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TradeNews
BritishDentalJournal190,309316(2001)
Publishedonline:24March2001|doi:10.1038/sj.bdj.4800959
SubjectCategory:Oralpathology

Toothdiscolourationandstaining:
Toothdiscolourationandstaining:areviewoftheliterature
AWatts1&MAddy2
ObjectiveTocarryoutanextensivereviewoftheliteratureontoothstainingwith
particularregardtosomeofthemorerecentliteratureonthemechanismsof
toothstaininginvolvingmouthrinses.
DesignComprehensivereviewoftheliteratureoverfourdecades.
ConclusionsAknowledgeoftheaetiologyoftoothstainingisofimportanceto
dentalsurgeonsinordertoenableacorrectdiagnosistobemadewhenexamining
adiscoloureddentitionandallowsthedentalpractitionertoexplaintothepatient
theexactnatureofthecondition.Insomeinstances,themechanismofstaining
mayhaveaneffectontheoutcomeoftreatmentandinfluencethetreatment
optionsthedentistwillbeabletooffertopatients.

Theappearanceofthedentitionisofconcerntoalargenumberofpeopleseekingdentaltreatmentandthe
colouroftheteethisofparticularcosmeticimportance.
Therehasbeenarecentincreaseininterestinthetreatmentoftoothstaininganddiscolourationasshown
bythelargenumberoftoothwhiteningagentsappearingonthemarket.Someoftheseagentsaresoldas
'overthecounter'productsandhavenoprofessionalinvolvementintheirapplication.Thecorrectdiagnosis
forthecauseofdiscolourationisimportantas,invariably,ithasaprofoundeffectontreatmentoutcomes.It
wouldseemreasonable,therefore,thatdentalpractitionershaveanunderstandingoftheaetiologyoftooth
discolourationinordertomakeadiagnosisandenabletheappropriatetreatmenttobecarriedout.
Thepurposeofthisarticleistoreviewtheliteratureonthecausesoftoothstaininganddiscolourationas
therehasbeenlittlementionoftheaetiologyofdiscolourationsinceVogel'sreviewin1973.1

Colourandcolourperception
Abasicunderstandingoftheelementsoftoothcolourisimportantformanyaspectsofrestorativedentistry.
Teetharetypicallycomposedofanumberofcoloursandagradationofcolouroccursinanindividualtooth
fromthegingivalmargintotheincisaledgeofthetooth.Thegingivalmarginoftenhasadarkerappearance
becauseofthecloseapproximationofthedentinebelowtheenamel.Inmostpeoplecanineteetharedarker
thancentralandlateralincisorsandyoungerpeoplecharacteristicallyhavelighterteeth,particularlyinthe
primarydentition.Teethbecomedarkerasaphysiologicalagechange,thismaybepartlycausedbythe
layingdownofsecondarydentine,incorporationofextrinsicstainsandgradualwearofenamelallowinga
greaterinfluenceoncolouroftheunderlyingdentine.Also,andtobediscussedfurther,toothwearand
gingivalrecessioncandirectlyorindirectlyaffecttoothcolour.
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Thescienceofcolourisimportantindentistrywithregardtocolourperceptionanddescription,andcanbe
improvedwithtraining.2Theviewingconditionsareextremelyimportantandvariablessuchasthelight
source,timeofday,surroundingconditionsandtheanglethetoothisviewedfromaffecttheapparenttooth
colour.Lightiscomposedofdifferingwavelengthsandthesametoothviewedunderdifferentconditionswill
exhibitadifferentcolour,aphenomenonknownasmetamerism.
Injudgingtoothcolouritisbestifthelightsourceusedisstandardisedtoreducetheeffectsofmetamerism.
Itisnotuncommontofindthreesourcesoflightinadentalsurgery3natural,fluorescentandincandescent.
Particularlightsourcesareknowntohaveaneffectatcharacteristicendsofthespectrum.Forinstance,
incandescentlightwillaccentuatetheredyellowendofthespectrumandweakentheblueend.Conversely,
afluorescentlightsourcehasmoreenergytowardsthebluegreenendofthespectrumandaccentuates
thesecoloursaccordingly.Speciallydevelopedcolourcorrectedlightsareavailablewhichhelptoreducethe
effectsofmetamerism,byprovidingevencolourdistribution.Naturalsunlightvariesinitscolour,atnoon
theskyappearsbluewithminimalatmospheretopenetrate.Earlymorningandlateeveningsunlighthasa
redorangetingeastheshorterwavelengthbluelightisscatteredbytheatmosphereandonlyredand
orangerayspenetrate.
Theaestheticaspectsoftoothcolouraredifficulttoquantifyandcolourperceptionishighlysubjectiveand
pronetoindividualvariation.Disagreementbetweendentistsinshadematchingthesametoothhasbeen
documentedbyCulpepper,4 notonlybetweendentists,butalsothesamedentistondifferentoccasions.
ColourcanbedescribedaccordingtotheMunselltermsofhue,valueandchroma.5Hueisthedescriptive
termtoenableonetodistinguishbetweendifferentfamiliesofcolour,forexamplereds,bluesandgreens.
Valueistherelativelightnessanddarknessofacolouronascalefromblacktowhite.Chromaisthedegreeof
coloursaturationanddescribesthestrengthofacolourasitchanges,forexample,frompinktocrimson.
Millerandcoworkershavesuggestedtheadditionofafourthdimensiontothisthreedimensionalcolour
system,intheformofopacity/translucency.3

Classificationoftoothdiscolouration6
Thecoronalportionofthetoothconsistsofenamel,dentineandpulp.Anychangetothesestructuresislikely
tocauseanalterationintheoutwardappearanceofthetoothcausedbyitslighttransmittingandreflecting
properties.Theappearanceoftoothcolourisdependentonthequalityofthereflectedlightandisalso,asa
consequence,dependentontheincidentlight.
Historically,toothdiscolourationhasbeenclassifiedaccordingtothelocationofthestain,whichmaybe
eitherintrinsicorextrinsic.Itmayalsobeofmerittoconsiderafurthercategoryofinternalisedstainor
discolouration.7
Intrinsicdiscolouration
Intrinsicdiscolourationoccursfollowingachangetothestructuralcompositionorthicknessofthedental
hardtissues.Thenormalcolourofteethisdeterminedbytheblue,greenandpinktintsoftheenamelandis
reinforcedbytheyellowthroughtobrownshadesofdentinebeneath.Anumberofmetabolicdiseasesand
systemicfactorsareknowntoaffectthedevelopingdentitionandcausediscolourationasaconsequence.
Localfactorssuchasinjuryarealsorecognised.

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1. Alkaptonuria
2. Congenitalerythropoieticporphyria
3. Congenitalhyperbilirubinaemia
4. Amelogenesisimperfecta
5. Dentinogenesisimperfecta
6. Tetracyclinestaining
7. Fluorosis
8. Enamelhypoplasia
9. Pulpalhaemorrhagicproducts
10. Rootresorption
11. Ageing
Extrinsicdiscolouration
Extrinsicdiscolourationisoutsidethetoothsubstanceandliesonthetoothsurfaceorintheacquired
pellicle.Theoriginofthestainmaybe:
1. Metallic
2. Nonmetallic
Internaliseddiscolouration
Internaliseddiscolourationistheincorporationofextrinsicstainwithinthetoothsubstancefollowingdental
development.Itoccursinenameldefectsandintheporoussurfaceofexposeddentine.Theroutesbywhich
pigmentsmaybecomeinternalisedare:
1. Developmentaldefects
2. Acquireddefectsa)Toothwearandgingivalrecessionb)Dentalcariesc)Restorativematerials

Themechanismsoftoothdiscolouration
Intrinsictoothdiscolouration
Theformationofintrinsicallydiscolouredteethoccursduringtoothdevelopmentandresultsinanalteration
ofthelighttransmittingpropertiesofthetoothstructure.Asmentionedintheclassificationsection,there
areanumberofmetabolicdisorderswhichaffectthedentitionduringitsformation,unliketheinherited
disordersinwhichonlythehardtissueformingatthetimemaybeinvolved.Thesedisorderswillnowbe
discussedindividually.
1.Alkaptonuria:Thisinbornerrorofmetabolismresultsinincompletemetabolismoftyrosineand
phenylalanine,whichpromotesthebuildupofhomogentisicacid.Thisaffectsthepermanentdentitionby
causingabrowndiscolouration.8
2.Congenitalerythropoieticporphyria:Thisisarare,recessive,autosomal,metabolicdisorderinwhich
thereisanerrorinporphyrinmetabolismleadingtotheaccumulationofporphyrinsinbonemarrow,red
bloodcells,urine,faecesandteeth.Aredbrowndiscolourationoftheteethistheresultandtheaffected
teethshowaredfluorescenceunderultravioletlight.9KingGeorgeIIIwassaidtohavesufferedwithacute
intermittentporphyriabutwiththelateronsetofthisdisorderhisteethareunlikelytohavebeenaffected
(Fig.1).
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Figure1:Congenitalerythropoieticporphyria
Fullsizeimage(72KB)

3.Congenitalhyperbilirubinaemia:Thebreakdownproductsofhaemolysiswillcauseayellowgreen
discolouration.Mildneonataljaundiceisrelativelycommon,butinrhesusincompatibilitymassive
haemolysiswillleadtodepositionofbilepigmentsinthecalcifyingdentalhardtissues,particularlyatthe
neonatalline.10,11
4.Amelogenesisimperfecta:Inthishereditarycondition,enamelformationisdisturbedwithregardto
mineralizationormatrixformationandisclassifiedaccordingly.Thereare14differentsubtypes,12the
majorityareinheritedasanautosomaldominantorxlinkedtraitwithvaryingdegreesofexpressivity.13,14
Theappearancedependsuponthetypeofamelogenesisimperfecta,varyingfromtherelativelymild
hypomature'snowcapped'enameltothemoreseverehereditaryhypoplasiawiththin,hardenamelwhich
hasayellowtoyellowbrownappearance(Fig.2).

Figure2:AmelogenesisImperfecta
Fullsizeimage(62KB)

5.Systemicsyndromes:Defectsinenamelformationmayalsooccurinanumberofsystemicallyinvolved
clinicalsyndromessuchasVitaminDdependentrickets,epidermolysisbullosaand
pseudohypoparathyroidism.Barabas15hasreportedareasofhypoplasticenamel,irregularitiesintheregion
oftheamelodentinalandthecementodentinaljunctionsinEhlersDanlosSyndrome.Inepidermolysis
bullosathereispittingoftheenamelpossiblycausedbyvesiculationoftheameloblastlayer.However,the
effectoftheseconditionsdependsondiseaseactivityduringthedevelopmentofthedentitionandisusually
aminorelement.
6.Dentinogenesisimperfecta:Dentinedefectsmayoccurgeneticallyorthroughenvironmental
influences.16Thegeneticallydetermineddentinedefectsmaybeinisolationorassociatedwithasystemic
disorder.ThemainconditionrelatedtothedentinealoneisDentinogenesisimperfectaII(hereditary
opalescentdentine).Bothdentitionsareaffected,theprimarydentitionusuallymoreseverelyso.Theteeth
areusuallybluishorbrownincolour,anddemonstrateopalescenceontransillumination.Thepulpchambers
oftenbecomeobliteratedandthedentineundergoesrapidwear,oncetheenamelhaschippedaway,to
exposetheamelodentinaljunction.Oncethedentineisexposed,teethrapidlyshowbrowndiscolouration,
presumablybyabsorptionofchromogensintotheporousdentine(Fig3).

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Figure3:Dentinogenesisimperfecta
Fullsizeimage(64KB)

DentinogenesisimperfectaI(associatedwithosteogenesisimperfecta,amixedconnectivetissuedisorderof
typeIcollagen)mayshowbonefragilityanddeformitywithbluesclera,laxjointsandopalescentdentine.
Theinheritancemaybedominantorrecessive,therecessivebeingmoresevereandoftenfatalinearlylife.
Opalescentteetharemorecommoninthedominantinheritancepattern,theprimaryteethbearastrong
resemblancetotheteethinDentinogenesisimperfectatypeIwhereastheappearanceofthesecondary
dentitionismuchmorevariable.Theenamelismuchlesspronetofracture,thepulpchamberisseldom
occludedbydentine(thismayhelptoradiographicallydifferentiatebetweentypesIandII),andtheoverall
prognosisforthedentitionisimproved.17
AthirdtypeofDentinogenesisimperfecta(typeIII,brandywineisolatehereditaryopalescentdentine)was
describedbyWiktop.17Inthiscondition,theteethmaybeoutwardlysimilartobothtypesIandIIof
Dentinogenesisimperfectahowever,multiplepulpalexposuresoccurintheprimarydentition.
Radiographically,theteethmaytakeontheappearanceof'shellteeth'asdentineproductionceasesafterthe
mantlelayerhasformed.ThistypeofDentinogenesisimperfectaisthoughttoberelatedmorecloselyto
typeII.
7.Dentinaldysplasias:Shields18reclassifiedtheinheriteddentinedefectsinareviewoftheliteraturein
1973andintroducedthetermdentinaldysplasias.Thisreclassificationallowsseparationoftheinherited
typesofdentinedefectsfromDentinogenesisimperfecta,withwhichtheyareoftenconfused.
IntypeIdentinedysplasiatheprimaryandsecondarydentitionareofnormalshapeandformbutmayhave
anambertranslucency.Radiographicallytheteethhaveshortrootswithconicalapicalconstrictions.The
pulpiscommonlyobliteratedintheprimarydentition,leavingonlyacrescenticpulpalremnantintheadult
dentitionparalleltothecementoenameljunction.Therearecharacteristicperiapicalradiolucenciesin
many,otherwisehealthy,teeth.Theconditionisinheritedasanautosomaldominanttrait.
TypeIIdentinedysplasiaisdescribedthroughasmallnumberofcasereportsinShields18review,themain
characteristicisthatofathistleshapedpulpchamberwithnumerouspulpstones.Abrowndiscolourationof
theteethwasmentionedintwooftheliteraturereportscited.
8.Tetracyclinestaining:Systemicadministrationoftetracyclinesduringdevelopmentisassociatedwith
depositionoftetracyclinewithinboneandthedentalhardtissues.19,20UristandIbsen21suggestedthat
tetracyclineanditshomologueshavetheabilitytoformcomplexeswithcalciumionsonthesurfaceof
hydroxyapatitecrystalswithinboneanddentaltissues.Dentinehasbeenshowntobemoreheavilystained
thanenamel.19Tetracyclineisabletocrosstheplacentalbarrierandshouldbeavoidedfrom29weeksin
uterountilfulltermtopreventincorporationintothedentaltissues.Sincethepermanentteethcontinueto
developintheinfantandyoungchilduntil12yearsofage,tetracyclineadministrationshouldbeavoidedin
childrenbelowthisageandinbreastfeedingandexpectantmothers.22Themostcriticaltimetoavoidthe
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administrationoftetracyclineforthedeciduousdentitionis4monthsinuteroto5monthspostpartum,with
regardtotheincisorandcanineteeth.Inthepermanentdentition,fortheincisorandcanineteeth,this
periodisfrom4monthspostpartumtoapproximately7yearsofage.22Thecolourchangesinvolveddepend
upontheprecisemedicationused,thedosageandtheperiodoftimeoverwhichthemedicationwasgiven.
Teethaffectedbytetracyclinehaveayellowishorbrowngreyappearancewhichisworseoneruptionand
diminisheswithtime.Exposuretolightchangesthecolourtobrown,theanteriorteethareparticularly
susceptibletolightinducedcolourchanges.Thevariousanaloguesoftetracyclineproducedifferentcolour
changes,forinstancechlortetracyclineproducesaslategreycolourandoxytetracyclinecausesacreamy
discolouration.23,24 Sincetetracyclinefluorescesunderultravioletlightsodoaffectedteeth,givingoffa
brightyellowcolour.Therehavebeenrecentreportsofadultsexperiencingchangeintoothcolourwiththe
useoflongtermtetracyclinetherapy.25Minocycline,asyntheticcompoundoftetracyclineantibiotics,isalso
implicatedincausingdiscolourationinanadultpatient,followingitslongtermusefortreatmentofacne.26,
27ThisphenomenonwasdescribedinasinglecasereportintheliteraturebyCaleetal.28Whenthe

appearanceofthedentinehadalteredfollowingthelongtermuseofminocyclineforacne,itwaspostulated
thatcalciumminocyclinecomplexesweredepositedinthedentine(Fig.4).

Figure4:Tetracyclinestaining
Fullsizeimage(57KB)

9.Fluorosis:TheassociationbetweenfluorideintakeanditseffectonenamelwasnotedbyDeanaslongago
as1932.29Thismayariseendemicallyfromnaturallyoccurringwatersuppliesorfromfluoridedeliveredin
mouthrinses,tabletsortoothpastesasasupplement.Theseverityisrelatedtoageanddose,withthe
primaryandsecondarydentitionsbothbeingaffectedinendemicfluorosis.BirdsongWhitfordetal.30gave
evidenceforthepossibleincreasedaffectoffluorosisataltitudewiththeirworkonrodents.Theenamelis
oftenaffectedandmayvaryfromareasoffleckingtodiffuseopaciousmottling,whilstthecolourofthe
enamelrangesfromchalkywhitetoadarkbrown/blackappearance.Thebrown/blackdiscolourationispost
eruptiveandprobablycausedbytheinternalisationofextrinsicstainintotheporousenamel.31
Thesefeaturesareoftendescribedasbeingpathognomonicoffluorosis,butcareshouldbetakennotto
confusetheconditionwiththehypomaturationtypeofameolgenesisimperfecta.32Fluorideonlycauses
fluorosisinconcentrationsofgreaterthan1ppmindrinkingwaterandisnotdistinguishable,clinicallyor
histologically,fromanyothertypeofhypoplasticorhypomineralizedenamel(Fig.5).

Figure5:Dentalfluorosis
Fullsizeimage(71KB)

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10.Enamelhypoplasia:Thisconditionmaybelocalisedorgeneralised.Themostcommonlocalisedcauseof
enamelhypoplasiaislikelytooccurfollowingtraumaorinfectionintheprimarydentition.33Suchlocalised
damagetothetoothgermwilloftenproduceahypoplasticenameldefect,whichcanberelated
chronologicallytotheinjury.
Disturbanceofthedevelopingtoothgermmayoccurinalargenumberoffoetalormaternalconditionseg
maternalvitaminDdeficiency,rubellainfection,drugintakeduringpregnancyandinpaediatric
hypocalcaemicconditions.34 Suchdefectswillbechronologicallylaiddownintheteethdependingonthe
stateofdevelopmentatthetimeofinterference,theeffectisdirectlyrelatedtothedegreeofsystemicupset.
Theremaybepittingorgroovingwhichpredisposestoextrinsicstainingoftheenamelintheregionoftooth
disturbed,oftenthenbecominginternalised(Fig.6).

Figure6:Localisedenamelhypoplasiaonbothuppercentralincisors
Fullsizeimage(53KB)

11.Pulpalhaemorrhagicproducts:Thediscolourationofteethfollowingseveretraumawasconsideredtobe
causedbypulpalhaemorrhage.Haemolysisoftheredbloodcellswouldfollowandreleasethehaemgroupto
combinewiththeputrefyingpulpaltissuetoformblackironsulphide.Grossmanassertedin1943thatthe
depthofdentinalpenetrationdeterminesthedegreeofdiscolouration35therewaslittleifanyscientific
investigationofthishypothesis.Invitrostudieshaverecentlyshownthatthemajorcauseofdiscolourationof
noninfectedtraumatisedteethistheaccumulationofthehaemoglobinmoleculeorotherhaematin
molecules.Intheabsenceofinfection,thereleaseofironfromtheprotoporphyrinringisunlikely.This
greaterunderstandingofthenatureoftoothstainingfollowingtraumatoteethmaybeofimportanceifthe
manufactureofbleachingagents,withspecificactivity,becomespossible.Forinstance,withfurtheranalysis
itmaybecomepossibletodevelopableachingagentforuseonteethstainedspecificallybyblood
pigments.36Incidentally,ithasbeenshownthatthepinkishhueseeninitiallyaftertraumamaydisappearin
2to3monthsifthetoothbecomesrevascularised(Fig.7).37

Figure7:Haemorrhagicproductsinanonvitalcentral
Fullsizeimage(56KB)

Postmortemchangesintoothcolourhavebeenwelldocumentedintheliterature.Apurplepink
discolourationhasbeennotedWhittakerstatesthatthisisnotseenincorpseslessthan4weeksold.38
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Otherauthorshavesuggestedthatthecauseofdeathhasaninfluenceonthediscolouration,itbeingmore
noticeableincarbonmonoxidepoisoninganddrowning.Simpsonfelttheattitudeofthebodyatthetimeof
deathalsohadaneffectonthedegreeofdiscolourationinafashionsimilartothe'lividstain'ofapost
mortemdependentpart.39Thisphenomenonisnotofsignificanceindeterminingthetimeofdeath.
12.Rootresorption:Rootresorptionisoftenclinicallyasymptomatic,however,occasionallytheinitial
presentingfeatureisapinkappearanceattheamelocementaljunction.Rootresorptionalwaysbeginsatthe
rootsurface,eitherfromthepulpalorperiodontalaspect,asinternalorexternalrootresorption
respectively.Itcanbedifficulttolocatearesorptivecavityonradiographuntilitreachesacertainsize(Fig.
8).40

Figure8:Pinkspotininternalresorbtion
Fullsizeimage(47KB)

13.Ageing:Thenaturallayingdownofsecondarydentineaffectsthelighttransmittingpropertiesofteeth
resultinginagradualdarkeningofteethwithage.
Extrinsicdiscolouration
Thecausesofextrinsicstainingcanbedividedintotwocategoriesthosecompoundswhichareincorporated
intothepellicleandproduceastainasaresultoftheirbasiccolour,andthosewhichleadtostainingcaused
bychemicalinteractionatthetoothsurface.
Directstaininghasamultifactorialaetiologywithchromogensderivedfromdietarysourcesorhabitually
placedinthemouth.Theseorganicchromogensaretakenupbythepellicleandthecolourimpartedis
determinedbythenaturalcolourofthechromogen.Tobaccosmokingandchewingareknowntocause
staining,asareparticularbeveragessuchasteaandcoffee.Thecolourseenonthetoothisthoughttobe
derivedfrompolyphenoliccompoundswhichprovidethecolourinfood.41
Indirectextrinsictoothstainingisassociatedwithcationicantisepticsandmetalsalts.Theagentiswithout
colouroradifferentcolourfromthestainproducedonthetoothsurface.Interestinthemechanismsof
extrinsictoothstainingwasrekindledin1971withtheobservationbyFlotraetal.,42thattoothstaining
increaseswiththeuseofchlorhexidine.
Extrinsictoothdiscolourationhasusuallybeenclassifiedaccordingtoitsorigin,whethermetallicornon
metallic.43
Nonmetallicstains:Thenonmetallicextrinsicstainsareadsorpedontotoothsurfacedepositssuchas
plaqueortheacquiredpellicle.Thepossibleaetiologicalagentsincludedietarycomponents,beverages,
tobacco,mouthrinsesandothermedicaments.Chromogenicbacteriahavebeencitedinchildren.Particular
coloursofstainingaresaidtobeassociatedwithcertainmouths,forinstance,greenandorangeinchildren
withpoororalhygieneandblack/brownstainsinchildrenwithgoodoralhygieneandlowcaries
experience.44 Conclusiveevidenceforthechromogenicbacterialmechanismhasnotbeenforthcoming.
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Themostconvincingevidencefortheextrinsicmethodoftoothstainingcomesfromthedifferingamountof
stainfoundinacomparisonofsmokersandnonsmokers.45Thestainingeffectofprolongedrinsingwith
chlorhexidinemouthrinses46andquarternaryammoniumcompoundsusedinmouthrinses47isof
considerableinteresttothedentalprofession.
Metallicstains:Extrinsicstainingofteethmaybeassociatedwithoccupationalexposuretometallicsaltsand
withanumberofmedicinescontainingmetalsalts.46Thecharacteristicblackstainingofteethinpeople
usingironsupplementsandironfoundryworkers48iswelldocumented.Coppercausesagreenstainin
mouthrinsescontainingcoppersalts49andinworkersincontactwiththemetalinindustrial
circumstances.50Anumberofothermetalshaveassociatedcolourssuchaspotassiumpermangenate
producingaviolettoblackcolour1whenusedinmouthrinsessilvernitratesaltusedindentistrycausesa
greycolour,50andstannousfluoridecausesagoldenbrowndiscolouration.51Itwaspreviouslythoughtthat
themechanismofstainproductionwasrelatedtotheproductionofthesulphidesaltoftheparticularmetal
involved.52Thisisperhapsnotsurprisingsincetheextrinsicstaincoincidedwiththecolourofthesulphide
ofthemetalconcerned.However,thoseproposingthehypothesisappearednottoconsiderthecomplexityof
thechemicalprocessnecessarytoproduceametalsulphide.
Asmentionedearliertheinterestarousedbythestainingnotedwithuseofchlorhexidinemouthrinsehas
promptedrenewedinterestinthemechanismofstainformation.Forthisreasonmostoftheresearchinto
stainformationhasbeencarriedoutonchlorhexidine,althoughthereareotherantisepticswhichcause
stainingtoalesserextentandthemechanismproposedcouldbeapplicabletostainingfoundwithpolyvalent
metals.ThecharacteristicstainingofthetongueandteethnotedbyFlotraandcoworkersin197142isnot
peculiartochlorhexidine,ithasbeenreportedinothercationicantiseptics,53theessentialoil/phenolic
mouthrinse'Listerine'52andfollowingprolongeduseofdelmopinolmouthrinses.53Thereisgreatindividual
variationinthedegreeofstainingfrompersontoperson,thismakesexplanationmoredifficultasitmaybe
causedbyintrinsicfactors,differencesinextrinsicfactorsorboth.Nolongeracceptedtheoriesofstain
formationwithchlorhexidineincludebreakdownofchlorhexidineintheoralcavitytoform
parachloraniline54 andalsothatchlorhexidinemayreducebacterialactivitysuchthatpartlymetabolised
sugarswerebrokendownandthendegradedovertimetoproducebrowncolouredcompounds.55Most
recentdebatehascentredaroundthreepossiblemechanisms.7
Nonenzymaticbrowningreactions:Berksuggestedthattheproteinandcarbohydrateintheacquired
pelliclecouldundergoaseriesofcondensationandpolymerisationreactionsleadingtodiscolourationofthe
acquiredpellicle.57Chlorhexidinemayaccelerateformationoftheacquiredpellicle58andalsocatalyze
stepsintheMaillardreaction.Observationoffurfurals,intermediateproductsinMaillardreactions,in
browndiscolouredpelliclehasleantsupporttothetheory,59buttheevidenceisinconclusive.60Moreover,
theseauthorsdidnotconsideratallthesamestainingphenomenonobservedwiththenumerousother
antiseptics.
Theformationofthepigmentedsulphidesofironandtin:thistheorysuggeststhatchlorhexidinedenatures
theacquiredpellicletoexposesulphurradicals.Theexposedradicalswouldthenbeabletoreactwiththe
metalionstoformthemetalsulphide.Warnerandcoworkers61haveshownincreasedlevelsofironin
chlorhexidinetreatedindividualscomparedwithwatercontrols,noevidencewasshownfortin.Theythen
wentontoconcludethatthechromophorewasnotasulphide,61butasulphurcontainingorganiccompound
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andmetalioncomplexandthatchlorhexidinepromotedthedepositionofsulphateproteins.However,
somewhatanomalouslyalthoughtheamountofstainandironlevelswereincreased,thelevelsofsulphide
werereduced.Studiesinvitro62havecontradictedaspectsofthemetalsulphide/denaturationtheory.54 For
instance,dietarystainingofchlorhexidinetreatedtoothsubstanceandacrylicoccurredintheabsenceof
salivarypellicle.Moreimportantlypelliclecoatedsurfacesexposedtoproteindenaturantsorchlorhexidine
didnotstainwhensubsequentlyexposedtosaltsofironandtin.Stainingofsalivacoatedtoothandacrylic
occurredonlywhenthechlorhexidinetreatmentwasfollowedbyadietarychromogensuchastea.Thishas
tosomeextentbeenreplicatedinvivo,54 wherereciprocalrinsingwithchlorhexidineandironsulphate
producednostaininginvolunteerswhoabstainedfromfoodandbeverages.However,chlorhexidineoriron
sulphatefollowedbytearinseproducedimmediatelythecharacteristicbrownandblackdiscolourationof
theteethandtonguereportedforchlorhexidineandironrespectively.
Precipitationofdietarychromogensbychlorhexidine:Plaqueinhibitionisdependentuponadsorptionof
chlorhexidineontothetoothsurface.55Daviesetal.suggestedthatlocallyadsorpedchlorhexidine
complexedwithionsfromtheoralenvironmentandshowedthisinvitrowiththecolourproducedbetween
chlorhexidineandfooddyes.56Followingthisobservation,invitroandinvivoexperimentsshowedthat
chlorhexidineandotherantisepticsknowntocausestaininginvivocouldbinddietarychromogensto
surfacestoproducestaining.57,58,59,60Oneobjectiontothedietarychromogentheorywasthatthereisno
knowncorrelationbetweenchromogenicstaininganddietaryconsumptionofbeverages.69However,teaand
coffeeandredwinearenottheonlydrinkstocontainchromogenicpolyphenols70capableofinteractingwith
chlorhexidineorpolyvalentmetalions.Thus,thefactthatstainingcanbeproducedinrabbitsanddogs,
whichdonotusuallyimbibehumanbeverages,canbeexplainedbythepresenceofotherpolyphenolswithin
thedietwhichareabletointeractwithchlorhexidine.Nevertheless,itwasofinteresttonotethatLeonardet
al.demonstratedthatstainingwasexaggeratedinbeagledogswhenteaandcoffeewasprovidedin
conjunctionwithchlorhexidinerinses.71
Mostevidenceindicatesthatthelikelycauseofstainingistheprecipitationofanionicdietarychromogens
ontoadsorpedcations.Thus,polyphenolsfoundindietarysubstances,beinganionic,areabletoreactwith
cationsadsorpedtosurfacessuchasthecationicantisepticsorpolyvalentmetalionstoproducestaining.7
Thedifferenceinthepotentialofvariouscationicantisepticstoproducestaininginvivocanbeexplainedby
theirdifferingsubstantivity,whichisconsistentwiththedietaryaetiology.Theapparentindividualvariation
instainingnotedinparticularwithchlorhexidineisofinterest.Itisworthyofnotethatfromthediet
controlledstudiesthisvariationcannotbeexplainedsolelyasadifferenceinthequantitiesofchromogenic
agentsinanyoneindividual'sdieteventhoughabstinencefromtea,coffeeorredwinevirtuallyeliminates
stainingfromeveryone.Clearlydifferencesdoexistinthepropensityofindividualstoproducestainanditis
worthyoffurtherinvestigationasitwouldberelevanttotheneedtousecosmetictoothwhiteningproducts.
Thereisnoevidencetoshowthatchlorhexidineisanylesseffectiveinpeoplewithalowsusceptibilityto
staining.
Internaliseddiscolouration
Thestainstakenupintothebodyofenamelordentinearethesameasthosecausingextrinsictooth
discolouration,includinginparticulardietarychromogensandthebyproductsoftobaccosmoking.Dental
defectspermittingtheentryofchromogenicmaterialcanbeclassifiedundertheheadingsof'developmental
andacquired'.

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1.Developmentaldefects:Themostimportantdefectsareconsideredunderthe'intrinsictooth
discolouration'sectionofthisreview.Asdescribedthesedevelopmentaldefectscreatetheirowncolour
changeinthetoothcausedbyinfluencesonlighttransmissionthroughthedentineandenamel.Post
eruptively,however,eithercausedbyincreasedenamelporosity,orthepresenceofenameldefects,
extrinsicstainscanpenetrateintotheenamel.Suchexampleswouldincludefluorosisandotherenamel
conditionsresultinginenamelhypoplasiaorhypocalcification.Alternatively,developmentaldefectsmay
exposedentineeitherdirectlyorlatercausedbyearlylossofenamelasindentinogenesisimperfecta.
Chromogensarethenabletoenterthedentinedirectlyorfacilitatedalmostcertainlybythetubulesystem.
2.Acquireddefects:Wearandtear,anddiseaseoftheteethandsupportingtissuesoccurthroughoutlife,all
ofwhichcanleaddirectlyorindirectlytotoothdiscolouration.Additionally,repairsonrestorationsofteeth
caninfluencethecolourofteeth(Fig.9).

Figure9:Internalisedstaininenamelcracks
Fullsizeimage(56KB)

a)Toothwearandgingivalrecession:Bothconditionsappeartohavemultifactorialaetiologies72buttodate
arepoorlyunderstood,therebeinglimitedscientificresearchonthetopics.Toothwearisusuallyconsidered
tobeaprogressivelossofenamelanddentineduetoerosion,abrasionandattrition.Asenamelthinsthe
teethbecomedarkerasthecolourofdentinebecomesmoreapparent.Oncedentineisexposedthepotential
ofchromogenstoenterthebodyofthetoothisincreased.Physicaltraumacanalsoresultinbulklossof
enamelorenamelcracks,bothofwhichfacilitateinternalisationofextrinsicstains.Althoughtoothwear
occursatthecervicalareaofteeth,whereenamelismostthin,exposureofdentineismorelikelycausedby
gingivalrecession.Again,thenetresultisdentineexposureandtheincreasedpotentialfortheuptakeof
chromogensintothetooth(Fig.10).

Figure10:Gingivalrecessionwithdentinediscolouration
Fullsizeimage(49KB)

b)Dentalcaries:Thevariousstagesofthecariousprocesscanberecognisedbychangesincolourasthe
diseaseprogresses.Forinstance,theinitiallesionischaracterisedbyanopaque,whitespot.Thewhitespot
lesiondiffersincolourfromtheadjacentenamelbyvirtueofitsincreasedporosityandtheeffectthishason
therefractiveindex.73EnamelhasaRefractiveIndexof1.62,comparedwith1.33forwaterand1.0forair.
Airdryingremoveswaterfromtheporesinpartiallydemineralizedenamelleavingairandmakesthe'white
spotlesion'conspicuousbythealterationinitslighttransmittingproperties.Thehard,arrestedlesionis
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black73havingpickedupstainfromexogenoussources.Earlyinvestigationintothechangeincolourwiththe
cariousprocesscentredaroundtheaminoacidsreleasedduringproteolysis,asaresultoftheproteolysis
chelationtheoryofcavityformation.74
ThesugarproteinreactionisalsoknownastheMaillardreactionornonenzymaticbrowning.Thereactionis
ofconsequencetothefoodindustryasitresultsinthebrowningofbreadduringthebakingprocess.Ahuge
numberofproductsandintermediatechemicalsareinvolvedintheMaillardreaction.Indeed,thebrown
pigmentfoundincariousdentinewascrudelyisolatedandinvestigatedaslongagoas1950byDriezenand
Spies75andshowntohaveasimilarspectroscopicpicturetoasyntheticMaillardpigment.However,ithas
proveddifficulttodistinguishmelaninfromMaillardpigmentsusingspectroscopy.
Anumberofstudieshavesuggestedmelaninasthecauseofdiscolourationincariousteeth.Kleterand
coworkersstatedthattheevidenceforthisispoorbecauseofthedifferentsiteswithinacariouslesionat
whichmelaninwasdiscovered.76Furthermore,thesilverstainusedisnotsensitiveenoughtodistinguish
melaninfrompigmentssuchaslipofuschinsandbileacids.Thesepigmentscouldformwithinthecarious
lesion,althoughexternalpigmentationisafurtherpossibility.Uptakeoffooddyesintocariouslesionshas
beendemonstratedinvivobyKiddetal.77Theevidenceregardingcarioustoothdiscolourationis
inconclusive.Fusayamaetaldescribedhowdiscolourationprecedesthebacterialpenetrationof
demineralizeddentine,78thusitseemsthatthediscolourationiscausedbycompoundsdiffusingaheadof
thebacteria.Intheabsenceofarelationshipbetweenthediscolourationandeitherpigmentedbacteriaor
metalionsKleteretal.havesuggestedtheformationofmelaninorlipofuschin,oraMaillardreaction.67As
bothmelaninandlipofuschinrequireaerobicconditionsfortheirproduction,itisthoughtthatsmall
aldehydescanreactwithproteinsunderanaerobicconditionstocausebrowning.Analternativeexplanation
oratleastacostainingfactorcouldagainbedietarychromogensenteringthedentineconsequentupon
increasedporositythroughthecariousprocess.
c)Restorativematerialsincludingamalgam:Someofthematerialsusedinrestorativedentaltreatment
mayhaveaneffectonthecolourofteeth.Eugenolandphenoliccompoundsusedduringrootcanaltherapy
containpigmentswhichmaystaindentine.Someofthepolyantibioticpastesusedasrootcanalmedicaments
maycauseadarkeningoftherootdentine.Cliniciansarefamiliarwiththedarkgreytoblackcolourof
dentinefollowingtheremovalofalongstandingamalgamrestoration.Itwaspreviouslythoughtthat
mercurywaspenetratingthedentinaltubulesandreactingwithsulphideions.Electronmicroscopicstudies
haveshownthatthisdiscolourationiscausedbythemigrationoftinintothetubules.79

Summaryandconclusions
Itcanbeseenfromtheforegoingdiscussionthatanunderstandingofthemechanismsbehindtoothstaining
isofrelevancetothegeneraldentalpractitioner.Inthemanagementofpatientswithtoothdiscolouration
suchinformationisvaluableinthedecisionmakingprocesswhenconsideringwhetherornottotreata
condition,orreferontoaspecialistforanopinionorfortreatment.Preventionofavoidablecausesoftooth
stainingisimportant,thegeneraldentalpractitionermaybeabletoofferadvicetomedicalcolleagueswhen
alternativetherapyisavailable.Agraspofthepathologicalprocessesinvolvedintoothstainingcanassistin
explainingthecausetoanxiousorconcernedparents.Knowledgeofthephysiologicalprocessinvolvedin
shadetakingwillenabledentiststocommunicatebetterwithtechnicalstaffandalsoinvolvethepatientin
theshadetakingprocess.Whenrecommendingorprescribingoralcareproductsknowntocausestaining,it
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isimportanttowarnpatientsofsuchpotentialsideeffects.Inunderstandingthemechanismofstain
formationassociatedwithcationicantisepticsandmetalsalts,notablystannousfluoride,advisingpatientsin
respectofthemorechromogenicdietaryfluidsmayhelppreventorlimittoothstaining.

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1. SpecialistRegistrarinRestorativeDentistry,BristolDentalHospitalandSchool,LowerMaudlin
Street,BristolBS12LY
2. Professor/HonoraryConsultant,DivisionofRestorativeDentistry,BristolDentalHospitalandSchool,
LowerMaudlinStreet,BristolBS12LY
Correspondenceto:MAddy2email:Martin.Addy@bristol.ac.uk

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