etiology and prevention of erosion

8/2/2019 Etiology and Prevention of Erosion

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LITERATURE REVIEW

Etiology and Preventionof Acid ErosionDavid Bartlett, BDS, PhD, MRD , FDS, RCS*Abstract: Acid erosion is the chemical effect of dietary orgastric acids on enam el and de ntine. Un like d ental caries,which is a bacterially mediated cond ition, acid erosion nor-mally is combined w ith physical forms of attrition and abra-sion. The clinical appearance of acid erosion in the earlystages isseen characteristically as hollo we d-ou t lesions onocclusal surfaces and on smooth surfaces as a subtle changein the too th contour. As the condition progresses, the le-sions coalesce and form widesprea d d entin exposure andcoronal des truction. Dietary acids that are present in bev-erages and fru its poten tially can cause acid erosion. How-ever, dietary habits involvin g frequen t consump tion ofacidsare believed to be important determinants in the risk ofdeve loping clinical signs of acid erosion. Prevention usingfluoride toothpastes, dietary mod if ications, and calcium-based products probably have a significan t clinical effect inreducing the risk of developing acid erosion.T he definitions of the components of tooth wearare recognized internationally.' Erosion is the lossof enamel and dentin caused by the action of acidsunrelated to bacterial a ction; attrition is the loss of toothstructure caused by tooth-to-tooth contact; and abrasion isthe loss of tooth structure caused by physical wear otherthan teeth. However, interpretations differ regarding howimportant each component is when analyzing a patient'spattern ofwear. Traditionally in Europe, the impact of aciderosion has been recognized as probably being the most im-portant component.^ However, the impact of abrasion,particularly tooth brushin g, often is emphasized in NorthAmerica. Recently, the role of acids in tooth w ear has be-come m ore acknowledged partly because of research andmounting clinical evidence.

It is challenging, based solely on the appearance of teeth,to separate the various components ot tooth wear. Insome

instances, the flattened incisai edges of incisors stronglysuggest that attr ition is a dominant factor. However, whenthere is cupping associated with the flattened surfaces,other factors will also be active, most notably erosion (Fig-ure I). The hollowed-out appearance of these types of le-sions, in theory, also could be attributed to abrasion, butthe force needed tocause this degree of wear is unlikely tooccur on the occlusal surfaces. Therefore, many profes-sionals consider acid erosion the predominant reason forcup-sbaped lesions.

The knowledge that acid was responsible for erosionwas first recognized in patients who had the eating disor-ders anorexia nervosa or bulimia nervosa. Th e appearanceof periomylosis on the palatal surfaces of upper incisorshas been acknowledged widely to be caused by acid rgur-gitation or vomiting (Figure 2). Periomylosis is the histor-ical term used todescribe the pattern of erosive tooth wearseen on the palatal surfaces of the upper incisor teeth. Itwas first recognized in patients with eating disorders andbelieved to be caused by vomiting and regurgitated gastricacids In the mouth.^ Eventually, clinical and laboratoryevidence suggested thepattern similar to a palatal veneerpreparation was caused by the low-pH gastric acid beingeither vomited or regurgitated.'* Some laboratory evidenceindicates tha t the shape ol the lesion is modified in someway by the abrasive action o: the tong ue.''Therefore, a hol-lowed-out or scooped-out appearance strongly suggests activeacid erosion.

APPEARANCEProbably the most easily recognizable component of toothwear is attrition. The action of bruxing opposing tooth sur-faces causes theflatteningof occlusal or incisai surfaces. Th ephysical force of the massester and temporalis muscles hasbeen predicted to approach 9 11 N.^ Theoretically, applying

*Professor, Department of Prosthodont ics, Kings College London Dental Inst itute, London Bridge, London, England


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Bartlettthis level of force to restorations increases the risk of frac-ture or chipping, particularly in those with porcelain bond -ed to metal. The site of attrition, by definition, will be alongthe incisai or occluding surfaces, whereas smooth surface le-sions, in theory, can be caused by abrasion or erosion.The etiology of cervical wear lesions has caused moredebate than any other aspect of tooth wear. Early literatureproposed excessive force applied by toothbrushing was acause of cervical wear.** However, clinical and laboratoryinvestigative work performed simulanteously co ntradictedthis clinical opinion and indicated that brushing of enam-el caused insignificant wear. Despite this research, manyclinicians continue to believe that too thbrush ing is a majorcause of cervical lesions. It is possible that excessive forceapplied while toothbrushing can cause cervical wear, butthis role has not been fully investigated. More recent re-search suggests that the cause of cervical wear is probablya comb ination of erosion and abrasion. '* It has been knownfor some time that mechanical wearin this case toothbrushingwhen combined with acid disolution is syner-gistic. Recent laboratory and clinical evidence indicatesthat bru shing with in 10 to 20 min utes following a die-tary acid increases wear to a signifantly greater extent thanpure brushing.*^

Dentin sensitivity, which often is present in associationwith cervical wear, has been suggested to be a direct clinicaloutcome of erosion. '^ These researchers suggested that sen-sitivity is a clinical sign of acid erosion because it does notoccur in patients with poor oral hygiene. Acid erosion, bydefinition, is caused by the action of dietary or gastric acidsdissolving tooth surfaces and is quite unlike dental caries,which is a subsurface etfect related to the metab olism ofplaque microorganisms. This clinical evidence suggests thatden tine sensitivity is a feature of clean too th surfaces. Theaction of acids removes the smear layer, which opens denti-nal tubules to the oral environment and increases the riskoi developing sensitivity.

It is probably safe to conclude that the impact of nor-mal toothbrushing in the absence of acid is unlikely tocause tooth wear.^ However, excessive pressure or brushingsoon after acid con sum ption may increase the risk of wearsignificantly." Smooth surface lesions are seen on the fa-cial surfaces of teeth and often noted adjacent to cervicalwear lesions. On occlusal surfaces, erosive lesions appear tobe hollowed-out, strongly suggesting the involvement ofacids in the fo rmation (Figtu"e 3).^

Figure 1 The outer r ing of enamel has been worn by attr it ion,but the shape of inner de nt in is caused by acids rather t ha nabrasion f rom toothbrushing.

Figure 2 The appearance of palatal dental erosion.

Figure 3 The wear on the facial surfaces of the pat ientseen in Figure 2. There is some cervical wear, and the shape ofthe upper left central incisor has been worn. The contributionfrom acids is l ikely to have an effect on the development ofthis lesion.


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Literature Review

Table 1 : Approximate pH of Acidified FoodsCitrus Fruits and Dr inksLemonsOrangesGrapefruitsLimesOther Fruits , ^ ^ ^ ^ HGrapesStrawberriesCranberriesApplesPearsAcidic D r i n k ^ ^ ^ ^ ^ ^ ^ lCola DrinksCarbonated Beverages(orange, lem on, etc)Lemon Tea or Herbal TeasWhite WineOth er Acidic Products Acidic CandiesChewable Vitamin C Tablets*NyA = not applicable.

p H2.03.73.22.0

3.53.22.33.34.3 2.53.23.13.7

N/A*N/A

ErosivityHighHighHighHigh

HighMedium

HighMedium

Lo w

MediumMediumMediumMedium

MediumHigh

Adapted from the US Food and Drug A dministration Web site.

ETIOLOGYTh e evidence tha t dietary or gastric acids cause erosion hasbeen extensively investigated, and its role has been subjectto a number of reviews.^''-^"''* The role of dietary acids isconsidered by many researchers probably to be the mostcommon cause of acid erosion and may account for thefinding that as much as 70% of patients have at least onetooth with wear.'^''*' Although gastric acids also cause aciderosion, the prevelance of rgurgitation, eating disorders,and alcoholism is insufficient to account tor the prevalencedata on erosion .' A comm on m isconception Is that allacidic foods an d drinks carry a high risk of acid erosion.Laboratory-based research strongly implicates chat dietaryacids have the potential to cause acid erosion.''*'"^''^ How-ever, the pH and titrability of an acid (the volume of al-kali needed for neutralization) are both important indicatorsof erosion risk.'^ Common dietary acids and their erosionrisk are shown in Table 1 .^^ The erosion risk from a strongacid, such as grapefruit, is higher than t hat of a cola drink.

Although the pH is similar in both, the amount of alkalineeded to neutralize the fruit means it is a stronger acid. Thetitrability of an acid is believed to give a stonger indicationof the risk of acid erosion whereas pH-a measure of theamo unt of hydrogen ions in a solutionis imprecise. Forexample, carbonated water has a relatively low p H , approx-imately 4 to 5. Its erosive potential is low whereas a coladrink with the same pH would have a much greater erosivepotential because of the much higher concentration of hy-drogen ions.^' T herefore, in the risk assessment of some-one with acid erosion, the type of acidic beverage or fruit isimportant to identify.

The other major risk factor with dietary acids is the fre-quency of consumption. Clinical evidence has suggestedthat the pattern of acid neutralization is unlike the patternobserved in dental caries.^^The typical drop and slow re-covery seen with acid production in dental plaque is notreplicated in acid erosion. Dietary acids cause an immedi-ate drop in oral pH, commensurate with the pH of thefood or drink. Then, after saliva has neutralized it, the pHreturns to physiologic pH 7 within a couple of minutes.These findings, along with clinical evidence, suggest thatit is the frequency of acid con sump tion that is imp ortan t.Any dietary habit, such as holding or swilling acids beforeswallowng, holding fruit against the incisors, or continualsnacking is indicative of an increased risk of developing

2' ' 2'^erosion. '

The concept of abfraction has been suggested by someclinicians as a possible cause of cervical wear. The laborato-ry support for this hypothetical cause is varied, with somelaboratory investigations supporting the view-'' and othersnot.^^ Evidence from finite-element analysis also supportsthis view, but the studies are computer models, which maynot provide sufficient complexity to model teeth.^" Also,no clinical studies support this hypothesis.^^ Despite thetemp tation that abfraction is a real phe nom ena, the evi-dence does not support it.~PREVENTIONThe epidemiologic evidence suggests that tooth wear andacid erosion are co mm on in adults,^ children,- and ado-lescents.^ ' Because of i ts widespread Impact, prevention'"of tooth w ear is impor tant . T he role of f luoride del iveredin a toothpaste has been investigated and observed to havea beneficial effect.'^-^^ Most evidence on fluoride's protec-tive effect has been based on laboratory i * ^ ^


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Bartlett

The fluoride ions appear to increase the microhardness offnamel and so improving its resistance to acid dissolution.-^-'Ihere are .some in situ studies that support the laboratory

evidence concluding fluoride is protective, but no clinicalintervention al research to date. ^"^^ Also, some clinical andlaboratory evidence suggests toothbrushing immediatelyatter consuming acids increases the risk of erosion andabrasion." Conjunctive application of a topical mouth-rinse containing fluoride also m ay be beneficial. Althoughthere is no research available to support frequent applica-tion of flouride, findings from caries studies suggest thatnitnithrinsing at times other than during normal brushingimproves the availability oi fluoride and hardens tooth sur-faces. In high-risk patients, there may be some justificationalso to consider brushing teeth at least 15 to 20 minutesafter consuming an acidic beverage or fruit.^'^ The syner-gisric action of the acid and brushing increases the potentialfor developing erosive wear lesions.

Dietary modification is probably im portan t in preven-tion. Clinical studies suggest that frequent c onsum ption ofacidic foods increases the risk of developing erosive too thwear.-''''^^ However, the strength of this evidence contin-ues to be based on association rather thnn causation. It re-mains challenging to properly investigate the role of die-tary acids in interventional studies because of ethical issues.Therefore, in a similar way to understanding the role ofrcFmed carbohydrates In dental caries, the evidence mustbe based on assimilating clinical knowledge, case reports,and laboratory investigations.^^ By amassing this data, thecurrent consensus is that frequent consum ption of carbo-hydrates causes caries. The strength of the evidence for asimilar statement in acid erosion is unavailable; however,increasing clinical knowledge strongly indicates that be-havior mo dification can be effective in preventing erosivetuoth wear."'

Early laboratory evidence implies that calcium-basedprodu cts have the potential to prevent erosive tooth wear.'**'Th e mo de of action is not fully understood, but these prod-ucts containing casein and calcium products might be pro-tective. The casein phosphopepride-amorphous calciumphosphate (CPP-ACP) complex is believed to maintain asufficiently high concentration of calcium and phosphateions to prom ote enam el rem ineral i zation. Fu rther, labora-tory studies indicate CPP-ACP may be absorbed into thesalivary pellicle**' and plaqtic"*^ and so provide a tich calci-um reservoir, improving the potential for remineralization.

Another method to improve the resistance of teeth coacid erosion is application of dentin-bondlng agents or fis-sure sealants to worn and eroded teeth. Clinical evidenceimplies that 3 - to 6-month protection is iifforded by a sin-gle application of a den tin- bo nd ing agent.** There alsomay be some benefit to the application of fissure sealantsto teeth to provide a barrier to erosive wear, which is moreresilient than a deinin-bonding agent.SUMMARYT he role of acids in too th wear is recognized as an imp orta ntreason why teeth wear. Increasingly, dietar)' habits rather thanthe quantity of acidic food and drinks is being recognized asthe most im porta nt factor in increasing the risk. Fluoride anddent in-bonding agents appear to have the potent ial to in-crease the teeth's ability to resist acidic attack, but behavioralchanges are likely to be as efFective in prevention.

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speaivethe North American and European imerpretationsoftootlivvcar. hit] Prosthodont. 1999;12(5):40l-408.

.1 . Bartlett DW, Smith BGN. Definition, classification and clin-ical assessment of attrition, erosion and abrasion of enameland dentine. In: Addy M, tmbery G, Edgar WM, eds. ToothWear and Sensitivity-Clinical Advances in Restorative Dentist1st ed. London, England: Martin D unitz; 2000 :87-93 .

4. Bartlett D. Intrinsic causes of etosion. Monogr Oral Sei. 2006:20:119-139.

5. Holst JJ, Lange F. Perimylolysis: a contribution towards the gen-esis of tooth w asting from non-mechanical causes. A w OdonulScatd. 1939;l:36-48.

6. Gregg T,Mace S, West NX, et al. A study in vitro of the abra-sive effect of the tongue on enamel and den tine softened byacid erosion. Caries Res. 2004;38(6):557-560.

7. Walcimo A. Nysirm M, Knncn M. Bite force .ind d cntofa-cial morphology in men with severe dental attrition. ScandfDent Res. l994;102(2):92-96.

8. Mannerbcrg F. Appearance of tooth surface as observed inshadowed replicas in various age group.s, in loni^-ccrm studies,after toothbrushing, in cases of erosion and after exposure tocitrus fruit juice. Odontologisb Reiiy I960;! 1(6 suppl):70-86.

9. Addy M, Absi EG, Adams D. Dctuinc hypersensitivity. Theeffects in vitro of acids and dietary siihstances on toot planedand burred dentine./ C7m Periodontol. 2000;l4(5):274-279.


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Literature Review10. Davis W B, W inter PJ. T he effect of abrasion on enamel and den-tine after exposure ro dietary acid.BrDentf. 1980:148:253-256.1 l.AttinT, Siegel S, BuchallaW, et al. Brushing abrasion of soft-ened and remineralLsed dentin: an in situ study. Caries Bes. 2004;38(l):62-66.12.Absi EG . Addy M, Adams D . D entine hypersen.sitivitytheeffect of toothbrushing and dietary acids on dendne in vitro:an SEM study, f Oral Rehabil. 1992;19(2):101-n0.13. Zero DT. Etiology of dental erosionextrinsic factors. Eurf

OralSci. 1996:104(2 pt 2):162 -t77.H.Lussi A, Khler N, Zero D, et al. A comparison of the erosivepotential of different beverages in primary and permanent teethusing an in vitro model. EiirJ 0mlSei. 2000:108(2);! 10-114.15. Harding MA, Whekon H, O'Mullanc D M, et al. Dental ero-sion in 5-year-old Irish school children and associated factors:

a pilot study. Community Dent Health. 2003:20(3): 165-170.16.Milosevic A, Young PJ, Lennon MA. The prevalence of toothwear in 14-year-old school children in Liverpool. CommunityDent Health. l994;ll(2):83-86.

17. Bartlett DW, Evans DF, Sm ith B GN , The relationship betweengastro-oesophageal reflux disease and dental erosion. / 0m lRehahii 1996;23(5):2a9-297.

18.Ganss C, Klimek J, Giese K. Dental erosion in children andadolescentsa cross-sectional and longitudinal investigationusing study models. Community Dent Oral Epidemiol. 2001;29(4):264-271.19 .G ren byT H. Method of assessing erosion and erosive potential.Eurf OralSci. 1996:104(2 pt 2):207-2 l4.20. Approximate pH of foods and food products. US Food andDrug Administration Gcnter for Food Safety and Applied nutri-tion. http://vm.cfsan.fda.gov/-comm/lacf-phs.htmi. PublishedApril 2007. Updated September 2008. Accessed: May 2009.21 . Bartlett DW . T'he role of erosion in tooth wear: aetiology, preveti-tion and management. Int Dentf. 2005;55(4 suppl l):277-284.22.Moazze-z R, Smith BGN, Bartlett DW, Oral pH and drinkinghabit during ingestion of a carbonated drink in a group o ado-lescents with dental ero sion ./D e/. 2000;28(6):395-.397.23.Mi!iward A, Shaw L., Harrington E, et al. Continuous moni-toring of salivary flow rate and pH at che surface of the denti-tion following consumption of acidic beverages. Caries Res.1997:31:44-49.24.Staninec M, Nalla RK. Hihon JF. et al. Dentin erosion simu-lation by cantilever beam tatiguc and pH change./ Dent Res.2005:84(4):371-375.25.Litonjua LA, Andreana S, Bush PJ, ct al. Wedged cervical le-sions produced by toothbrushing. Am f Dent. 2004; 17(4):237-240.26 . Rees JS, Hammadeh M, Jagger DC. Abfraction lesion forma-tion in maxillary incisors, canines and premolars: a finite ele-ment study. fwr/Ora/iV/. 2003;l 11(2): 149-154.

27 . Estafan A, Furnarl PC, Goldstein G, et al. In vivo correlationof noncarious cervical lesions and occlu.sal wcAr. f Pimthrt Dem2005;93(3):221-226.28 . Bartlett DW, Shah P. A critical review of no n-carious cervical(wear) lesions and the role of abfraction, erosion, and abra-sion. / Dent Res. 2006;85(4);306-312.29.Van't Spijker A, Rodrigues JM, Kreulen CM, et al. Prevalenceof tooth wear in adults, ntf hvsthodant. 2009:22(l):35-42.

30.Dugmore CR, Rock WP. The prevalence of tooth erosion in12-year-old children. .r Df M i/20 04 ;! 96(5):279-282.31 . Bartlett DW, Coward PY, Nikkah G, et al. The prevalence of"tooth wear in a cluster sample of adolescent schoolchildrenand its relationship with potential explanatory factors. Br Dent

f. 1998;184(3);125-129.32 . Bartlett DW, Smith BG, Wilson RK Comparison of the effectof fluoride and non-fluoride toothpaste on tooth wear in vitroand the influence of enamel fluoride concentration and fiard-ness of enamel. BrDentf 1994;]76(9):346-348.33 . Gans-s G, Klimek J, Schaffet U, et al. Effectiveness of two fluor-idation measures on erosion progression in human enamel anddentine in vitro. Caries Res. 2O01;35(5):325-33O.34 . Attin T,Zirkel C, Hellwig E. Brushing abrasion of eroded de n-tin after application of sodium fluoride solutions. Caries Res1998;32(5):.M4-350.35.Zero DT, Hara AT, Kelly SA, et al. Evaluation oa de-sensiti*/.-ing test dentifrice using an in situ erosion remineralizationmodel./C/mDf/.2006:17{4):l 12-116.36 . Wiegand A. Egert S. Attin T. Toothbrushing before or after anacidic challenge to minimize tooth wear? An in situ/ex vivostudy./imyOfwi. 2008:21(1):]3-16.37.Lussi A, Schaffner M, Holtz P, et al. Dental erosion in a pop-tilation of Swiss adults. Community Dent Oral Epidemiol. 199I9(5):286-290.38.Lussi A, Jaeggi T, Jaeggi-Schrer S, Prediction of the erosivepotential of some beverages. Caries Res. I995:29(5):349-354.39 . Edgar W M , O'Mullane DM , eds. Saliva an d Oral Health. 2nded. London, England: British Dental Journal; 1996.4O.Ranjitkar .S, Rodriguez JM , Kaidonis JA, et al. Th e effect ofcasein phosphopeptide-amorphotis calcium phosphate on ero-sive enamel and dentine wear by toothbrush abrasion./c/.2009;37(4):250-254.41.Schpbach P, Necser JR, Golliard M, ct al. Incorporation ofcaseinoglycomacropeptide and caseinophosphopeptide intothe salivary pellicle inhibirs adherence of mutans streptococci.

f Dem Res. 1996;75(10):779-1788.42. Rose RK. Effects of an anticartogenic casein phosphopcptideon calcium diffusion in streptococcal model den tal plaques.Arch Oral Biol. 2000;45{7):569-575.

43.SundaramG, Wilson R, Watson T, et al. Clinical measurementof palatal tooth wear following coating by a resin sealing sys-tem. Oper Dent. 2007;32(6):539-543.


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etiology and prevention of erosion

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