Artículo 3 - Fluor (Cury-Tenuta 2008)

7/27/2019 Artculo 3 - Fluor (Cury-Tenuta 2008)

1/4

SSince the primary effect of fluoride (F) on caries controlis post-eruptive, any method of fluoride use, to beeffective, should be able to maintain a constant fluorideconcentration in the oral environment. Fluoridated water

and F dentifrice are still regarded, respectively, as systemicand topical methods of F use, and they are considered to bethe most effective F regimens for interfering with the cariesprocess. However, our understanding of how these apparentlydifferent methods of F use maintain F in the oral environment

has not been fully elucidated. Thus, the aim of this article isto consider evidence that fluoridated water and F dentifricediffer only in the manner that F is kept in the oral environmentduring the intervals that water is not being drunk or the teethare not being brushed.

IntroductionThe history of the importance of fluoride (F) in caries controlcan be divided into two phases: before its use for waterfluoridation in the 1950s, and before the widespread use of Fdentifrices in the 1980s. Also, on the basis of our understandingof fluorides effect on the caries process, it is apparent that,in the past, it was considered to be essentially systemic inaction, but now is considered to be primarily a topical agent

(Featherstone, 1999).Water fluoridation and F dentifrice are recognized asthe most effective methods to control caries (Ellwood andFejerskov, 2003). Fluoridated water had a relevant role in cariescontrol until the 1980s-90s, when, in some countries, it was theonly source of fluoride at the community level, and it is stillconsidered important for many countries (see other articles inthis issue). Since the 1990s, however, the widespread use ofF dentifrice has had a tremendous effect on caries decline atthe population level (Rlla et al., 1991). The epidemiologicalchanges in caries promoted by F from drinking water ordentifrices have been observed both in developed (Brunelleand Carlos, 1990; Rlla et al., 1991)and developing countries.Brazil is an example of a developing country in which the anti-caries benefits of these two sources of F delivery are clearly

evident (Cury et al., 2004). Thus, caries decline has occurredin Brazil in two phases (steps)one from 1970 to 1980 andanother after 1990which may be attributed to the programof water fluoridation and the widespread use of F dentifrice,respectively. Currently, 45% of the Brazilian population hasaccess to water fluoridation, mostly in south and southeastregions, but all dentifrices are fluoridated (90% containingMFP, i.e., sodium monofluorophosphate).

However, fluoridated water and F dentifrice are stillconsidered, respectively, systemic and topical methods of Fuse, which clouds the explanation of how these apparentlydifferent sources of F work efficiently on caries control by thesame mechanism. Rationally, this may be facilitated by ourunderstanding of the disease and how F may interfere with it.

Dental CariesThere is evidence to support dental caries as a dietary

carbohydrate-modified bacterial infectious disease (vanHoute, 1994). Its key feature is a dietary carbohydrate-inducedenrichment of the plaque microbiota with organisms such asmutans streptococci and lactobacilli, which causes an increaseof plaques pH-lowering and cariogenic potential. Amongthe dietary carbohydrates, sucrose is considered the mostcariogenic, due to the changes provoked in plaque (biofilm)matrix composition (Rlla, 1989), which depend on theconcentration and frequency of sucrose use (Cury et al., 1997;Aires et al., 2006; Ccahuana-Vsquez et al., 2006).

Changes in the mineral structure of the enamel depend onthe equilibrium between demineralization and remineralizationprocesses occurring in dental biofilm fluid. Thus, every timesugar penetrates a cariogenic biofilm and is converted toacids by bacterial metabolism, the biofilm fluid becomes

undersaturated with respect to enamel solubility properties,and demineralization occurs (Dawes, 2003). A critical lowpH for tooth dissolution is maintained for a certain time, butit returns to physiological values when exposure to sugarceases. Therefore, when the pH is raised and supersaturatingconditions are again reached, a certain amount of mineral losscan be recovered by enamel, and this process has been namedremineralization, a well-known salivary phenomenon.

Ideally, any disease control should focus on the etiologicalfactors involved, and for caries this would be the removal(or regular disorganization) of dental biofilm, and dietarycounseling. However, the success of these strategies has beenshown to be limited (Duggal and van Loveren, 2001; Nyvad,2003), reinforcing the use of F as the most relevant method forcontrolling caries. In contrast, the mechanism explaining how

F works to control this disease is not that hypothesized whenthe anti-caries benefits of F added to the water supply weredemonstrated (Fejerskov et al., 1981).

How Fluoride Controls CariesToday, there is consensus that the predominant effect of F isnot systemic, pre-eruptively changing enamel structure, butmainly local, interfering with the caries process. Hence, Fmust be present in the right place (biofilm fluid, saliva) andat the right time (sugar exposure) to interfere with de- andremineralization events. For this effect, even sub-ppm valuesof available F are effective.

Thus, as described previously, enamel is dissolved by thelow pH reached in dental plaque due to acid production every

time sugar is ingested (Fig. 1). However, if F is present in thebiofilm fluid, and the pH is not lower than 4.5, at the same

How to Maintain a Cariostatic FluorideConcentration in the Oral Environment

J.A. Cury*, L.M.A. Tenuta

Piracicaba Dental School, University of Campinas, Piracicaba, SP, Brazil;

*corresponding author, [email protected]

Adv Dent Res 20:13-16, July, 2008

Key Words

Fluoride, caries, dentifrice, drinking water.

Presented at a symposium entitled Fluoride and Caries Decline,sponsored by the IADR Cariology Research, Behavioral, Epidemiologic& Health Services Research, and Pharmacology/Therapeutics/Toxicology Groups, presented during the 35th Annual Meeting ofthe American Association for Dental Research and the 83rd AnnualSession of the American Dental Education Association, March 9, 2006,Orlando, Florida, USA, and supported by the Colgate-Palmolive Co.

13by on April 19, 2010http://adr.sagepub.comDownloaded from
http://adr.sagepub.com/http://adr.sagepub.com/http://adr.sagepub.com/


2/4

14 Cury & Tenuta Adv Dent Res 20:13-16, July, 2008

time that hydroxyapatite (HA) is dissolved, fluorapatite (FA)is formed (ten Cate et al., 2003). The net result is a decrease inenamel dissolution, since a certain amount of calcium (Ca) andinorganic phosphorus (Pi) that was lost as HA is recovered byenamel as fluorapatite.

This indirect effect of F reducing enamel demineralizationwhen the pH drops is complemented by its effect onremineralization when the pH rises (Fig. 2). It is well-knownthat saliva is able to remineralize enamel (Edgar and Higham,1995), but this effect is enhanced in the presence of F (Dijkmanet al., 1990). Consequently, small amounts of Ca and Pi lost byenamel during the pH drop can be more efficiently recoveredif F is still present in the oral environment after the cariogenicchallenge.

This physicochemical effect of F, reducing demineralizationand enhancing remineralization of dental enamel (or dentin),could be supplemented by some antibacterial effect if anappropriate concentration of F can be maintained in the oralenvironment (see other articles in these Proceedings) by thecurrent methods of F use.

Therefore, although F does not have a direct effect onthe etiological factors responsible for the disease, by reducingtooth demineralization and enhancing remineralization, Fis extremely effective in helping saliva to control the caries

process, resulting in reduction of caries lesions. If the current

methods of F use were able to interfere with biofilm formationor its metabolism when dietary sugars are consumed, thedisease could be controlled more efficiently.

Nevertheless, the aim is the maintenance of a constant lowlevel of F in the oral environment, and this could be achievedby any method of F administration, either systemic or topic.Also, if this is acceptable, the classification of methods of F useshould be re-evaluated, since it is conceptually misleading.Among these different methods of F delivery (Ellwood andFejerskov, 2003), drinking water and dentifrices presentunique properties to control the caries process, since the oralenvironment is daily exposed to low concentrations of F.

Water Fluoridation

In individuals drinking fluoridated water and eating a normaldiet, the baseline F concentration in saliva is higher thanthat found in persons exposed to F-deficient water (Olivebyet al., 1990). Actually, blood is considered as the centralcompartment responsible for F distribution to any part ofthe organism and, of course, to the oral cavity (Fig. 3). Wheneither optimally fluoridated water or food prepared with it isingested, a transient increase in salivary F levels is observed.Absorbed F will be taken up by bone, especially in children,

in whom newly forming bone canretain up to 90% of the absorbed F,compared with 50% in adults. Fromthe sub-compartment of bone thatundergoes constant remodeling, F can

return to the blood. Thus, an increasedblood concentration is maintainedby both daily F intake and exchangewith F accumulated in remodelingbone. As a consequence, with regularintake, salivary F concentration ismaintained at a higher level, reflectingF concentrations in the blood.However, there is no homeostaticmechanism to maintain bloodfluoride concentration (Waterhouseet al., 1980), and, consequently, thesalivary F steady state is dependenton F intake.

Thus, when the external supply

Fig. 1 -Enamel demineralization in the presence of F in dental biofilm. Sugars(sucrose, glucose, fructose) are converted to acids in the biofilm. When thepH decreases to below 5.5, undersaturation with respect to hydroxyapatite(HA) is reached in the biofilm fluid, resulting in mineral dissolution. However,if the pH is higher than 4.5 and in the presence of F, the biofilm fluid issupersaturated with respect to fluorapatite (FA), and there is reprecipitation ofminerals in enamel. As a consequence, net demineralization is reduced.

Fig. 2 -Enamel remineralization in the presence of F in dental biofilm. Afterexposure to sugars has ceased, acids in the biofilm are cleared by saliva andconverted to salts. As a result, the pH increases, and at pH 5.5 or above, thebiofilm fluid is supersaturated with respect to HA and FA. Thus, Ca and Pi lostby enamel can be more efficiently recovered if F is still present in the biofilm.

Fig. 3 -Schematic illustration of how fluoride levels from drinking water intake are kept constant in the oralenvironment.

by on April 19, 2010http://adr.sagepub.comDownloaded from
http://adr.sagepub.com/http://adr.sagepub.com/http://adr.sagepub.com/


3/4

Adv Dent Res20:13-16, July, 2008 Maintaining a Cariostatic F Concentration in the Oral Environment 15

of F is interrupted, the concentration in the blood decreases,as well as that in the exchangeable bone sub-compartment(Rao et al., 1995). Since this decrease in F concentration in thebone sub-compartment can last several days (Likins et al., 1956;Zipkin et al., 1956), an apparent equilibrium may be suspected,but in fact does not exist. As a result, the higher F concentrationin saliva can no longer be sustained.

If this model is valid, an optimal level of F could not bemaintained in dental biofilm (the right place!) if the supply offluoridated water is interrupted. In fact, the concentration ofF in dental biofilm of children drinking optimally fluoridatedwater decreased almost 20-fold when the ingestion ceased

(Nobre dos Santos and Cury, 1988) (Table 1). This interruptionwas transient, lasting 6 months, and after intake from waterfluoridation resumed, the F concentration in dental biofilmreturned to the same level found previously (Cury, 1989).Analysis of these data gives support to the absence of ahomeostatic mechanism to control F in the oral environment,as opposed to Ca, which did not decrease significantly duringthis period (unpublished observations). Also, the findingssupport past epidemiological data showing a caries increasewhen children living in areas with high F concentration in thewater moved to low-F areas (Fejerskov et al., 1981).

It should be emphasized, however, that the example inTable 1 illustrates the need for constant exposure to fluoridatedwater in a region where, 20 years ago, the only source ofcommunity F was drinking water. It is important to notice that

F levels in the dental biofilm were shown to be maintained,even after interruption of water fluoridation, in a low-cariespopulation using F dentifrice on a regular basis (Sepp et al.,1996). This means that an additive effect on F concentrationin the biofilm would not be expected to occur when thesemethods of F delivery are simultaneously available.

Furthermore, it should be cautioned that this approachto explaining how F from drinking water fits the currentconcepts on the mechanism of action of F may not be used torecommend any other method of F ingestion (i.e., supplements),since water fluoridation is unique as a public health strategyfor F delivery.

Fluoride Dentifrice

Similarly to fluoridated water ingestion, the concentrationof F in saliva increases every time teeth are brushed withF-containing dentifrice. After 3 min, the F concentration insaliva is more than 100 times higher than the baseline value,but after 2 hrs, it returns almost to baseline values (Bruun et al.,1984; Duckworth and Morgan, 1991).

However, during toothbrushing, F is spread throughoutthe oral cavity and is stored in some compartments (Ekstrandand Oliveby, 1999), such as the enamel surface and anyremaining dental biofilm. In this way, after toothbrushing,salivary clearance dilutes the residual F in saliva, but theenamel surface and remaining biofilm are able to take upfluoride, as calcium-fluoride (CaF2)-like deposits, maintainingcertain F levels in the right place to control caries. Thesereservoirs would release F to the fluid of the biofilm during

pH-cycling due to sugar exposure (Rlla et al., 1993; ten Cate,1997), reducing enamel demineralization and enhancing itsremineralization.

If this is true, F should be found in dental biofilm eithersoon after toothbrushing or preferably for longer periods. Inan in situ study, 10 hrs after toothbrushing, the F concentrationin dental biofilm of the group using F dentifrice was 30 timeshigher than that found in the control group (Paes Leme etal. , 2004) (Table 2). Also, even 14 days after APF fluoride

application, which forms a high quantity of CaF2-like deposits,a high concentration of F was found in the biofilm (Table2). Thus, the effect on reduction of enamel demineralizationobserved could be attributed to this residual F maintained inthe biofilm by these modes of F use.

ConclusionSince F must be available in the biofilm to interfere with thecaries process, systemic and topical F act in caries controlessentially by the same mechanism, differing only in the mannerin which F is maintained in the oral environment between theintervals of intake/use. Exchangeable bone deposits of F mayfunction as a fluorapatite reservoir and release F to the blood,from where it will be subsequently released to saliva. Also,

CaF2-like deposits on the tooth surface and biofilm increaseF availability in the biofilm fluid at times after the use of Fproducts. Therefore, the effect of an anti-caries regimen maybe limited by F storage in these different reservoirs. Oncefluoridated water or F-dentifrice is no longer used, its protectiveeffect cannot be maintained, since the reservoirs will beexhausted within several days, and F would not be available inthe oral environment to interfere with de- and remineralizationprocesses. This would explain why slow-fluoride-release devicesare effective in caries control (Toumba, 2001).

ReferencesAires CP, Tabchoury CP, Del Bel Cury AA, Koo H, Cury JA (2006).

Effect of sucrose concentration on dental biofilm formed in situ

and on enamel demineralization. Caries Res40:28-32.Brunelle JA, Carlos JP (1990). Recent trends in dental caries in US

children and the effect of water fluoridation.J Dent Res 69:723-727.Bruun C, Givskov H, Thylstrup A (1984). Whole saliva fluoride after

toothbrushing with NaF and MFP dentifrices with different Fconcentrations. Caries Res 18:282-288.

Ccahuana-Vsquez RA, Vale GC, Tabchoury CPM, Tenuta LMA,Del Bel Cury AA, Cury JA (2007). Effect of frequency ofsucrose exposure on dental biofilm composition and enameldemineralization in the presence of fluoride. Caries Res 41:9-15.

Cury JA (1989). Fluoride use. In: Operative dentistry: preventive andrestorative procedures. Baratieri LN, editor. Rio de Janeiro: EditoraSantos, pp.43-67 [in Portuguese].

Cury JA, Rebello MA, Del Bel Cury AA (1997). In situ relationshipbetween sucrose exposure and the composition of dental plaque.

TABLE 1. Means SD of Fluoride Concentration in DentalPlaque from Schoolchildren According to the Conditions

of Water Fluoridation (Piracicaba, SP, Brazil, 1986-1987)

Water Fluoridation Status mg F/g Biofilm Wet Weight

Fluoridated (0.8 ppm F) 3.2 1.8 (n = 91)

Interrupted (0.06 ppm F) 0.2 0.09 (n = 41)

Re-fluoridated (0.7 ppm F) 2.6 1.9 (n = 55)

TABLE 2. Means SD (n=15) of Fluoride Concentration

in Dental Biofilm and Enamel Demineralization (DZ),According to the Treatments

Treatments mg F/g Biofilm Wet Weight DZa

Non-F dentifrice (control) 1.5 0.5 1253.6 697.2

APFb+ non-F dentifrice 7.1 12.0 971.4 671.5

F dentifrice 46.6 46.6 405.4 216.4

a

Area of mineral loss as measured by cross-sectional microhardness determination(Paes Leme et al., 2004).b APF = acidulated phosphate fluoride (one application at the beginning of the study).

http://adr.sagepub.com/http://adr.sagepub.com/http://adr.sagepub.com/http://adr.sagepub.com/


4/4

16 Cury & Tenuta Adv Dent Res 20:13-16, July, 2008

Caries Res 31:356-360.Cury JA, Tenuta LMA, Ribeiro CCC, Paes Leme AF (2004). The

importance of fluoride dentifrices to the current dental cariesprevalence in Brazil. Braz Dent J 15:167-174.

Dawes C (2003). What is the critical pH and why does a tooth dissolvein acid?J Can Dent Assoc 69:722-724.

Dijkman A, Huizinga E, Ruben J, Arends J (1990). Remineralization ofhuman enamel in situ after 3 months: the effect of not brushingversus the effect of an F dentifrice and an F-free dentifrice. CariesRes 24:263-266.

Duckworth RM, Morgan SN (1991). Oral fluoride retention after use of

fluoride dentifrices. Caries Res 25:123-129.Duggal MS, van Loveren C (2001). Dental considerations for dietarycounselling. Int Dent J 51:408-412.

Edgar WM, Higham SM (1995). Role of saliva in caries models. AdvDent Res 9:235-238.

Ekstrand J, Oliveby A (1999). Fluoride in the oral environment. ActaOdontol Scand 57:330-333.

Ellwood R, Fejerskov O, Cury JA, Clarkson B (2008). Fluoride in cariescontrol. In: Dental caries: the disease and its clinical management.Fejerskov O, Kidd E, editors. 2nd ed. Oxford: BlackwellMunksgaard, pp. 287-323.

Featherstone JD (1999). Prevention and reversal of dental caries: role oflow level fluoride. Community Dent Oral Epidemiol 27:31-40.

Fejerskov O, Thylstrup A, Larsen MJ (1981). Rational use of fluoridesin caries prevention. A concept based on possible cariostatic

mechanisms.Acta Odontol Scand 39:241-249.Likins RC, McClure FJ, Steere AC (1956). Urinary excretion of fluoride

following defluoridation of a water supply. Public Health Rep71:217-220.

Nobre dos Santos M, Cury JA (1988). Dental plaque fluoride is lowerafter discontinuation of water fluoridation. Caries Res 22:316-317.

Nyvad B (2003). The role of oral hygiene. In: Dental caries: the diseaseand its clinical management. Fejerskov O, Kidd EAM, editors.Copenhagen: Blackwell Munksgaard, pp. 171-177.

Oliveby A, Twetman S, Ekstrand J (1990). Diurnal fluorideconcentration in whole saliva in children living in a high- and alow-fluoride area. Caries Res 24:44-47.

Paes Leme AF, Dalcico R, Tabchoury CP, Del Bel Cury AA, RosalenPL, Cury JA (2004). In situ effect of frequent sucrose exposure onenamel demineralization and on plaque composition after APFapplication and F dentifrice use.J Dent Res 83:71-75.

Rao HV, Beliles RP, Whitford GM, Turner CH (1995). A physiologicallybased pharmacokinetic model for fluoride uptake by bone. RegulToxicol Pharmacol 22:30-42.

Rlla G (1989). Why is sucrose so cariogenic? The role of gluco-

syltransferase and polysaccharides. Scand J Dent Res 97:115-119.Rlla G, Ogaard B, Cruz RA (1991). Clinical effect and mechanism ofcariostatic action of fluoride-containing toothpastes: a review. IntDent J 11:442-447.

Sepp L, Hausen H, Karkkainen S (1996). Plaque fluoride and mutansstreptococci in plaque and saliva before and after discontinuationof water fluoridation. Eur J Oral Sci 104:353-358.

ten Cate JM (1997). Review on fluoride, with special emphasis oncalcium fluoride mechanisms in caries prevention. Eur J Oral Sci105:461-465.

ten Cate JM, Larsen MJ, Pearce EIF, Fejerskov O (2003). Chemicalinteractions between the tooth and oral fluids. In: Dental caries:the disease and its clinical management. Fejerskov O, Kidd EAM,editors. Copenhagen: Blackwell Munksgaard, pp. 49-69.

Toumba KJ (2001). Slow-release devices for fluoride delivery to high-

risk individuals. Caries Res 35 (Suppl 1):10-13.van Houte J (1994). Role of micro-organisms in caries etiology. J Dent

Res 73:672-681.Waterhouse C, Taves D, Munzer A (1980). Serum inorganic fluoride:

changes related to previous fluoride intake, renal function andbone resorption. Clin Sci (Lond) 58:145-152.

Zipkin I, Likins RC, McClure FJ, Steere AC (1956). Urinary fluoridelevels associated with use of fluoridated waters. Public Health Rep71:767-772.

http://adr.sagepub.com/http://adr.sagepub.com/http://adr.sagepub.com/http://adr.sagepub.com/

Artículo 3 - Fluor (Cury-Tenuta 2008)

Documents

Transcript of Artículo 3 - Fluor (Cury-Tenuta 2008)