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w w w . r e u m a t o l o g i a . c o m . b r

REVISTA

BRASILEIRA

DE

REUMATOLOGIA

Review

article

What

rheumatologists

should

know

about

orofacial

manifestations

of

autoimmune

rheumatic

diseases

Aline

Lauria

Pires

Abrão

a,∗

,

Caroline

Menezes

Santana

b

,

Ana

Cristina

Barreto

Bezerra

a

,

Rivadávio

Fernandes

Batista

de

Amorim

b

,

Mariana

Branco

da

Silva

c

,

Licia

Maria

Henrique

da

Mota

d

,

Denise

Pinheiro

Falcão

b

aProgramadePós-Graduac¸ãoemCiênciasdaSaúde,FaculdadedeCiênciasdaSaúde,UniversidadedeBrasília(UnB),Brasília,DF,Brazil bProgramadePós-Graduac¸ãoemCiênciasMédicas,FaculdadedeMedicina,UniversidadedeBrasília(UnB),Brasília,DF,Brazil

cFaculdadedeCiênciasdaSaúde,UniversidadedeBrasília(UnB),Brasília,DF,Brazil dServic¸odeReumatologia,HospitalUniversitáriodeBrasília(UnB),Brasília,DF,Brazil

a

r

t

i

c

l

e

i

n

f

o

Articlehistory:

Received4February2015 Accepted28August2015 Availableonline16March2016

Keywords:

Autoimmunerheumaticdiseases Orofacialmanifestations Saliva

Orallesions Periodontaldisease

a

b

s

t

r

a

c

t

Orofacial manifestationsoccur frequently inrheumatic diseases andusually represent earlysignsofdiseaseorofitsactivitythatarestillneglectedinclinicalpractice.Among theautoimmunerheumaticdiseaseswithpotentialfororalmanifestations,rheumatoid arthritis(RA),inflammatorymyopathies(IM),systemicsclerosis(SSc),systemiclupus ery-thematosus(SLE),relapsingpolychondritis(RP)andSjögren’ssyndrome(SS)canbecited. Signsandsymptomssuchasoralhyposalivation,xerostomia,temporomandibularjoint dis-orders,lesionsoftheoralmucosa,periodontaldisease,dysphagia,anddysphoniamaybe thefirstexpressionoftheserheumaticdiseases.Thisarticlereviewsthemainorofacial man-ifestationsofrheumaticdiseasesthatmaybeofinteresttotherheumatologistfordiagnosis andmonitoringofautoimmunerheumaticdiseases.

©2016ElsevierEditoraLtda.ThisisanopenaccessarticleundertheCCBY-NC-ND license(http://creativecommons.org/licenses/by-nc-nd/4.0/).

O

que

o

reumatologista

deve

saber

sobre

as

manifestac¸ões

orofaciais

das

doenc¸as

reumáticas

autoimunes

Palavras-chave:

Doenc¸asreumáticasautoimunes Manifestac¸õesorofaciais Saliva

Lesõesbucais Doenc¸aperiodontal

r

e

s

u

m

o

Manifestac¸õesorofaciaisocorremcomfrequêncianasdoenc¸asreumáticase,comumente, representamsinaisiniciais oude atividadeda doenc¸aqueaindasãonegligenciadosna práticaclínica.Entreasdoenc¸asreumáticasautoimunescompossíveismanifestac¸õesorais, incluem-se a artrite reumatoide(AR),miopatiasinflamatórias (MI), esclerosesistêmica (ES), lúpuseritematososistêmico(LES), policondriterecidivante(PR)esíndromede Sjö-gren (SS). Sinais e sintomas orofaciais como hipossalivac¸ão, xerostomia, disfunc¸ões

Correspondingauthor.

E-mail:alinelauria@hotmail.com(A.L.Abrão).

http://dx.doi.org/10.1016/j.rbre.2016.02.006

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temporomandibulares, lesões na mucosa bucal, doenc¸a periodontal, disfagia e disfo-nia podem ser a primeira expressão dessasdoenc¸as reumáticas.Esse artigo revisaas principais manifestac¸ões orofaciais das doenc¸as reumáticasque podem ser de inter-esse doreumatologista, para diagnóstico e acompanhamentodas doenc¸as reumáticas autoimunes.

©2016ElsevierEditoraLtda.Este ´eumartigoOpenAccesssobumalicenc¸aCC BY-NC-ND(http://creativecommons.org/licenses/by-nc-nd/4.0/).

Introduction

Autoimmunerheumaticdiseasesconstituteaheterogeneous group of conditions characterized by immune tolerance breakdownandproductionofautoantibodiesandofa num-ber of substances responsible for lesions in several body structures.Inthiscategory,rheumatoidarthritis(RA), inflam-matory myopathies (IM), systemic sclerosis (SSc), systemic lupuserythematosus(SLE)andSjögren’ssyndrome(SS)can beincluded.1

Somerheumaticdiseasesshowmucocutaneous manifes-tations.Generally,thechangesareconsequencesofsystemic disordersandmanifestthemselvesinsidiously,showingsigns andsymptomsintheoralcavity(Table1).However,inthe con-textofautoimmune diseases,the oralapproachappearsto havenotyetarousedscientificinterest.Inthispaper,some dentalclinicalfindingsoftenfoundinpatientstreatedatthe RheumatologyOutpatientClinicofBrasília,Hospital Univer-sitáriodeBrasilia (HUB)–UNBwillbediscussed,basedon a narrativeliteraturereview.Forthisreview,thefollowingterms wereenteredinPubMeddatabase(AutoimmuneRheumatic Disease[allfields])AND“dentistry”[allfields],limitedtothose studiesconductedonhumansubjects.Itwasfoundthatare onlysixty-eightstudieswere publisheduntilJune21,2015. Somestudiespointtoepidemiologicaldata ofmedicaland dentalinterest.Inthiscontext,clearlyonerealizesthelimited approachtothesubject.However,thepaperschosen demon-stratethatthedentistcanandshouldactintheearlydiagnosis andmanagementofthesedisorders,sincethesepatientshave specificneeds.

Thus,thisnarrativereviewaimstoaddressthemain orof-acialmanifestationsinautoimmunerheumaticdiseasesthat maybeofinterest totherheumatologist fordiagnosis and clinicalfollow-up.

Literature

review

Rheumatoidarthritis

Rheumatoidarthritis(RA)isachronicautoimmune inflam-matorydiseaseofunknownetiology.2Theclassicfeaturesof

thisdiseasearechronic,bilateralandsymmetric polyarthri-tis,jointpainandinflammationthatcanresultindeformity, instability and destruction of synovial joints.3,4 RA affects

more often the synovial membrane of small joints of the extremities,resultinginswelling,edemaandpain,andcan leadtoboneandcartilagedestruction,severedisabilityand untimelymortality.3

ThemostcommonoralmanifestationsinpatientswithRA are:

Temporomandibulardisorder(TMD)

The temporomandibularjoint (TMJ) isasynovial joint and can be affected bydisorders innon-articular tissues, with manifestationsofmusclespasm,fibromyalgia,andmyotonic dystrophy,amongothers.However,TMJjointtissuesmayalso beaffectedbymechanicaltrauma,infection,iatrogenic disor-ders,andgout,aswellasbyautoimmunerheumaticdiseases suchasRAandpsoriasis.5Onecanobservethepresenceof

typical inflammatorymediators ofosteoarthritis, including tumornecrosisfactor(TNF)-␣,interleukin(IL)-1␤,IL-6and IL-8.Thesefindingsmaintaincorrelationwiththeextentofthe disease,i.e.,clinicalsymptoms,numberofjointeffusionsor morphologicalchanges.6,7

TMDsareconsideredtobethemostcommonconditions causingorofacialpainofnon-dentalorigin,and thedentist isthe professional responsibleforthe clinicalexamination ofTMJ andforrequestingimagingexams ofthis anatomi-calregion.ATMDcanmanifestsymptomssuchasearpain, headache,non-specificnervepain,andtoothache.Its diagno-sisrequiresamedicalanddentalapproach,whichmakesthe evaluationoftheprevalenceofTMDacomplexissue,andits studyisoftenoverlookedintheclinicalpracticeofrheumatic autoimmunediseases.8,9

TMD can occur bothin adultsand –more commonly– in children with RA. A study that evaluated 223 children with juvenile idiopathic arthritis revealed that 38.6% had some TMJinvolvement (pain, swelling and/orlimitation in range of motion).10 When TMJ involvement is manifested

during a child’s development, there may be a mandibu-lar growth restriction, resulting in micrognatia and/or ankylosis.11

Inadults,studiesontheprevalenceofTMDinRApatients resultedinextremelyvariedvalues(5–86%),dependingonthe populationstudied,diagnosticcriteriaused,andassessment methods.4,5TMDisthemostcommonorofacialmanifestation

inRApatients.Thepatientmayshowabilateral,profound and pervasiveacute pain, which isexacerbated duringthe function.Theclinicalexaminationmayreveal:malocclusion, sensitivity andinflammationofpre-auricular regions, joint stiffnessuponwaking,limitationofjawmovement, intracap-sularcrepitusorclickingandpaininmasticatoryand/orneck muscles.4,12Imagingstudiesmayshowbonestructurelossat

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Table1–Oralmanifestationsofautoimmunerheumaticdiseasesandtheirclinicalimplications.

Oralevents Autoimmunerheumaticdiseases

RA IM SSc SLE SS Clinicalimplications

PM DM

Periodontaldisease X X X •Worseningfactorfordiabetesandrheumatic

andheartdiseases

Dentalcaries X X X •Dependingontheextentoftheinjury,pain,

chewinginvolvement,andfociofinfectioncan occur,likelyworseningdiabetesandrheumatic andheartdiseases

Candidiasis X X •Itchingand/orburninginthemucosa

•Riskofesophagealinfection •Inappetence

Hyposalivation X X X X •Dysphonia

•Dysphagia

•Thrushandulcersintheoralmucosa •Greatertendencytooralandoropharyngeal

infections30

•Recurrentesophagitis

•Sleepinterruptedforwaterintakeand urination

Xerostomia X X X X X •Decreaseinqualityoflife

Halitosis X •Decreaseinqualityoflife

Mouthburning X X X X •Dysgeusia

•Eatingdifficulty •Cancerphobia

Oralulcers X X X •Pain

•Difficultyinfeedingandoralhygiene

TMD X X X X •Headache

•Otalgiaand/ortinnitus •Afeelingofeartamponade •Anirradiatingcervicalpain •Chronicheadache •Limitedmouthopening •Difficultytochewandspeak12

Microstomia X •Limitedmouthopening

•Difficultyineatingandtohaveagoodoral hygiene46

Regionalresorptionof jawbone/TMJ

X •Limitedmouthopening

Dysphagia X X X •Dehydration

•Malnutrition

Aspirationofsecretionsand/orfoodtothe lung–aspirationpneumonia

Dysphonia X X X X •Decreaseinqualityoflife

Changesinlanguage X X X •Difficultytoperceivefood,speechand

swallowing.

Anglecheilitis X •Painandlimitedmouthopening

Alterationsintooth morphology

X •Facialestheticsandmasticatoryfunction

changes

Pathologicalchangesin salivaryglands

X X •Hyposalivation

Changesinmimicand chewingmusclesand inthepharynx

X •Dysphagia

•Dysphonia •Difficultytochew

Trigeminalneuralgia •Episodesofintensepainintheeyes,lips,nose,

scalp,foreheadand/orjaw

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Fig.1–Computedtomographyoftemporomandibularjointofapatientwithrheumatoidarthritisandcomplaintofclicking whilechewing.Presenceofsubchondralcystintheupperportionoftherightmandibularhead(a),erosionoflateralportion oftheleftmandibularhead(b)andflatteningofarticulareminences(c).

Periodontaldisease(PD)

PDisachronicinfectiousdiseasecausedbyGram-negative anaerobic bacteria, affectingthe tissues of protection and supportof the tooth, suchas gums, periodontal ligament, cementum and alveolar bone. Under PD designation, both reversible(gingivitis)andirreversible(periodontitis)processes areincluded.Whenundiagnosedanduntreated,PDcancause progressivedestructionofalveolarbone,causingtooth mobil-ity and subsequent dental loss.14 According to the World

Health Organization, periodontal disease affects approxi-mately10–15% ofthe world population.14 Brazilian official

datashowthat19.4%ofadultsaged35–44yearsarecarriers ofthisdisease.15

Somerecentstudiesalsosuggestasignificantassociation betweenRAandPD.13,16–18TherelationshipbetweenRAand

progressionofinflammatoryconditions(p.ex.,periodontitis) isnotclear.Themainreasonforthisscenarioisthelackof uniformityintheclassificationofthevariousformsofboth diseases.19ItisestimatedthattheprevalenceofPDincreases

twiceinRApatientscomparedtothegeneralpopulation.17

Thus,thepresenceofamoderate-to-severeRAalsoincreases morethan twicetheriskofdevelopingformsof moderate-to-severeperiodontitiscomparedtoindividualswithoutthe disease.17–19

Furthermore,thereisevidenceofsimilarityinthe patho-genesisofRAandPD.MicroorganismssuchasPorphyromonas gingivalismayplayaroleinbothconditions,16beingableto

invadeisolatedhumanchondrocytesinthekneejoint, inter-feringwithcellcycle andinducingthesecells’apoptosis.20

AnotherimportantfactorwouldbethatP.gingivalisexpresses the peptide argininedeiminase (PAD),which converts argi-nine to citrulline by a citrullination process. Thisprocess, which is common to some human proteins, is associated withthepathophysiologyofRA.Ithasalowimmune toler-ancetocitrullinatedproteinsinsynovialfluid,whichtriggers thedevelopmentofimmunoglobulinsagainsttheseproteins, presentinjointsandtendons.21,22 Inaddition,studieshave

demonstratedthepresenceofantibodiesinresponsetooral anaerobicbacteriainthesynovialtissueandserum.Others authorsalsofoundthepresenceoforalbacterialDNAinthe synovialfluidofRApatients.18Infact,RAandPDhavea

vari-etyofmarkedlysimilarclinicalandpathophysiologicfeatures (Table2).23,24

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Table2–Pathophysiologicalsimilaritiesinthe characteristicsofrheumatoidarthritisandperiodontal disease.23,24

Pathophysiological characteristics

RA PD

Cellinfiltrate Macrophages,T lymphocytes, plasmacellsand PMN

Equivalent

Immune phenomenon

Immunecomplex deposition, complement fixation

Equivalent

Cytokines IL-1␣,IL-1␤,IL-6, IL-8,TNF-␣and TGF-␤

Equivalent

Localcellsaffected Chondrocytesand synoviocytes

Gingival fibroblast, osteoblast,and keratinocytes

Inductionofbone resorption

PGE2,TNF-␣,IL-1␤ LPS,PGE2, TNF-␣,IL-1␤

TissueDestruction Metalloproteinase, phospholipase andelastase

Equivalent

Granulationtissue Presentin cartilage/bone interface

Presentinthe cement/bone interface

IL-1␣, interleukin-1 alpha; IL-1␤, interleukin-1 beta; IL-6, interleukin-6; IL-8, interleukin-8; LPS, lipopolysaccharide; PD, periodontaldisease;PGE2,prostaglandinE2;PMN, polymorphonu-clearleukocytes;RA,rheumatoidarthritis;TNF-␣,tumornecrosis factoralpha;TGF-␤,growthtransformingfactorbeta.

improvementinendothelialfunction,withadecreaseinlocal andsystemicinflammatoryprocesses.25

Hyposalivation/xerostomia

Amongoral changes,it turns out that hyposalivation (low salivaryflow) and xerostomia (dry mouth) are common in autoimmunerheumaticdiseases,andxerostomiaaffects1% ofRApatients.26 About one thirdofRApatientshave

sec-ondary SS.27 A study including 604 RA patients showed a

decrease in salivary flow in43% ofsubjects.28 The risk of

developinghyposalivationincreaseswiththeseverityofthe disease.Itisworthmentioningthatanotherstudyconducted in483hospitalizedpatientsduetocomplicationsofarthritis foundthatonly17.7%ofxerostomia-positivepatientswere treatedforxerostomia.Incontrast,84.8%ofpatientstreated forxerophthalmiaweretreatedforthiscondition.Itwasalso observed that the therapeutic modalities administered for xerostomia were not effectiveand alsowere notin accor-dancewithcurrentrecommendationsfoundinthemedical literature.29

Therefore,atimelydiagnosisandpropermonitoringofSS associatedwithRAareimportantstepstopromotegainsin thequalityoflifeofthesepatients(aswillbediscussedinthe

SSsection),takingintoaccountthatsalivaperformsfunctions ofsystemicinterest,forinstance,thesenseoftaste, epithe-lialrepairoforopharynxandesophagus,andesophagealacid contentbuffering,amongotherfunctions.30

Inflammatorymyopathies

Polymyositis(PM)anddermatomyositis(DM)areautoimmune diseases classified as idiopathic inflammatory myopathies, beingcharacterizedbymusculoskeletalinflammation.31

PMisasystemicconnectivetissuedisease,characterizedby bilateral,symmetrical,proximalmuscleweakness.Itaffects muscles of the shoulder and pelvic girdle and progresses towardproximalmusclesofthelimbs.Itsonsetisfrequently gradualandprogressive.PMexhibitsageographicallyvariable incidence,withaboutonecaseforevery100,000inhabitants, predominantlyaffectingfemales.32

Impairment of skeletal muscles ofposterior pharyngeal wall and proximal third of the esophagus can lead to oropharyngeal dysphagia, with aspiration and dysphonia. Consequently, thepatient cancomplain ofhypersalivation. Thiscomplication,however,willbeduetoanimpaired func-tionalactivityofswallowingmusclesinassociationwiththe salivary reflexcaused byreflux.Two thirds ofthe patients present involvementoftheneckflexormuscles, whichcan cause difficulty in neck support. Constitutional symptoms includefatigue,low-gradefever,weightloss,andarthralgia orarthritisofsmallandmediumjoints.33

Somerarecasereportsrelatepresenceofulcerationsonthe entiretongue,ofalinearaspectandwithawhitesecretionon theedges,andalsotongueatrophy,inwhichonecanobserve areddenedmucosa.34

DMisanautoimmunediseaseofunknownetiologythat is characterized by a systemic small-vessel vasculopathy predominantlyinvolvingmusclesandskin.Besidesthe cuta-neousinvolvement,thecharacterizationofDMisbasedinthe patternofmuscleinvolvement,presenceofassociatedclinical manifestations,andhistopathologicalchanges.35

The prevalenceoforal involvementinDM is unknown. Mostoftheinformationavailablecomesfromindividualcase reportsorsmallcaseseries,andsomeearlyreportsofcases didnotclearlyseparateMSfromPM.36

Aninvolvementofmimicmusclesmayoccur,whichleads toadecreaseinfacialexpression.Similarly,theinvolvement ofthemasticatoryandpharyngealmusclesmayresultin dys-phagia,dysphonia,andhypersalivation.Theinvolvementof striatedmuscleofthepharynxoresophagusalsocontributes totheoccurrenceofdysphagia.Inpatientswithdysphagia, DM reaches18–50%ofpatientsand correlateswithdisease severity.36,37Inaddition,thepresenceofdysphagiaincreases

theriskofaspirationpneumonia.Mortalityratesrangefrom1 to5years,reaching31%ofpatientswithDManddysphagia.37

However, the occurrence of hypersalivation is not always attributable toan excess insaliva production, but may be causedbyaninabilitytoretainsalivaandswallowingit,dueto theweaknessofperioralmuscletone,orbecauseofdysphagia. Theinvolvementoftonguemuscle resultsinmacroglossia, inadditionofhypotonia,whichcanalsomakeitmore diffi-cult chewing,swallowingand speech.38 Involvementofthe

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Mucosaledema, erythemaand telangiectasia are the com-monestoralchanges.38

Although27.5%ofpatientswithDMalsosufferarthritis, TMJinvolvementisrare,withonlyonecasereportedinthe literature.Insomereports,thepresenceofprominentblood vesselsthroughouttheoralmucosaandaphthousstomatitis/ ulcer-likelesionsweredescribed.40About10–46%ofpatients

developpainfuloralandgingivalulcers.41Theteethhaveshort

andbulgingroots,withobliterationofrootcanalsaswellas pulpchambercalcification.Xerostomiaisalsoseenasa com-moncomplaint.42

Systemicsclerosis

Systemic sclerosis (SSc)isan autoimmune disease charac-terizedbyinflammationandhyper-reactivity ofmicro-and macrovascularcirculationassociatedwithexcessivecollagen deposition intissues, withsubsequent fibrosis ofthe skin and/orinternalorgans.43SSchasapredilectionforfemales,

withanincidenceof2–10/onemillioninhabitantsinthe gen-eralpopulation.44Inaddition,thereisaconsensusaboutan

increaseinmorbidityandmortality,withanestimated66% survivalat10years.45

The oral manifestationsare scarcely studied and often neglectedbyclinicians,althoughleadingtomajorfunctional disability.Microstomiaisthemostcommonoralfindingand developsduetocollagendepositioninperioraltissues, caus-inglimitation ofmouth opening,perioralgroovewrinkling, and soft palate, larynx and oral mucosa stiffness.46

Fur-thermore, hyposalivation and/or dry mouth are secondary manifestationsofthedisease.TMDcanalsooccur,with vary-ingdegreesofsubsequentresorptionofmandibularbranch, coronoidprocess,menton and condyle.5 Itisbelieved that

these areas are reabsorbed due to the chronic collagen deposition.Tonguecancerhasasignificantlyincreased fre-quencyinpatientswithSScthat presentamouth opening <30mm.47

Theresorptionofsometeethhasalsobeenreportedwith somefrequencyinthesepatients.There maybean abnor-malincrease in the frequency ofdecayed teethand of an

atypical tooth eruption. Apparently there is also a predis-position forthe occurrenceofPD,due toincreasedplaque buildup.Thisproblemarisesfromthedifficultyofcleaningthe mouth(causedbyasmallermouthopening)andintheuse ofthedentalbrush.Thislattercomplicationisdueto scle-roticchangesinfingersandhands.Furthermore,theuseof systemiccorticosteroidsforlongperiodsinfluencein reduc-ingtheperiodontalinflammatoryresponse,thusmakingthis processaprogressiveandofteninsidiousone.48

Systemiclupuserythematous

SLE isan autoimmune disease ofunknown etiology, influ-enced by environmental and genetic factors, and which mainly affects women inthe second and thirddecades of life.49 The prevalence of oral lesions in patients with SLE

variesbetween6.5%and21%.SLEaffects primarilytongue, oralmucosa,lipsandpalate.Forthisreason,oralulcersare considered primaryevents,thatare includedinthe follow-ingactivityindexesofthisdisease:BILAG(BritishIslesLupus AssessmentGroup),50SLEDAI(SystemicLupusErythematosus

Disease Activity Index),51 SELENA-SLEDAI (Safety of

Estro-gens in LupusErythematosus National Assessment),SLAM (SystemicLupusActivityMeasure),52 andECLAM(European

ConsensusLupusActivityMeasurement).53

Thelesionsappearindifferentways,suchasblemishes and plaques on the mucosa. The lesions may be erythe-matous, ulcerated,ofa recurrentaphthousstomatitis, and lichenplanus-orleukoplakia-likelesions(Fig.2).Thesizeof these lesionsisalsovariable,from asmall surface erosion to ulcers covering a wide and extensive area.54,55 The few

studiesonorallesionsinpatientswithSLEshow, microscop-ically,parakeratosisororthokeratosis,acanthosis,epithelial atrophy,vacuolardegenerationofthebasalmembranewith necrosisofbasalkeratinocytes,basementmembrane thick-ening,lichenoidmononuclearinfiltrate,anddeepconnective tissuevasculitis.Injuriesinthevermilionborderoflips (espe-cially in the lower lip), deserve special attention,as these lesions may be related to lupus cheilitis, with or without epithelialdysplasia.54,56

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Othersecondaryorofacialsigns/symptomsinclude:mouth burning,hyposalivation,xerostomia, salivary glanddisease (suchasfocal necrosisofthe parotidgland),TMD, desqua-mative gingivitis and PD.54 Hyposalivation can lead to an

increasedoccurrenceofdentalcariesandtoapredisposition tocandidiasis,especiallyifimmunosuppressiveagentssuch ascorticosteroidsarebeingused.56

Sjögren’ssyndrome(SS)

SSisaninflammatoryautoimmunediseasepresentinga fre-quentchroniccourse,inwhich thelymphocyticinfiltration ofexocrineglands,particularlylacrimalandsalivaryglands, impairs its secretory function.55 Simultaneously, systemic

manifestationsofcutaneous,respiratory,renal,hepatic, neu-rologicand vascular naturecan occur. SS hastwo distinct forms:primarySS–notassociatedwithanotherdisorder;and secondarySS–inwhichthepatientexpressesthissyndrome inassociationwithotherautoimmunediseases.57,58

ItisestimatedthatSSaffects0.2%oftheworld popula-tion,mainlywomen,inaratioof9:1.57,58InBrazil,duetothe

absenceofofficialestimatesorscientificallyconfirmeddata onitsincidence,nooneknowstheexactnumberofpatients withthissyndrome.However,itwasstatedthatthemajorityof diagnosedcasesarerelatedtomenopausal,orolder,women.59

SSfollowsavariablecourseandexhibitsawidespectrum ofclinicalmanifestations.Inaddition,manyofitssymptoms arenon-specific,makingdifficultanddelayingthediagnosis. EightypercentofpatientswithSSexhibitaninsidiousonsetof symptomsofdrynessthatdevelopoveraperiodfromseveral monthstoyears.58

TheoralmanifestationsobservedinpatientswithSSare attributedtotheinvolvementofsalivaryglands,whichleads tolesssalivarysecretion.Inconsequence,theworse lubrica-tionandlossofbufferingandantimicrobialactionofsalivary secretion increase the incidence of oral/dental infections, mucosal friability, and symptomsof irritationand burning mouth(Fig.3).57Ontheotherhand,somepatientscomplain

ofxerostomia,whichmaynotbeaccompaniedbyadecrease insalivary secretion.30 However,in the initialstage ofthe

disease, when the diagnosis has not yet been well estab-lished,patientsmaycomplainofxerostomiaduetochangesin

salivarycomposition,ortoareductionofsalivarysecretion fromthesmallersalivaryglands(fromlipmucosaandpalate). Thus,sialometrymay revealthatthe patienthasanormal salivaryflow;however,salivarycompositiontestswillindicate qualitativechanges.60

Usually,dentalcariesandfungalinfectionsareobservedin mucousmembranes(especiallycandidiasis)thatcanmanifest aspseudomembranousorerythematouslesions.Thefriability of the mucosa in patients with SS often leads tosoft tis-sueinjuries.Suchsignsincludedryandcrackedlips,median rhomboidglossitisorafissuredtongue,lossoflingual papil-lae,stomatitis,angularcheilitis,aphthousinjury,lipmucosal ulcers,difficultyinswallowingsolids,andodynophagia.57

SS patients oftendisplay voice disorders andcorrelated symptomsthatareassociatedwithadecreaseintheirquality oflife.Itisknownthatthelubricationofthevocalcordsis carriedoutbysaliva.61Thus,thisbiologicalfluidisimportant

foraproperphonation.

Another relevantpoint referstothe drop inthe quality oflifeofpatientswithSS,becauseoftheirchangingeating habits,causedbydrymouth.62ThereisaStrongcorrelation

amongoraldrynessandfatigue,pain,psychologicaldistress, andaworsequalityofsleep;andthatitisconsideredasa car-diovascularriskfactor.63Inthisstudy,theauthorsconcluded

thatamultidisciplinarytherapeuticapproachmaybethebest waytominimizedrymouthanditsconsequencesinpatients withprimarySS.63

Finally,anothercommonoralmanifestationisan asymp-tomaticandself-limitingincreasesofparotidglandsorother majorsalivaryglands,55whichmaybepointingtotheearly

stageofSS.

Therefore,theestablishmentofanearlydiagnosisofSSis essentialforthechoiceofthecorrecttreatment,which con-sistsinrelievingthesignsandsymptomsinordertominimize oravoidsequelsthatcanimpactonthehealthandqualityof lifeofpatients.64

Gustatory,mechanicalandchemicalsialogogueshavebeen usedtostimulatesalivaproduction.However,the effective-ness of these resources is low, because they provide only temporaryrelief,requiringfrequentapplications.65Many

top-icaltreatmentssuchassprays,lozenges,mouthwashes,gels, oilsortoothpasteshavebeenevaluated,butthereisnostrong

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evidencethatanyofthesetopicaltreatmentsiseffectiveto alleviatethepatientwithdrymouth.66 Oxygenatedtri-ester

glycerol-basedlubricantsaremoreeffectivethanwater-based electrolytesprays.Chewinggumincreasessalivaproduction, butthereisnoevidencethattheseproductsarebetterorworse than saliva substitutes. However, acidic secretagogues and those containingsugar shouldbe avoided,66 because these

productsloweroralpH,promotegreatertooth demineraliza-tionandirritateamucousalreadyverysensitive.Oneshould optfortheuseofsugar-freechewinggum,butcontaining flu-orideandbicarbonateinitscomposition.Thesecomponents increasesalivarypHandassistinpreventingtoothdecay.67,68

Chemical sialagogues, such as pilocarpine and cevime-line,areeffectiveinrelievinghyposalivation,butmaycause adverseeffects.65Electricalstimulationappliedtothe

affer-entpathways(throughtheoralmucosaorskin)inareasof salivaryglands,showedincreasedsalivaproductionandrelief ofdrymouthinpatientswithSS65andinpatientsundergoing

cervical-brainradiotherapy.69

Asystematicreviewofrandomizedcontrolledtrialswas conductedtogatherevidenceondrugtherapyinprimarySS. Theauthorssuggestedthatsalivasubstitutesandsugar-free chewinggumsmaybeeffectiveincasesofmild-to-moderate drymouth.Consumptionofalcoholandsmokingshouldbe avoided, and it is a critical factor the establishment of a thoroughoralhygiene.Thetreatmentofchoiceforpatients withresidual functionofsalivaryglandsiscevimelineand oralpilocarpine. However,nostudywas published compar-ing theefficacy ofthese twodrugs. Thedoses which have shown better effects in terms ofefficacy and safety were: pilocarpine5mgevery 6h; andcevimeline 30mgevery 8h. N-acetylcysteinecouldbeanalternativeinpatientswith con-traindicationsorintolerancetomuscarinicagonists.70

Conclusion

Orofacial manifestations in patients with autoimmune rheumaticdiseasesarecommonproblems,butstillsparsely addressed by rheumatologists in their everyday clinical practice.Thisarticleproducedasummaryofthemain mani-festationsobserved,inordertofamiliarizetheseprofessionals withtheirdiagnoses,underlyingthepossibleneedforanearly referraltothedentist.

Conflicts

of

interest

Theauthorsdeclarenoconflictsofinterest.

Acknowledgements

TheauthorswouldliketoacknowledgeNathalyaLopesSilva, RafaellyStavale,TalithaGiovannadaSilvaandFrancisca Ires-daniaAlvesMacedofortheircollaboration.Thesecondand seventhauthorsarealsogratefulforthefinancialsupportof CAPES–Coordenac¸ãodeAperfeic¸oamentodePessoaldeNível Superior.

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Imagem

Table 1 – Oral manifestations of autoimmune rheumatic diseases and their clinical implications.
Fig. 1 – Computed tomography of temporomandibular joint of a patient with rheumatoid arthritis and complaint of clicking while chewing
Table 2 – Pathophysiological similarities in the characteristics of rheumatoid arthritis and periodontal disease
Fig. 2 – Patient with systemic lupus erythematosus with gingival and tooth sensitivity complaint
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