Denof r

V. Kim Kutsch, D

This study was presented to the Am

Chief Executive Officer, Oral BioTech

The Journal of Prosthetic

tal caries: An updated medical modelisk assessment

MDOral BioTech, Albany, Ore

Dental caries is a transmissible, complex biofilm disease that creates prolonged periods of low pH in the mouth, resulting ina net mineral loss from the teeth. Historically, the disease model for dental caries consisted of mutans streptococci andLactobacillus species, and the dental profession focused on restoring the lesions/damage from the disease by using a surgicalmodel. The current recommendation is to implement a risk-assessment-based medical model called CAMBRA (cariesmanagement by risk assessment) to diagnose and treat dental caries. Unfortunately, many of the suggestions of CAMBRAhave been overly complicated and confusing for clinicians. The risk of caries, however, is usually related to just a few commonfactors, and these factors result in common patterns of disease. This article examines the biofilm model of dental caries,identifies the common disease patterns, and discusses their targeted therapeutic strategies to make CAMBRA more easilyadaptable for the privately practicing professional. (J Prosthet Dent 2014;111:280-285)

Dental caries is a transmissible bio-film dysfunction of the teeth marked byprolonged periods of low pH, whichresults in a net mineral loss.1 Histori-cally, the disease model for dentalcaries consisted of mutans streptococ-ci and Lactobacillus species.2 However,more recent scientific evidence indicatesthat the disease is more complex thanthis model suggests and that it hastraits in common with other biofilmdiseases.

Biofilm research using DNA se-quencing identification of bacteria hasidentified some 40 bacterial speciesto date as having a role in dental caries,and that list continues to grow.In recent independent studies, Bifido-bacterium species, Scardovia wiggsiae,Slackia exigua, and Propionibacterium acid-ifaciens have been implicated.3-5 Next-generation sequencing technologiespromise to add to these species as thebiofilm model of dental caries becomesbetter understood. Dental caries alsohas potential systemic effects.6 Studiesfrom randomly collected coronary pla-que specimens during surgery indicatethat when found in the mouth, themost common oral bacteria found inthe coronary plaque is also Streptococcus

erican Aca

; Private

Dentis

mutans.6 The authors concluded that Smutans was responsible for most bac-terial endocarditis and that by com-parison, the presence of periodontalpathogens was negligible. S mutans isalso able to invade endothelial cellsdirectly by means of its cnm (collagen-binding protein) gene.7 Further studieshave also implicated caries-causingbacteria in impaired cognitive func-tion, ulcerative colitis, and acceleratedplaque growth after angioplasty.8-10

Dental caries also has apparent hered-itary characteristics and genetic associ-ations.11,12 Early studies found thatindividuals with the G20A poly-morphism for beta-defensin-1, a sali-vary bacteriolytic enzyme, had 5 timesthe decayed, missing, and filled teeth(DMFT) scores seen in those withother variations of this gene.11 Heredi-tary associations with the TAS2R38taste-bud gene increase the risk fordental caries.12 A recent genome-wide-association study indicated multiplegene site associations with an increasedrisk for caries, the strongest of whichwas LYZL2 (lysozyme-like 2), which en-codes another bacteriolytic enzyme.13

The data from this study also indi-cated 5 distinct patterns of decay

demy of Restorative Dentistry, Chicago, Ill, Feb

practice, Albany, Ore.

try

geographically in the mouth, with theLYZL2 gene being associated withcarious lesions only in the mandibularincisors.13 Additional genetic associa-tions have been attributed to a muta-tion in matrix metalloproteinase 13(MMP13) and the HLA antigen alleleHLA-DQ2.14,15 Regardless of howcomplex the biofilm disease model be-comes, however, dental caries stillmeans prolonged periods of low pH,resulting in a net mineral loss from theteeth. With the continued developmentof next-generation sequencing technol-ogies, examining the biofilm and itsmetabolic outcome differently will bepossible. Nyvad et al16 have exploredthe novel idea of viewing the biofilm asa single organism, as first proposed byBuchen.17 Biofilm is a collection ofdistinct and separate organisms, but itbehaves collectively as one superor-ganism. As such, it is less important toidentify which specific bacterial speciesare present. Instead, the authors pro-posed a metagenomic study to identifywhich genes were present in the biofilmin total. The genes that are active pro-duce the proteins resulting in metabolicoutput from the biofilm. In the case ofdental caries, the concern is that acid

ruary 2013.

Kutsch

April 2014 281

output creates prolonged periods oflow pH. Future dental caries biofilmresearch, therefore, should not befocused on specific bacteria but on thefunction and output of the biofilm.16

CARIES RISK ASSESSMENT

As the scientific evidence has grown,the dental profession has progressedfrom an intuitive model of medicine(educated guess; drill and fill lesions) toan empirical model (probabilisticmodel based on systematic reviews ofrandomized controlled trials; fluorideand nonfluoride anticaries therapies).Continued growth in the evidence basewill lead the profession into a future ofprecision medicine, in which the causeof a disease is known and can bemeasured and targeted for therapy.18

Results to date have been mixedregarding the sensitivity and specificityof various caries risk assessment (CRA)tools. Pediatricians who identified pla-que on the maxillary central incisors (acaries risk factor) in children duringwell-care visits had a 55% sensitivityand an 80% specificity.19 Another studyexamined the caries risk assessmenttool (CAT) of the American Academy ofPediatric Dentistry, independently ofsocioeconomic status, and comparedthe results with mutans streptococcalcultures. The CAT had a high sensitivityof 100% and a low specificity of 2.9%,whereas the mutans streptococcal cul-ture alone resulted in an 86.5% sensi-tivity and a 93.4% specificity. Themutans streptococcal culture aloneoutperformed the CAT.20 A studyexamining the Cariogram risk assess-ment tool over a 2-year period inschool-age children found both a highsensitivity (83%) and a high specificity(85%), and a strong correlation wasfound between caries risk profiles andcaries incidence after 2 years.21 A 6-yearretrospective analysis of the CAMBRA(caries management by risk assess-ment) CRA form reported a higherincidence of cavitated lesions amongthose assessed as being at extreme riskcompared with those diagnosed asbeing at low risk initially.22 Finally,

Kutsch

a systematic review of 4 CRA toolsconcluded that the evidence for thevalidity of existing systems for CRAis limited and that valid and reli-able methods for CRA are urgentlyneeded.23

CAMBRA is the next attempt toexplain the underlying risks and causesof dental caries in an individual.24

Identifying the risks allows for individ-ualized, targeted therapy. There areknown and validated common riskfactors for dental caries, as well asdisease indicators.22 The same 6-yearretrospective study examined 12 954individuals, and the odds ratios (ORs)of these factors and indicators havebeen established and validated.22 Thedisease indicators include visible cavi-tation or radiographic radiolucenciespenetrating to dentin (OR, 8.21), activewhite spot lesions (OR, 2.77), and ahistory of a restored cavity in the pre-vious 3 years (OR, 1.46). Risk factorsinclude noticeable plaque buildup onthe teeth (OR, 2.55), frequent snacking(OR, 1.77), hyposalivation (OR, 1.27),exposed roots (OR, 1.19), deep pitsand fissures (OR, 1.80), and recrea-tional drug use (OR, 1.95). These newdata have added to the factors andchanged the picture for dental caries,but this change has simplified thesituation for those in clinical practice.By identifying pattern recognition forcommon clinical causes of dentalcaries, the new factors include bacteria(either too much bacterial load or highacid output of the biofilm); diet (eitherexcessive sugar consumption or snack-ing too frequently); saliva (eitherhyposalivation or poor buffering ca-pacity); and genetics (multiple possibleassociative genes).

CAMBRA is a simple process, con-sisting of 3 separate steps: assessment,diagnosis, and prescription. CRA isperformed with a standardized CRAform. CRA forms are available from theAmerican Dental Association, the Cali-fornia Dental Association Foundation,the American Academy of PediatricDentistry, and other organizations.Assessment consists of identifyingknown risk factors for an individual

patient and noting any disease in-dicators. Various biometrics have beenused in clinical practice for dentalcaries, but most have involved culturingsaliva to measure mutans streptococcaland Lactobacillus levels. A current bio-metric uses the adenosine triphosphate(ATP) bioluminescence of a dentalbiofilm specimen, which correlates withoverall bacterial load and the func-tioning/metabolic output of the bio-film.25,26 High ATP presence indicateseither high bacterial load or highmetabolic output.27

One of the challenges of imple-menting CAMBRA in clinical practicestems from the lack of time available toperform this task, as it is usuallyassigned to an already burdened hy-giene appointment. A recent CRA formdeveloped for clinical practice ad-dresses this issue beginning with 3motivational interview questions, fol-lowed by the self-reporting of risk fac-tors by the patient (Fig. 1). This can beaccomplished in the reception areabefore a dental hygiene visit. The dentalprofessional can then identify diseaseindicators and discuss the risk factorswith the patient.2

The caries diagnosis is made byexamining all of the patient data: theCRA form, oral examination, radio-graphs, history, and any biometrics (ifused). The American Dental Associa-tion Council on Scientific Affairs pub-lished definitions for the various riskcategories for children and adults in aspecial supplement to the Journal of theAmerican Dental Association in 2006.28

Once the caries diagnosis is deter-mined, the next step is to design ther-apeutic strategies for the patient,specifically targeting individual risks.

Prescriptive strategies can be orga-nized into 3 categories: reparative stra-tegies, therapeutic materials, andbehavioral changes. Reparative strate-gies are well developed by the dentalprofession and include remineralizationand restoration. The best scientific evi-dence for remineralization is with fluo-ride, although most of the compellingscientific evidence is from studieson children, and the results are

1 Caries risk assessment form adapted for clinical practice.

282 Volume 111 Issue 4

extrapolated to all age groups.29,30

Whereas fluoridated water has beenfound to reduce the overall decay ratein populations, the best form of pro-fessionally applied fluoride is fluoride

The Journal of Prosthetic Dentis

varnish.31,32 Patient-applied fluoride isbest in the form of a 0.05% fluoriderinse or a 5000-ppm fluoride gel. Forpatients with a high risk of caries, therecommendation for fluoride varnish is

try

every 3 months; more frequent appli-cation does not add benefit.

Current remineralization researchalso involves several forms of cal-cium phosphate, including nanoparticle

Kutsch

April 2014 283

hydroxyapatite.33,34 Although more re-search is indicated, it has been found thatthe nanoparticle hydroxyapatite is bio-mimetic for the natural building blocks ofenamel and reduces biofilm formation.35

Restoration of active cavitated lesions isrequired. The clinician may elect to stagethe treatment of lesions in thepatientwitha high risk of caries, first restoring all le-sions with an intermediate material suchas glass ionomer cement while workingwith the patient tomodify the biofilm andbehaviors. Patients at high risk or extremerisk (such as, because of hyposalivation)may develop new lesions within 1 year,36

so it is appropriate to stage their restor-ative care.

Therapeutic strategies include an-timicrobial, metabolic, pH, andpotentially probiotic categories. Anti-microbial strategies typically include theuse of povidone-iodine, chlorhexidine,or sodium hypochlorite rinse. Biofilmsare resistant to change, and it may take2 or more years of using these rinses tomodify the biofilm and reduce the pa-tient’s caries risk.36 Whereas it isappropriate to use an antimicrobialagent for a patient with a high biofilmload, patients that lack a high biofilmload but have other risk factors may notbenefit from an antimicrobial strategy.One potential metabolic strategy forthe biofilm is xylitol. Xylitol hasbeen found to potentiate even smallamounts of fluoride, so it might bebeneficial to combine xylitol with fluo-ride strategies.37 However, there isconflicting evidence for xylitol; a recentstudy in adults found that long-termdaily use of xylitol mints alone did notdecrease the caries outcome in those athigh risk.38 This multisite study perhapsindicates that a 1-dimensional treat-ment of xylitol in patients with highcaries risk may not be effective given thecomplex biofilm nature of the cariesdisease. Conversely, numerous studieshave found that xylitol is an effectiveanticaries agent.39-41 Recently, a studyhas indicated that xylitol seems tohave an anticaries effect on rootsurface lesions in caries-active adults.42

Xylitol may be effective when applied ina combined approach with other

Kutsch

strategies targeted to the patient’s spe-cific risk factors but may be ineffectiveas a solo strategy. In addition, pHmodification may reverse both the se-lection pressure and therefore theoutput of the biofilm, with the addedbenefit that it also drives remineraliza-tion.1 For patients with inadequatesaliva, neutralization strategies supple-ment the protective role of the saliva.

Probiotics deserve mention. A pro-biotic is a therapeutic agent that con-sists of living microorganisms, primarilybacteria; that is safe for human con-sumption; and that when ingested hasbeneficial effects beyond just nutrition.The strategy is to influence the makeupof the biofilm by consuming less-pathogenic organisms. Probiotics havebeen used with great success in treatingconditions such as diarrhea and Crohndisease.43 In dental caries, the probioticmust be able to adhere to and integrateinto the biofilm, compete with andantagonize cariogens, and have low-acid-production metabolism. Althoughadditional research is indicated, pro-biotics offer a potential additionalstrategy for the future.44

Behavioral issues include strategies toalter behavior and also to account forrisks that cannot be modified. Some be-haviors are theoretically modifiable andsome are not. Diet and home care bothplay significant roles in dental caries.Excessive plaque buildup or bacterialload, accompanied by infrequentdisruption, leads to site-specific demin-eralization of the teeth. Home care in-structions such as daily brushing andflossing continue to be important. Di-etary issues tend to stem from excessivesugar intake or from snacking toofrequently. Both of these behaviorsshould be modifiable, but humanbehavioral change is not easy, nor is itlinear.45,46 In a recent clinical trial in pa-tients improving their oral hygiene be-haviors, some improved during the term,some stayed the same, and someimproved and then relapsed.47 Motiva-tional interview and wellness coachingprinciples can help patients manage theirown behavioral changes, but realisticallythese changes take time and consistent

reinforcement.48,49 A recent study alsoprovides some discouraging results; itfound that it is easier to change patients’alcohol intake than it is to change theirsugar consumption.50

Nonmodifiable issues typically involvemedication-induced hyposalivation, ag-ing, reduced cognitive or physical func-tion, and special needs. Hyposalivation isa significant risk factor for dental cariesand most often relates to medicationuse.51 The more medications involved,the greater the risk and severity ofhyposalivation.

Designing an appropriate andeffective treatment strategy for an indi-vidual patient is straightforward. Thecauses drive the treatment strategies.The patient in Figure 2 is at high risk fordental caries, as is the patient inFigure 3. However, the risk factorsassociated with these 2 patients aresignificantly different and require atargeted approach for their treatmentto be successful. If the patient has abacterial issue (see Fig. 2), it should beaddressed with antimicrobials, pHmodification, and home care in-structions. For the patient with a di-etary issue, the strategy should focus onmodifying their sugar consumption orsnacking habits. The patient withhyposalivation (see Fig. 3) will likelybenefit from maintaining hydrationlevels and from pH neutralization ma-terials, both of which support a healthyoral environment. The patient with agenetic risk for dental caries will beharder to diagnose but will benefit fromminimizing acid exposure during theday and maintaining good health. Forthe clinician, it is important to have anappreciation and understanding of thecomplexity of the dental caries biofilmdisease model. But perhaps moreimportantly, being able to identify thecommon disease patterns and associ-ated therapies presented in this articleshould make CAMBRA more easilyadaptable in clinical practice.

SUMMARY

Dental caries is a complex biofilmdisease with many associated risk

2 Patient with high caries risk with bacterial load and homecare risk factors.

3 Patient with high caries risk with medication-inducedxerostomia.

284 Volume 111 Issue 4

factors and disease indicators. Thedental profession has historicallytreated the disease by focusing onrestoring cavitated lesions. CAMBRA,an emerging philosophy, also includesidentifying specific risk factors and dis-ease indicators for an individual patientand designing targeted therapies toaddress those risks. CAMBRA providesthe next step toward precision medicineand the more effective treatment ofdental caries in clinical practice.

REFERENCES

1. Marsh PD. Dental plaque as a biofilm: thesignificance of pH in health and caries.Compend Contin Educ Dent 2009;30:76-90.

2. Kutsch VK, Young DA. New directions in theetiology of dental caries disease. J Calif DentAssoc 2011;39:716-21.

3. Beighton D, Al-Haboubi M, Mantzourani M,Gilbert SC, Clark D, Zoitopoulos L, et al.Oral Bifidobacteria: caries associated bacte-ria in older adults. J Dent Res 2010;89:970-4.

The Journal of Prosthetic Dentis

4. Tanner AC, Mathney JM, Kent RL Jr,Chalmers NI, Hughes CV, Loo CY, et al.Cultivable anaerobic microbiota of severeearly childhood caries. J Dent Res 2011;90:1298-305.

5. Wolff D, Frese C, Maier-Kraus T, Krueger T,Wolff B. Bacterial biofilm composition incaries and caries-free subjects. Caries Res2013;47:69-77.

6. Nakano K, Nemoto H, Nomura R, Inaba H,Yoshioka H, Taniguchi K, et al.Detection of oral bacteria in cardiovascularspecimens. Oral Microbiol Immunol2009;24:64-8.

7. Abranches J, Miller JH, Martinez AR,Simpson-Haidaris PJ, Burne RA, Lemos JA.The collagen-binding protein cnm is requiredfor Streptococcus mutans adherence to andintracellular invasion of human coronaryartery endothelial cells. Infect Immun2011;79:2277-84.

8. Chen X, Clark JJ, Naorungroj S. Oral health innursing home residents with different cogni-tive statuses. Gerodontol 2013;30:49-60.

9. Kojima A, Nakano K, Wada K, Takahashi H,Katayama K, Yoneda M, et al. Infection ofspecific strains of Streptococcus mutans, oralbacteria, confers a risk of ulcerative colitis.Sci Rep 2012;2:332.

try

10. Kesavalu L, Lucas AR, Verma RK, Liu L,Dai E, Sampson E, et al. Increased athero-genesis during Streptococcus mutans infection inApoE-null mice. J Dent Res 2012;91:255-60.

11. Ozturk A, Famili P, Vieira AR. The antimi-crobial peptide DEFB1 is associated withcaries. J Dent Res 2010;89:631-6.

12. Wendell S, Wang X, Brown M, Cooper ME,DeSensi RS, Weyant RJ, et al. Taste genesassociated with dental caries. J Dent Res2010;89:1198-202.

13. Shaffer JR, Feingold E, Wang X, Lee M,Tcuenco K, Weeks DE, et al. GWAS of dentalcaries patterns in the permanent dentition.J Dent Res 2013;92:38-44.

14. Tannure PN, Küchler EC, Falagan-Lotsch P,Amorim LM, Raggio Luiz R, Costa MC, et al.MMP13 polymorphism decreases risk fordental caries. Caries Res 2012;46:401-7.

15. Valarini N, Maciel SM, Moura SK,Poli-Frederico RC. Association of dentalcaries with HLA class II allele in Brazilianadolescents. Caries Res 2012;46:530-5.

16. Nyvad B, Crielaard W, Mira A, Takahashi N,Beighton D. Dental caries from a molecularmicrobiological perspective. Caries Res2013;47:89-102.

17. Buchen L. Microbiology: the new germtheory. Nature 2010;468:492-5.

18. Christensen CM. The innovator’s prescrip-tion. New York: McGraw-Hill; 2009. p. 43.

19. Dumas SA, Weaver KE, Park SY, Polk DE,Weyant RJ, Bogen DL. Accuracy of visibleplaque identification by pediatric cliniciansduring well-child care. Clin Pediatr 2013;52:645-51.

20. Yoon RK, Smaldone AM, Edelstein BL. Earlychildhood caries screening tools: a compari-son of four approaches. J Am Dent Assoc2012;143:756-63.

21. Campus G, Cagetti MG, Sale S, Carta G,Lingström P. Cariogram validity in school-children: a two-year follow-up study. CariesRes 2012;46:16-22.

22. Doméjean S, White JM, Featherstone JD.Validation of the CDA CAMBRA caries riskassessmentda six-year retrospective study.J Calif Dent Assoc 2011;39:709-15.

23. Tellez M, Gomez J, Pretty I, Ellwood R,Ismail A. Evidence on existing caries riskassessment systems: are they predictive offuture caries? [e-pub ahead of print]. Com-munity Dent Oral Epidemiol 2012. Sep 15.

24. Young DA, Kutsch VK, Whitehouse J.A clinician’s guide to CAMBRA: a simpleapproach. Compend Contin Educ Dent2009;30:92-4, 96, 98.

25. Fazilat S, Sauerwein R, Kimmell I,Finlayson T, Engle J, Gagneja P, et al. Appli-cation of ATP driven bioluminescence forquantification of plaque bacteria andassessment of oral hygiene in children. PedDent 2010;32:195-204.

26. Pellegrini P, Sauerwein R, Finlayson T,McLeod J, Covell DA Jr, Maier T, et al. Plaqueretention by self-ligating vs. elastomeric or-thodontic brackets: quantitative comparisonof oral bacteria and detection with ATPbioluminescence. Am J Orthod DentofacialOrthop 2009;135:426.e1-9; discussion426-7.

Kutsch

April 2014 285

27. Hallett KB, O’Rourke PK. Oral biofilm activ-ity, culture testing and caries experience inschool children. Int J Paed Dent2009;19(suppl 1):4.

28. American Dental Association Council onScientific Affairs. Professionally appliedtopical fluoride: evidence-based clinicalrecommendations. J Am Dent Assoc2006;137(suppl):1151-9.

29. Suwansingha O, Rirattanapong P. Effect offluoride varnish on caries prevention ofpartially erupted of permanent molar in highcaries risk. Southeast Asian J Trop MedPublic Health 2012;43:808-13.

30. Divaris K, Preisser JS, Slade GD. Surface-specific efficacy of fluoride varnish in cariesprevention in the primary dentition: results ofa community randomized clinical trial. CariesRes 2013;47:78-87.

31. Slade GD, Sanders AE, Do L, Roberts-Thomson K, Spencer AJ. Effects of fluori-dated drinking water on dental caries inAustralian adults. J Dent Res 2013;92:376-82.

32. Greig V, Conway DI. Fluoride varnish waseffective at reducing caries on high caries riskschool children in rural Brazil. Evid BasedDent 2012;13:78-9.

33. Hannig M, Hannig C. Nanotechnology andits role in caries therapy. Adv Dent Res2012;24:53-7.

34. Kutsch VK, Kois JC, Chaiyabutr Y,Milicich GW. Reconsidering remineralizationstrategies to include nanoparticle hydroxy-apatite. Compend Contin Educ Dent2013;34:170-7.

35. Hannig C, Basche S, Burghardt T,Al-Ahmad A, Hannig M. Comparison ofdifferent live/dead stainings for detection andquantification of adherent microorganisms inthe initial oral biofilm. Clin Oral Investig2013;17:841-50.

Kutsch

36. Featherstone JDB, White JM, Hoover CI,Rapozo-Hilo M, Weintraub JA, Wilson RS,et al. A randomized clinical trial of anticariestherapies targeted according to risk assess-ment (caries management by risk assess-ment). Caries Res 2012;46:118-29.

37. Maehara H, Iwami Y, Mayanagi H,Takahashi N. Synergistic inhibition by com-bination of fluoride and xylitol on glycolysisby mutans streptococci and its biochemicalmechanism. Caries Res 2005;39:521-8.

38. Bader JD, Vollmer WM, Shugars DA,Gilbert GH, Amaechi BT, Brown JP, et al.Results from the Xylitol for Adult Caries Trial(X-ACT). J Am Dent Assoc 2013;144:21-30.

39. Thorild I, Lindau B, Twetman S. Caries in4-year-old children after maternal chewing ofgums containing combinations of xylitol,sorbitol, chlorhexidine and fluoride. Eur ArchPaediatr Dent December 2006;7:241-5.

40. Alamoudi NM, Hanno AG, Masoud MI.Effects of xylitol on salivary mutans strepto-coccus, plaque level, and caries activity in agroup of Saudi mother-child pairs: an18-month clinical trial. Saudi Med J 2012;33:186-92.

41. Shinga-Ishihara C, Nakai Y, Milgrom P,Söderling E, Tolvanen M, Murakami K.Xylitol carryover effects on salivary mutansstreptococci after 13 months of chewingxylitol gum. Caries Res 2012;46:519-22.

42. Ritter AV, Bader JD, Leo MC, Preisser JS,Shugars DA, Vollmer WM, et al. Tooth-surface-specific effects of xylitol: randomizedtrial results. J Dent Res 2013;92:512-7.

43. Parvez S, Malik KA, Ah Kang S, Kim HY.Probiotics and their fermented food productsare beneficial for health. J Appl Microbiol2006;100:1171-85.

44. Beighton D. Can the ecology of the dentalbiofilm be beneficially altered? Adv Dent Res2009;21:69-73.

45. Fineberg HV. The paradox of disease pre-vention: celebrated in principle, resisted inpractice. JAMA 2013;310:85-90.

46. Duncanson K, Burrows T, Holman B,Collins C. Parents’ perceptions of childfeeding: a qualitative study based on thetheory of planned behavior. J Dev BehavPediatr 2013;34:227-36.

47. Wade KJ, Coates DE, Gauld RD,Livingstone V, Cullinan MP. Oral hygienebehaviours and readiness to change using theTransTheoretical Model (TTM). N Z Dent J2013;109:64-8.

48. Weinstein P. Motivational interviewing con-cepts and the relationship to risk manage-ment and patient counseling. Cal Dent AssocJ 2011;39:742-5.

49. Harrison RL, Veronneau J, Leroux B. Effec-tiveness of maternal counseling in reducingcaries in Cree children. J Dent Res 2012;91:1032-7.

50. Evans D. Some evidence that one-to-onedietary interventions in the dental settingcan change behaviour. Evid Based Dent2012;13:42.

51. Moore PA, Guggenheimer J. Medication-induced hyposalivation: etiology, diagnosis,and treatment. Compend Contin Educ Dent2008;29:50-5.

Corresponding author:Dr V. Kim Kutsch2200 14th Street SEAlbany, OR 97322E-mail: kimkutsch@aol.com

Copyright ª 2014 by the Editorial Council forThe Journal of Prosthetic Dentistry.