was postu-lated that fluoride may be released from

the enamel surface at low pH in sufficientconcentrations to interfere with glycoliticenzymes and to prevent further increasein hydrogen ion concentration54.

However, more recent studies suggestthat fluoride present in the surface ena-mel does not significantly prevent acidproduction. The concentrations of fluo-ride present in the saliva are too low toaffect bacterial metabolism. On the otherhand, appreciable amounts of fluoride

may accumulate in dental plaque. How-ever, fluoride concentrations needed forantimicrobial effects surpass significan-tly the concentrations which can reducethe solubility of apatite. Since less than 1ppm of fluoride will cause rapid precipita-tion of fluorapatite from high concentra-tions of calcium and phosphate present inthe plaque it is unlikely that fluoride in-hibition of bacterial production in plaqueis of any significance55. This is an impor-tant argument in debates on the effect of

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fluoride in dental plaque and its contribu-tion to caries prevention51.

In order to provoke any antimicrobial

effect fluoride has to enter the bacterialcell. Fluoride diffuses into cariogenic bac-teria in the form of HF (a weak acid, pKa3.15). At the lower external pH, more HFis formed and more of it diffuses into thecell. Once inside the cell the HF dissoci-ates into H + and F , because of a higherinternal pH of cells, such as oral strepto-cocci, than external. This continued diffu-sion and dissociation leads to the accu-mulation of fluoride in the cell and theacidification (accumulation of H+) of thecytoplasm. The result is a reduction inboth the proton gradient and the enzymeactivity. Current information indicatesthat fluoride ions within the cell interferewith the glycolitic enzyme (enolase) activ-ity and proton-extruding adenosine tri-phosphatase (H +/ATP -ase), which is in-volved in the generation of protongradients through the efflux of protonsfrom the cell at the expense of ATP56.Thus, fluoride inhibit effectively the car-

bohydrate metabolism of acidogenic oralbacteria, including the uptake of su-gars51. In spite of these known effects,there is no general agreement that theantimicrobial effects of F contribute tothe anticaries effect of fluoride56.

Many investigators tend to dismissthe role of fluoride in the metabolic activ-ity of bacteria, on the grounds that onlylarge concentrations are effective, andthat there are no differences in the Strep-

tococcus mutans populations in personsresiding in fluoridated and in non-fluori-dated areas57. In addition, the wide-spread use of toothpastes, which havebeen responsible for the decrease in car-ies prevalence over the last three deca-des, did not result in a reduction in thenumber of the mutans streptococci58.White et al.59 suggested that topical fluo-ride from the over-the-counter dentifriceaffects only minimal reductions in acuteplaque metabolic activity (acid produc-

tion). Van Loveren58 summarized theantimicrobial action of fluoride and sug-gested that the continuous daily applica-tion of fluoride reduces the acidogenicity

of plaque, although there is no direct linkwith clinical inhibition of caries. A singleapplication of professionally applied topicalfluoride at a high concentration, althoughtransient, reduces the plaques ability toproduce acid, but has little clinical signifi-cance in controlling dental caries.

Adaptation ofStreptococcus mutans tofluoride has been suggested as the reasonfor the reduced cariogenic potential of thebacterial cells. Possible adaptation of

streptococci in dental plaque to frequentexposure to fluoride will not necessarilydecrease the caries preventive effectscaused by topically applied fluoride agents(i.e. fluoride lacquer)60. Van Loveren etal.61 showed that the use of fluoride tooth-paste does not affect plaque composition,or fluoride tolerance or acidogenicity ofmutans streptococci. In general, the clini-cal contribution fluoride anti-plaque ef-fects to caries is poorly understood62.

Recommendations for the FutureUse of Fluoride

Two theories of the cariostatic mecha-nism of fluoride are suggested in cariesprevention. One stresses the importanceof an ample supply of fluoride duringtooth formation, and the other a lifelongdaily supply. Larsen63 pointed out, thatthe two theories may complement each

other, and neither of the theories exclu-des the other. On the basis of present in-formation, it is suggested that the post--eruptive effect of fluoride is by far themost important. There is considerable ev-idence to suggest that low concentrationsof fluoride decrease the rate of demineral-ization and enhance the rate of remi-neralization. Thus, the effectiveness offluoride as a cariostatic agent depends onthe availability of free fluoride in plaqueduring cariogenic challenge, i. e. during

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K. Ro{in-Grget

Department of Pharmacology, School of Dental Medicine, University of Zagreb,[alata 11, 10000 Zagreb, Croatia

TUMAÊNJE ANTIKARIJESNOG MEHANIZMA DJELOVANJA FLUORIDA

S A @ E T A K

U ovom je radu opisano mogu}e novo tuma~enje uloge fluorida i njihovog meha-nizma djelovanja u prevenciji karijesa. Ranije se inhibicija karijesa fluoridima pripi-sivala smanjenoj topljivosti cakline zbog ugradnje F u minerale cakline (~vrsto veznifluoridi ili fluorapatit). Temeljem novih nalaza, ~ini se da su otpu{teni fluoridi u teku}ufazu koja oplakuje tvrdo tkivo ili fluoridi prisutni u njoj, mnogo va`niji za smanjenjerazvoja i progresije karijesa. Dokazano je da fluoridi imaju glavni u~inak na demine-ralizaciju i remineralizaciju tvrdog zubnog tkiva i da interferiraju s kariogenim bakte-rijama koje stvaraju kiseline. Prisutnost otopljenih fluorida klju~ je uspje{ne terapije.Ovi fluoridi mogu poticati iz fluorapatita ili precipitata (poput) kalcij fluorida (CaF 2),koji se stvaraju na caklini i u plaku nakon primjene topikalnih fluorida. Precipitatikalcij fluorida ne otapaju se tako brzo kao {to se ranije mislilo. Razlog tomu je, prineutralnom pH, oblaganje kalcij fluorida proteinima pelikule i fosfatima. Osloba|anjefluorida iz kalcij fluorida ovisno je o pH. Pri nièm pH, omota~ nestaje i pove}ava sebrzina otapanja. Zbog toga CaF2 djeluje kao u~inkovit izvor slobodnih iona fluora uvrijeme kariogenih zbivanja. Ioni se zatim inkorporiraju u caklinu kao hidroksilfluo-rapatit ili fluorapati

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