887

2000;131;887-899 J Am Dent Assoc

JOHN D.B. FEATHERSTONE CARIES PREVENTION

THE SCIENCE AND PRACTICE OF

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JADA, Vol. 131, July 2000 887

Although the prevalence of dental

caries in children has declined

markedly over the last 20 years in

most countries in the Western world,

the disease continues to be a major problem for both adults

and children everywhere.

The trends in caries in U.S. children during the last 30

years were recently summarized1 on the basis of results of

four national surveys.2-5 By the late 1980s, although

approximately 75 percent of children aged 5 to 11 years

were caries-free, about 70 percent of the 12- to 17-year-olds

still had caries. Approximately 25 percent of children and

adolescents in the 5- to 17-year age range accounted for 80

percent of the caries in permanent teeth. By age 17 years,

however, 40 percent of the population accounted for 80 per-

cent of the caries.1-6 These findings illustrate the need for

management of caries by individual risk assessment and

for measures more specifically directed to high-risk people

and populations.

Although these prevalence rates still leave much to be

desired, the overall caries prevalence in children has

indeed declined in the United States. Smaller epidemiolog-

ic studies in recent years indicate, however, that the

decline in caries has not continued during the 1990s and

that it may have plateaued.6

THE SCIENCE AND PRACTICEOF CARIES PREVENTIONJOHN D.B. FEATHERSTONE, M.SC., PH.D.

Background and Overview. Dentalcaries is a bacterially based disease. Whenit progresses, acid produced by bacterialaction on dietary fermentable carbohy-drates diffuses into the tooth and dis-solves the carbonated hydroxyapatite min-eral—a process called demineralization.Pathological factors including acidogenicbacteria (mutans streptococci and lacto-bacilli), salivary dysfunction, and dietarycarbohydrates are related to caries pro-gression. Protective factors—whichinclude salivary calcium, phosphate andproteins, salivary flow, fluoride in saliva,and antibacterial components or agents—can balance, prevent or reverse dentalcaries.Conclusions. Caries progression orreversal is determined by the balancebetween protective and pathological fac-tors. Fluoride, the key agent in battlingcaries, works primarily via topical mech-anisms: inhibition of demineralization,enhancement of remineralization andinhibition of bacterial enzymes.Clinical Implications. Fluoride in drink-ing water and in fluoride-containingproducts reduces caries via these topicalmechanisms. Antibacterial therapy mustbe used to combat a high bacterial chal-lenge. For practical caries managementand prevention or reversal of dentalcaries, the sum of the preventive factorsmust outweigh the pathological factors.

A B S T R A C T

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The reasons for the reduc-tions in caries prevalence dur-ing the last 20 years are diffi-cult to pinpoint. Strong evi-dence exists, however, that thenear universal use of fluoride-containing products such asdentifrice, mouthrinses and top-ical gels applied in the dentaloffice have been major contribu-tors.7,8 Earlier caries reductionsof 40 to 70 percent (before the1970s) had resulted from thefluoridation of public water sup-plies in many communities.9-12

Dental caries in adults alsocontinues to be a major prob-lem, as illustrated by a recentU.S. survey.13 The surveyreported that 94 percent of alldentate adults (aged 18 yearsor older) had evidence of treat-ed or untreated coronal caries.

Caries obviously still is amajor problem in adults, aswell as children, and we needan improved approach to pre-vention and therapy. This arti-cle reviews and summarizes thescientific basis for and practiceof successful intervention in the caries process.

THE CARIES PROCESS

Bacterial plaque and acidproduction. The caries processis now well-understood; much ofit has been described extensivelyin the dental literature. Somedetails of the caries processremain to be unraveled, but, ingeneral, we understand theprocess well enough to initiatebetter-targeted methods of cariesprevention and intervention.

The mechanism of dentalcaries formation is essentiallystraightforward.1 Plaque on thesurface of the tooth consists of abacterial film that producesacids as a byproduct of itsmetabolism.14,15 To be specific,certain bacteria within the

plaque are acidogenic—that is,they produce acids when theymetabolize fermentable carbo-hydrates.12,14,15 These acids candissolve the calcium phosphatemineral of the tooth enamel ordentin in a process known asdemineralization.16-18 If thisprocess is not halted or re-versed via remineralization—the redeposition of mineral viasaliva—it eventually becomes afrank cavity.

Dental caries of the enameltypically is first observed clini-cally as a so-called “white-spotlesion.” This is a small area ofsubsurface demineralizationbeneath the dental plaque. The

body of the subsurface lesionmay have lost as much as 50percent of its original mineralcontent and often is covered byan “apparently intact surfacelayer.”19 The surface layer formsby remineralization. Theprocess of demineralization con-tinues each time there is carbo-hydrate taken into the mouththat is metabolized by the bac-teria. The saliva has numerousroles, including buffering (neu-tralizing) the acid and reminer-alization by providing mineralsthat can replace those dissolvedfrom the tooth during deminer-alization.1,20,21

Any fermentable carbohy-drate (such as glucose, sucrose,fructose or cooked starch) canbe metabolized by the acido-genic bacteria and create theaforementioned organic acids asbyproducts.22 The acids diffusethrough the plaque and into theporous subsurface enamel (ordentin, if exposed), dissociatingto produce hydrogen ions asthey travel.17,23 The hydrogenions readily dissolve the miner-al, freeing calcium and phos-phate into solution, which candiffuse out of the tooth. Mostimportantly, lactic acid dissoci-ates more readily than theother acids, producing hydrogenions that rapidly lower the pHin the plaque.17 As the pH islowered, acids diffuse rapidlyinto the underlying enamel ordentin.

The two most importantgroups of bacteria that predom-inantly produce lactic acid arethe mutans streptococci and thelactobacilli.14 Each group con-tains several species, each ofwhich is cariogenic. Mutansstreptococci include Strep-tococcus mutans and S. sobri-nus. The lactobacilli speciesalso are prolific producers oflactic acid and appear in plaquebefore caries is clinicallyobserved.24,25 These two groupsof bacteria, either separately ortogether, are the primarycausative agents of dentalcaries.

HOW FLUORIDECOMBATS THECARIES PROCESS

The ability of fluoride to pre-vent and arrest caries has beenresearched extensively. Fluo-ride has three principal topicalmechanisms of action:dinhibiting bacterial metabo-lism after diffusing into the

888 JADA, Vol. 131, July 2000

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The mutans streptococci andthe lactobacilli,

either separatelyor together, are

the primarycausative agents of

dental caries.



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bacteria as the hydrogen fluo-ride, or HF, molecule when theplaque is acidified;dinhibiting demineralizationwhen fluoride is present at thecrystal surfaces during an acidchallenge; denhancing remineralizationand thereby forming a low-solubility veneer similar to theacid-resistant mineral fluorap-atite, or FAP, on the remineral-ized crystals.

Inhibiting bacterialmetabolism. Several investiga-tors have studied the possibleeffects of fluoride on oral bacte-ria.26-28 The most significantfinding reported is that the ion-ized form of fluoride, or F-, can-not cross the cell wall and membrane but can rapidly trav-el into the cariogenic bacterialcells in the unchanged form asHF.26-28

When the pH in the plaquefalls as the bacteria produceacids, a portion of the fluoridepresent in the plaque fluid thencombines with hydrogen ions toform HF and rapidly diffusesinto the cell, effectively drawingmore HF from the outside.1,26-28

Once inside the cell, the HF dis-sociates, acidifying the cell andreleasing fluoride ions thatinterfere with enzyme activityin the bacterium. For example,fluoride inhibits enolase, anenzyme necessary for the bacte-ria to metabolize carbohydrates.As fluoride is trapped in thecell, the process becomes cumu-lative.

In summary, fluoride fromtopical sources is converted par-tially to HF by the acid that thebacteria produce and diffusesinto the cell, thereby inhibitingessential enzyme activity.

Inhibiting demineraliza-tion. The mineral of our teeth(enamel, cementum, dentin)

and bones is a carbonatedhydroxyapatite29 that can beapproximately represented bythis simplified formula:

Ca10-x(Na)x(PO4)6-y(CO3)z

(OH)2-u(F)u

The substitutions in thehydroxyapatite crystal lattice(the arrangement of atoms andions in the crystal) occur as themineral is first laid down dur-

ing tooth development, with thecarbonate (CO3) ion in particu-lar causing major disturbancesin the regular array of ions inthe crystal lattice.30,31 Duringdemineralization, the carbonateis lost, and during remineral-ization it is excluded from thenewly formed mineral. The cal-cium-deficient, carbonate-richregions of the crystal are espe-

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Figure 1. High-resolution electron microscope images (magnificationapproximately ¥2,000,000) of individual enamel crystals. The blacklines are rows of calcium atoms, which are visualized by this tech-nique. A. Normal enamel crystal showing white patches (arrows),which are calcium-deficient and carbonate-rich defect regions. B. Demineralized crystal from the body of a natural caries lesion showing “large” hexagonal holes coinciding with the “small” defectregions seen in normal enamel. (Adapted from Featherstone and col-leagues30,31 with permission from Karger, Basel.)

A

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cially susceptible to attack bythe acid hydrogen ions duringdemineralization, as has beenshown by several investiga-tors.21,29-33 High-resolution lat-tice imaging, which imagescrystals almost to atomic reso-lution (viewed at about ×2,000,000 magnification), wasused to illustrate the appear-ance of hexagonal holes in theearly stages of enamel crystaldissolution in dental caries(Figure 1), which coincided withthe calcium-deficient, carbon-ate-substituted regions of thecrystal.30-33

The carbonated hydroxyap-atite, or CAP, of our teeth ismuch more soluble in acid thanhydroxyapatite, or HAP (HAP = Ca10(PO4)6(OH)2), andthat in turn is much more solu-ble than fluorapatite, or FAP(FAP = Ca10(PO4)6F2),

21 in which

the OH- ion in pure hydroxyap-atite is completely replaced byan F- ion. The resulting mineralFAP is highly resistant to disso-lution by acid.

Fluoride inhibits demineral-ization. Sound enamel, exceptin its outer few micrometers,generally contains fluoride atlevels of about 20 to 100 partsper million, or ppm, dependingon the fluoride ingestion duringtooth development.34 Teeth inchildren who lived in areaswith fluoridated drinking waterduring tooth development havefluoride content toward thehigher end of this range. Theouter few micrometers of en-amel can have fluoride levels of1,000 to 2,000 ppm.34

Fluoride in the solution sur-rounding CAP crystals has beenshown to be much more effec-tive in inhibiting demineraliza-

tion than fluoride incorporatedinto the crystals at the levelsfound in enamel.21,35 Ten Cate,21

Nelson and colleagues35 andFeatherstone and colleagues36,37

found no measurable reductionin the acid solubility of synthet-ic CAP (3 percent CO3 byweight, comparable to that ofdental enamel mineral) withabout 1,000 ppm fluoride incor-porated. Importantly, thismeans that fluoride incorporat-ed during tooth mineral devel-opment at normal levels of 20to 100 ppm (even in areas thathave fluoridated drinking wateror with the use of fluoride sup-plements) does not measurablyalter the acid solubility of themineral. Even when the outerenamel has higher fluoride lev-els, such as 1,000 ppm, it doesnot measurably withstand acid-induced dissolution any betterthan enamel with lower levelsof fluoride. Only when fluorideis concentrated into a new crys-tal surface during remineraliza-tion is it sufficient to beneficial-ly alter enamel solubility. Thefluoride incorporated develop-mentally—that is, systemicallyinto the normal tooth mineral—is insufficient to have a measur-able effect on acid solubility.21,38

In contrast to the lack ofeffect of fluoride incorporatedinto the CAP crystals of toothmineral developmentally, as lit-tle as 1 ppm in the acid solutionreduced the dissolution rate ofCAP to a rate equivalent tothat of HAP.36 Further increas-es in fluoride in the acid solu-tion in contact with the CAPmineral surface decreased thesolubility rate logarithmically.These results indicate that iffluoride is present in the aque-ous solution surrounding thecrystals, it is adsorbed stronglyto the surface of CAP carbonat-

890 JADA, Vol. 131, July 2000

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00 5 10 15 20 25 30

TIME (MINUTES)

pH

Subjects withnormal salivary flow

who ingestedsucrose

Subjects withxerostomia

who ingestedsucrose

Subjects who ingesteda sugar-free

sweetened product

▲

Figure 2. Typical pH curves for normal subjects with normal salivaryflow and for subjects with xerostomia (mean for each group) afteringestion of sucrose. A curve for ingestion of a sugar-free sweetenedproduct is shown for comparison. (Reproduced from Featherstone1

with permission of the publisher. Copyright ©1999, Munksgaard.)



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ed apatite (enamel mineral)crystals and thus acts as apotent protection mechanismagainst acid dissolution of thecrystal surface in the tooth’ssubsurface region. If fluoride isin the plaque fluid at the timethat the bacteria generate acid,it will travel with the acid intothe subsurface of the tooth and,therefore, adsorb to the crystalsurface and protect it againstbeing dissolved.

In summary, fluoride presentin the water phase at low levelsamong the enamel or dentincrystals adsorbs to these crystalsurfaces and can markedlyinhibit dissolution of tooth min-eral by acid.21,36 Fluoride thatacts in this way comes from theplaque fluid via topical sourcessuch as drinking water andfluoride products. Fluorideincorporated during toothdevelopment is insufficient toplay a significant role in cariesprotection. Fluoride is neededregularly throughout life to pro-tect teeth against caries.

Enhancing remineraliza-tion. As the saliva flows overthe plaque and its componentsneutralize the acid, raising thepH (Figure 2), demineralizationis stopped and reversed. Thesaliva is supersaturated withcalcium and phosphate, whichcan drive mineral back into thetooth.21,39 The partially deminer-alized crystal surfaces withinthe lesion act as “nucleators,”and new surfaces grow on thecrystals (Figure 3). Theseprocesses constitute remineral-ization—the replacement ofmineral in the partially de-mineralized regions of the cari-ous lesion of enamel or dentin(including the tooth root).20,21

Fluoride enhances remineral-ization by adsorbing to the crys-tal surface and attracting calci-

um ions, followed by phosphateions, leading to new mineralformation. The newly formed“veneer” excludes carbonateand has a composition some-

where between HAP and FAPas described above (Figure 4).FAP contains approximately30,000 ppm F and has a verylow solubility in acid. The new

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Figure 3. High-resolution electron microscope images (magnificationapproximately ×2,000,000) of individual enamel crystals that visualizeremineralization at the atomic level. The black lines are rows of calciumatoms, which are visualized by this technique. A. Normal enamel crystaldissected from the inner region of enamel, showing “small” whitepatches of calcium-deficient, carbonate-rich regions. B. Crystal onwhich a “remineralized” surface veneer has been grown after treat-ment with fluoride, calcium and phosphate. (Adapted from Featherstoneand colleagues, 198130 with permission from Karger, Basel.)

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remineralized crystal now willbehave like low-solubility FAPrather than the highly solubleCAP of the original crystal surface.36

In summary, fluoride in solu-tion from topical sources en-hances remineralization byspeeding up the growth of anew surface on the partiallydemineralized subsurface crys-tals in the caries lesion. Thenew crystal surface veneer isFAP-like, with much lower sol-

ubility than the original CAPtooth mineral. Subsequent acidchallenges must be quite strongand prolonged to dissolve theremineralized enamel.

Saliva and caries. Saliva hasa critical role in the preventionor reversal of the caries process;it provides calcium, phosphate,proteins that maintain super-saturation of calcium in theplaque fluid, proteins and lipidsthat form a protective pellicleon the surface of the tooth, anti-

bacterial substances andbuffers.40 The saliva compo-nents neutralize the acids pro-duced by bacterial metabolismin the plaque, raise the pH andreverse the diffusion gradientfor calcium and phosphate.Thereby, they return calciumand phosphate to the subsur-face lesion, where these ionscan regrow new surfaces on thecrystal remnants that were pro-duced by demineralization.These so-called “remineralized”crystals have a veneer of muchless soluble mineral. Saliva alsoclears carbohydrates and acidsfrom the plaque.

In the case of salivary dys-function,41 all of the above bene-fits of saliva are reduced oreliminated (as is illustratedpartially in Figure 2 by the pHprofile of the subjects withxerostomia).

THE CARIES BALANCE

Fluoride’s three extensivelystudied and documented princi-pal mechanisms of action relyon the presence of fluoride insaliva, in the plaque at thetooth surface and in the fluidamong the crystals in the sub-surface of the enamel or dentin.The clinical effects of fluoride,therefore, can be optimized byusing delivery methods thatbring fluoride to the surface ofthe tooth and into the plaquerather than incorporating fluo-ride into the tooth mineral crys-tals during tooth development.These topical delivery methodsare equally applicable to adultsand children and include fluo-ride in beverages and foods,dental products and drinkingwater. The benefits of continu-ally providing low levels of fluo-ride in the saliva and plaquefrom the aforementioned topicalsources are described more fully

892 JADA, Vol. 131, July 2000

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Enamel crystal =carbonated apatite

ACIDPartly dissolved

crystal

Crystalnucleus

Remineralization Calcium +phosphate+ fluoride

Ca10 (PO4)6 (F)2 =fluorapatitelike

coating on crystals

Protective Factors

NO CARIES CARIES

Salivary flow and componentsProteins, antibacterial components and agentsFluoride, calcium and phosphateDietary components: protective

Reduced salivary functionBacteria: mutans streptococci, lactobacilliDietary components: frequency carbohydrates

Pathological Factors

Figure 4. Schematic representation of demineralization followed byremineralization in the caries process. If remineralization is successful,the final result is a crystal with a surface veneer of “fluorapatitelike”mineral of low solubility. (Reproduced from Featherstone1 with permis-sion of the publisher. Copyright ©1999, Munksgaard.)

Figure 5. The caries balance: a schematic diagram of the balancebetween pathological and protective factors in the caries process.(Reproduced from Featherstone1 with permission of the publisher.Copyright ©1999, Munksgaard.)



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in a recent review article.1

Pathological and protec-tive factors in the caries bal-ance. Caries progression, asopposed to reversal, consists ofa delicate balance between theaforementioned factors—name-ly, a bacterially generated acidchallenge and a combination ofdemineralization inhibition andreversal by remineralization.1,42

The balance between pathologi-cal factors (such as bacteria andcarbohydrates) and protectivefactors (such as saliva, calcium,phosphate and fluoride) is adelicate one that swings eitherway several times daily in mostpeople (Figure 5).

Protective factors. Saliva isessential for the protection ofthe tooth against dental cariesand provides many natural pro-tective factors summarized ear-lier,40,41 including calcium, phos-phate, antibacterial componentsand other proteins with variousfunctions. Extrinsic antibacteri-al agents such as chlorhexidinealso can be considered as pro-tective factors in this balance,as can fluoride from externalsources. The mechanisms ofaction of fluoride described inthis article apply primarily tofluoride from topical sources;systemically incorporated fluo-ride has only a minor role inprotecting against dental caries.This conclusion is supported notonly by laboratory data asdescribed previously, but alsoby epidemiologic studies. Forexample, a four-year study inEngland found a 27 percentlower caries incidence amongchildren who were 12 years oldwhen water fluoridation beganin their communities, relativeto the incidence in control sub-jects of the same age in nonfluo-ridated areas.43 This was a well-conducted study, and it clearly

showed the posteruptive (topi-cal) effects of fluoride in thedrinking water. Other studieshave illustrated the weak pre-eruptive effects of fluoride. Forexample, in two groups ofOkinawa nursing students aged18 to 22 years, there was no dif-ference in caries status betweenthose who had received fluori-dated water only until about 5to 8 years of age (and nonethereafter) and those who hadnever received fluoridateddrinking water.44

The cariostatic effects of fluo-ride are, in part, related to thesustained presence of low con-centrations of ionic fluoride inthe oral environment,1,21,38

derived from foods and bever-ages, drinking water and fluo-ride-containing dental productssuch as toothpaste. Prolongedand slightly elevated low con-centrations of fluoride in thesaliva and plaque fluid decreasethe rate of enamel demineral-ization and enhance the rate ofremineralization.21,36,38,45-48 Forexample, fluoride at 0.04 ppmin saliva can enhance reminer-alization. Remineralization ofearly lesions also requires calci-

um and phosphate, which arederived primarily from salivaand plaque fluid.

Pathological factors. Patho-logical factors obviously includecariogenic bacteria and the fre-quency of ingestion of ferment-able carbohydrates that sustainthese bacteria. The importanceof mutans streptococci (whichincludes S. mutans and S.sobrinus) in the development ofdental caries has been reviewedextensively.12,14,15,49,50 Numerouscross-sectional studies inhumans have shown that great-er numbers of mutans strep-tococci and lactobacilli in salivaor plaque are associated withhigh caries rates.15,25,49,51-54

Longitudinal studies haveshown that an increase overtime in numbers of both ofthese bacterial groups is associated with caries onset and progression.24,55,56

CARIES INTERVENTION

The methods of caries interven-tion can be summarized by join-ing the principal components ofthe caries process with theinterventional possibilities(Table).

Cariogenic bacteria andhigh bacterial challenge.Dental caries is a transmissible,bacterially generated disease.There is the mistaken beliefthat drilling out a caries lesionand placing a restoration elimi-nates the bacteria and therebystops caries progression. Al-though traditional restorativework may eliminate the bacte-ria at the site of the restoration,the remainder of the mouth isleft untouched, caries continuesunchecked in the remainder ofthe mouth and recolonizationcommences rapidly at the margins.57

It is logical, therefore, to use

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There is the mistaken beliefthat drilling out a caries lesion and placing a

restoration eliminates thebacteria andthereby stops

caries progression.



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antibacterial therapy—such astreatment with chlorhexidinegluconate rinse—as a caries-preventive measure. Althoughthis has been proposed formany years58-60 and used in sev-eral European countries, anantibacterial approach almostnever is used in the UnitedStates for the prevention of theprogression of dental caries.

One of the difficulties in per-suading clinicians to use theantibacterial approach is thatthere have not been rapid andaccurate methods of determin-ing the levels of cariogenic bac-teria in the mouth. Further-more, although numerous studies have indicated thatmutans streptococci and lacto-bacilli definitely are risk factorsfor dental caries, there is no

one-to-one direct correlationbetween levels of these bacteriaand caries progression.24,49

However, it now is well-estab-lished that high levels ofmutans streptococci, high levelsof lactobacilli or both constitutea “high bacterial challenge.”24

This bacterial challenge can bebalanced by the protective fac-tors described earlier, whichinclude salivary components—especially calcium, phosphateand fluoride—and the amountof saliva present.42

Figure 5 illustrates the bal-ance between pathological fac-tors (including cariogenic bacte-ria, reduced salivary functionand frequency of use of fer-mentable carbohydrates) andprotective factors. If thesepathological and protective fac-

tors are in balance, caries doesnot progress. If they are out ofbalance, caries either progressesor reverses.

Antibacterial therapy forcaries control. Currently, themost successful antibacterialtherapy against cariogenic bac-teria is treatment by chlorhexi-dine gluconate rinse or gel.47,61

Chlorhexidine is available byprescription in the UnitedStates. Studies have shown thata daily dose of chlorhexidinerinse for two weeks canmarkedly reduce the cariogenicbacteria in the mouth and that,as a result, recolonization takesplace in three to six monthsrather than immediately.58 Inpatients with high levels of bac-teria, therefore, chlorhexidinetreatments at three-month

894 JADA, Vol. 131, July 2000

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CARIES COMPONENT INTERVENTION METHOD

Bacteria

Carbonated Hydroxyapatite

Fermentable Carbohydrates

Organic Acids Produced byOral Bacteria

Saliva

Fluoride

SUMMARY: THE CARIES PROCESS AND METHODS OF CARIES INTERVENTION.

TABLE

Antibacterial therapy such as treatment withchlorhexidine gluconate (see text)

Make the mineral less soluble by transformingit to other crystalline forms such as hydroxy-apatite without carbonate (future caries-preventive treatments by specific laser irradia-tion will enable this to be done69,70)

Reduce the frequency of ingestion; substitutewith noncariogenic sweeteners (this method iswell-accepted and used in patient education)

Recommend use of sugar-free chewing gum,which reduces frequency of fermentable carbo-hydrate ingestion and also enhances reminer-alization

Neutralize the acid by providing extra buffer-ing or enhancing saliva; sugar-free gum assistsin this as well

Enhance the saliva flow and function

Exploit its known effects on bacteria, inhibi-tion of demineralization and enhancement ofremineralization by using “topical” fluoridedelivery by means of dental products, drinkingwater, beverages and foods



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intervals are indicated. The problem faced by clini-

cians is how to determine, in atimely fashion, whether thebacterial challenge is high,medium or low. For manyyears, commercial “dip slides”have been available in Europe,and they recently becameavailable in the UnitedStates.58 A saliva sample istaken from the patient andincubated on the dip slide; twodays later, a result is providedof the levels of S. mutans andlactobacilli bacteria in themouth.58 Although these slidesare a major advance in conven-ience and are the best toolsavailable at the time of thiswriting, it has been shownthat this technology is notwell-correlated with tradition-al bacterial plating. It is antic-ipated that methods of rapidchairside assessment of bacter-ial challenge, based on molecu-lar biology, will be available inthe future.

Several investigators haveexplored the possibility ofusing modern molecular biolo-gy for better and more rapidmethods of bacterial assess-ment,62 but they were unableto overcome a number of com-plications. An exciting devel-opment is work by Shi and col-leagues,63 who recently pub-lished a method using species-specific monoclonal antibodiesthat recognize the surface ofcariogenic bacteria. With thistechnology, it is not necessaryto split open the bacterial cellsto assess the internal DNA orRNA. These probes can betagged either with a fluo-rescent molecule or with amarker that can be measuredquantitatively in a simplespectrophotometer.

It is anticipated that these

probes will be available com-mercially in the near future,and that clinicians will be ableto use them chairside andobtain results within a fewminutes. This will enable clini-cians to determine the quanti-tative levels of bacteria in apatient’s mouth while he orshe is in the operatory and tofactor these numbers into anoverall risk assessment ofcaries for that patient. It isenvisaged that computer pro-grams will be available thatwill include the assay num-bers, as well as other data.The practitioner will receiveguidance as to the level of

caries risk and what regimenor regimens to use to preventfurther caries and to reducethe bacterial challenge. Withthe new monoclonal antibodyprobes, the levels of bacteriaand success of the interventioncould readily be followed overtime. This is an exciting, inno-vative tool that may becomewidely used and acceptedwithin a few years.

CARIES RISKASSESSMENT

Several studies have attempt-ed to determine risk factorsthat can be reliably used to

assess the level of risk ofcaries progression in individ-ual patients. Studies still areunder way, and there is nodefinitive formula yet avail-able. The status of risk assess-ment was summarized, how-ever, by the authors of a spe-cial supplement to TheJournal of the AmericanDental Association in 1995;this publication can be used asa guide until more definitiveinformation is available.64

Figure 5 represents a basis fordetermining caries risk withthe information currentlyavailable.

It has been established thathigh-risk patients includethose who have a high bacteri-al challenge, which may con-sist of a combination of highnumbers of mutans streptococ-ci, lactobacilli or both.Although fluoride has excel-lent properties in terms of bal-ancing caries challenge, if thechallenge is too high, thenfluoride—even at increasedconcentrations, with increaseduse or both—cannot balancethat challenge. Therefore, inthe case of high bacterial chal-lenge, the bacterial infectionmust be dealt with, typicallywith a chlorhexidine rinse, aswell as the enhancement ofsalivary action by topicaldelivery of fluoride. Theseprinciples apply equally wellto adults and children.Accurate detection of earlycaries can increase the relia-bility of caries risk assess-ment, particularly if thosemeasurements are made atthree- or six-month intervalsand caries progression can bemeasured. In the case of cariesprogression, obviously, inter-vention is needed either anti-bacterially, with fluoride or

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Methods of rapid chairsideassessment of

bacterial challenge, based

on molecular biology, will beavailable in the

future.



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with other techniques, some ofwhich are described in the fol-lowing material.

Caries management byrisk assessment. As thecaries risk assessmentmethodologies are refined, wewill have more definitive bio-logical and chemical riskassessment measures to guideclinical decision making.These measures form thebasis for assessing the direc-tion in which the caries bal-ance is likely to move for aparticular patient. Earlycaries detection, especially inocclusal surfaces, is an essen-tial part of caries managementby risk assessment.

Caries management by riskassessment now is receivingconsiderable attention, andsoftware programs are beingdeveloped that will aid practi-tioners in assessing risk andlead them to the use of cur-rent and new technologies byspecifying treatments recom-mended for the various riskcategories.59,60 As we move intothe future, tooth restorations

will become less and lessdesirable as a treatment andwill be used only as a finalresort when new interventionmeasures have failed or whenpeople have not participatedin caries intervention pro-grams such as those indicated previously.

CARIES MANAGEMENTTOOLS FOR THE FUTURE

Several technological advance-ments are currently close toclinical reality and will beembraced if they are provensuccessful.

Assessment of bacterialchallenge by chairsidemolecular probes. The use of chairside bacterial probesfor assessing a patient’s cario-genic bacterial challenge willbe an essential component ofcaries management by riskassessment.

Caries immunization. Ina program of caries manage-ment by risk assessment, it islogical that all available toolsshould be used. One such toolthat has been investigated for

many years is an immuniza-tion against caries. There aremany obstacles to the successof immunization, as caries isnot a systemic infection thatcan be dealt with simply byadministering a specific anti-biotic. The infection must bedealt with in the mouth, wherethe internal body fluids do notpass and, therefore, the normalimmune response is not rele-vant. However, IgA that is pro-duced by the saliva naturallycan interfere with the coloniza-tion of the surface of the toothby specific bacteria.

Recent studies by Ma andcolleagues 65,66 have illustratedthe effectiveness of specific IgAin the inhibition of recoloniza-tion of mutans streptococci.The next logical step is to usethis technology as one of thetools for caries intervention. Itis possible to use geneticallyengineered plants, such astobacco or alfalfa, to produceimmunoglobulins.66.67 A study isin progress at the University ofCalifornia, San Francisco, totest IgA that has been pro-duced using genetically engi-neered tobacco plants. At presstime, the results were notknown, but if the trial is suc-cessful, this IgA can be appliedto the teeth after chlorhexidinetreatment has removed the car-iogenic bacteria, with the aimof inhibiting future recoloniza-tion by mutans streptococci.

Early caries detectionand intervention. Successfuluse of the innovative methodsdescribed here for caries inter-vention will require accuratemethods for the early detectionof dental caries in enamel and dentin. Early-detectionmethods such as fluorescence, optical coherence tomography,electrical impedance and

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Pulsed laser light with highabsorption coefficient

Removes carious tissue;minimal heat deposition

Walls of preparation heatedto 800-900 C

Heat conduction

Pulp temperature rise < 4 C

Enamel

Dentin

Pulp

Figure 6. Schematic diagram showing the potential use of specificlasers for precise removal of carious enamel and modification of thesurrounding enamel for prevention of further caries progression afterrestoration. The laser would be set first to remove a minimum of cari-ous tissue. Then the walls and base of the cavity preparation would betreated with the laser to inhibit subsequent caries progression.(Reproduced from Featherstone71 with the permission of the publisher.Copyright © 2000 Indiana University School of Dentistry.)



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ultrasonography are likely tobecome available for use by cli-nicians in the near future.68 Itwill be possible to detectlesions in the occlusal surfaceand to determine whether theyhave progressed into the dentinand, if so, how far. This is notpossible with current radio-graphic technology.

Once new methods are intro-duced for the early detection ofcaries, they can be used in twoopposing fashions. Clinicianswith traditional training arelikely to use these methods tointervene physically at an ear-lier stage with cariouslesions—drilling, filling andplacing restorations. This out-come is of concern, as manymore restorations would beplaced than may be necessary,which weakens the tooth struc-ture. Early detection and inter-vention by placing a restorationalso does not take advantage ofthe body’s natural protectivemechanisms of inhibition ofdemineralization and enhance-ment of remineralization viasaliva.

Alternatively, early detectionof caries can be used as anopportunity to promote re-mineralization via salivaryenhancement, use of topical fluoride and chlorhexidine andmeticulous oral hygiene. Inaddition, as innovative meth-ods for early caries interven-tion are introduced, the needfor restorations may be elimi-nated for many patients, there-by preserving the tooth struc-ture and halting or reversingprogression of dental caries.

Caries prevention bylaser treatment. In May 1997,the U.S. Food and DrugAdministration approved theuse of an erbium:yttrium-aluminum-garnet, or Er:YAG,

laser for use on teeth. This wasthe first approval for laser useon dental hard tissues. Thisapproval by the FDA was forthis particular laser to be usedfor the removal of dental cariesand the cutting of sound tissuebefore the placement of restora-tions. This event has usheredin a new era for lasers in den-tistry. Since then, other lasershave been approved for thesame purpose, and additionalhard-tissue uses are likely tobe approved in the future,including the use of lasers forthe inhibition of progression ofdental caries by altering thecomposition of surface enamel

or dentin mineral. Kantorowitz and colleagues69

and Featherstone and col-leagues70 have studied theeffects of lasers on hard tissuesfor almost 20 years. The overallobjective of these studies is toestablish the scientific basis forthe choice of laser parametersthat can be used clinically forthe prevention, removal ortreatment of caries lesions.Their studies have demonstrat-ed that specific pulsed carbondioxide, or CO2, laser treat-ment of dental enamel caninhibit subsequent carieslikeprogression in a severe de-

mineralization-remineraliza-tion model in the laboratory byup to 85 percent. They havedemonstrated that carbonate islost from the CAP mineral ofthe tooth during specific laserirradiation, making the miner-al highly resistant to dissolu-tion by acid. Although theyhave demonstrated in the labo-ratory, using pH cycling mod-els, that as little as 20 pulses of100 microseconds each can pro-duce a preventive effect similarto daily use of fluoride denti-frice, these promising andexciting results have not yetbeen tested in human mouths.70

For practical purposes, itwould be desirable to develop alaser that can remove carioustissue and subsequently beused to treat the walls of thearea from which carious tissueis removed to make themresistant to subsequent carieschallenge71 (Figure 6). Friedand colleagues72 recently pub-lished a report on a new CO2laser that efficiently removescarious tissue. After caries anda minimal amount of surround-ing tissue are removed, it willbe possible to change the laserparameters to perform caries-preventive treatment on thesame area. This would be fol-lowed by placement of a resin-based composite restoration,thereby inhibiting subsequentcaries around that restoration.For example, if an early oc-clusal lesion was detected (bythe new methods described pre-viously) that was deemed to bebeyond hope of remineraliza-tion, this lesion could be con-servatively removed with anappropriate laser. Then thesurrounding cavity preparationwalls could be treated for cariesprevention by the laser and asmall conservative restoration

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placed. The cavity walls will behighly resistant to acid attackand therefore resistant to sec-ondary caries. Providing bacter-ial intervention via chlorhexi-dine rinse was also part of thetreatment in the same patient,future caries would be unlikely.

SUMMARY ANDCONCLUSIONS

The mechanism of dental cariesis well-established to the pointwhere new approaches arebeing made for caries preven-tion based on a scientific under-standing of the processesinvolved. Several existingmethodologies are available toenable successful managementof dental caries by risk assess-ment. Understanding the bal-ance between pathological fac-tors and protective factors is the key. Beyond the well-established and currently usedmethods, some innovative andexciting techniques have shownearly research successes thatmost likely will be used forearly caries intervention in thefuture. These methods includefluoride therapy for inhibition ofdemineralization and enhance-ment of remineralization, mole-cular probes for the quantita-tive detection of cariogenic bac-teria at chairside, computerizedcaries risk assessment pro-grams, genetically engineeredIgA for inhibition of recoloniza-tion of cariogenic bacteria, spe-cific lasers for conservativeremoval of carious tissue andspecific lasers for the preven-tion of caries progression.

The use of these technologieswill require extensive retrainingof clinical dentists. But it willdramatically alter the way inwhich dentists diagnose, inter-vene, treat and manage caries,with major benefits to the oral

health of their patients. ■

Dr. Featherstone is a professor and thechair, Department of Preventive and Restorative Dental Sciences and Departmentof Dental Public Health and Hygiene, University of California, San Francisco, 707Parnassus Ave., Box 0758, San Francisco,Calif. 94143, e-mail “[email protected]”.Address reprint requests to Dr.Featherstone.

The author sincerely acknowledges contri-butions from numerous colleagues over manyyears to much of the work reviewed here.

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Documents

management of caries

caries progression

battling caries

prevalence of dental

reversal of dental caries

reverse dental caries

caries process plaque

overall caries prevalence