فاينال ميديسن.pdf diseases of the lips and other

Medicine

1. Diseasesofthelips
Dr.FahedHabash

2. SWELLINGOFTHELIPS
Thereisconsiderableindividualandracial
variationinthesizeoflips.Abnormal
swellingofthelipscaneitherbediffuseor
localizedtoa particularareaoflip.
Diffuse:
Angioedema
Oedemaduetotruamaorinfection
cellulites
Orofacialgranulomatosis,crohn’sdisease
Haemangioma
lymphangioma

7. Localizedcausesforswellingofthe
lips
Mucocele
Abcess
Haematoma
Salivaryadenoma
Basalcellcarcinoma
Squamouscellcarcinoma

10. Angioedema
Angioedema (soft-tissue swelling) can be allergic or non-
allergicin aetiologyand mayoccurwithorwithouturticaria
(raisedwhealsorplaquesontheskin).
Mostcasesofangioedemaareidiopathic.
Itcanoccurinhereditaryformbutmainlyinacquiredform.
Acute angioedema can, however, occur as an allergic
response to a wide range of stimuli, including food stuffs
(for example, peanuts) drugs (for example, penicillin),
insectbitesandnaturalrubberlatex.
theseareresultofatypeIhypersensitivityreactionthatis
IgE-mediated
Angiotensin-convertingenzymedrugsthatareusedfor
treating hypertensioncancauseangioedema
Attacks of acute angioedema can result in widespread and
often dangerous soft-tissue swelling that may affect the
facial, oral, and pharyngeal regions and compromise the
airway..

14. Treatment
Prescriptionofantihistamine,steriods
Identificationandwithdrawalof
allergicstimuli
Stressreduction

16. Hereditaryangiodema
Arareautosomaldominantgeneticdisease.
ComeasaresultofC1esteraseinhibitor
deficiency,theactionofthecomplement
systemisuncontrolledandthisincreased
capillarypermeability.
Initsfullydevelopedformitisaserious
andlife-threatenconditionthatmaybe
precipitatedbyminimallocal traumasuch
as dentaltreatment.

17. ➢Angularchelitis:
❖ItistypicallycausedbyleakageofCandida
infectedsalivaat theangleofthemouth.
❖Itoccursindenturewearers(denture
stomatitis)andlessfrequentlywithother
types of oral candidosis.
❖Staphylococcus aures,orlessfrequently
streptococcimaybeinvolved(duetospread
fromanteriornares.
❖Inmanycases,combination(Mixed)ofthese
organismareimplicated.

19. ➢Clinically:
❖Soreness,erythema,andfissuringofthecornersofthe
mouth.
❖Deepfoldsofskinattheangles,duetoloseofocclusal
heightmaybecontributoryfactors.
❖Insomecasesangularchelitisistheresultofunderlying
systemicdisease(anemia,orofacialgranulomatosis,HIV
infection,Sjogren’ssyndrome)ornutritionaldeficiencies
inparticulariron-defandvitBI2,folicacid.
❖Facial eczema may present at the angles of the mouth
andmimic asimpleangularchelitis.Diagnosishere
dependon thehistory(unlikelyforeczema tostartatthe
angle of mouth)andtherapidresponseto localsteriod.
❖Management antifungalandfucidicacid(cream)1*4
FOR4WEEKS.Twotubesshouldbeusedoneforthe
anglesandtheotherfortheanteriornares.

21. Lipfissures
Vertical cracks in the lipsandthe
most common siteisinthemidlineof
thelower lip.
Chronic lip fissures are often resistant
to consevativetreatmentandmay
requiresurgical treatmentorlaser
treatment.
The majorityofthese fissuresare
infectedbyS.aureus

25. Treatment
Elimination of secondary infection by
theuseof antibioticcreamsuchas
fusidicacid followedbythe useof
steriodcreams.
Withsucharegimemostofthese
cracks can be healed, at least
temporarily.
A short course of a systemic antibiotic
may be required in some persistent
cases.

26. Actiniccheilitis
Actinic cheilitis is a clinical lesion of the lower lip caused by
excessivesolar radiationdamage.
Older, fair-skinned men with outdoor occupations are
typicallyaffected,
In early stages, the lower lip is mildly keratotic with
bleedingofthevermilionborderwiththe adjacentskin.
Actiniccheilitisiscausedbychronicandexcessive
exposuretoultravioletradiationinsunlight. Additional
factors mayalso playarole,includingtobaccouse,lip
irritation
Withincreasedexposuretothesun,focalwhitezonesthat
havedistinct or diffusebordersbecome apparent.
Thelipslowlybecomesfirm,scaly,slightlyswollen,
fissured,andeverted.
Ulcerationwithencrustationistypicalofthechronic
condition.
Theulcersmaybecausedbylossofelasticity,ortheymay
be anearlysignofcarcinomatoustransformation.

27. Biopsy is recommended to rule out
similarsun-relateddiseases suchas
epithelialdysplasia, carcinomain situ,
basal cell carcinoma, squamous cell
carcinoma.
Actinic cheilitis isconsidered a
precancerous condition.
Cliniciansshouldwarnthepatientofthe
likelihoodofdiseaseprogression without
the use ofsunscreenprotective agents.
Dysplasticchangesshouldbe treated
surgicallyorbytopicalapplicationof
chemotherapy orlasertherapy.

31. Exfoliativecheilitis
Exfoliativecheilitisisapersistentcondition
affectingthelipsthatis characterizedby
the productionof excessiveamountsof
keratin,fissuring,andtheformationof
hemorrhagiccrusts.
Sometimes brown scales formed that may
spontaneouslyshed.
Itisnotpremalignantlesion.
Oralsepsis,stress,andhabitualliplicking
andbitingareetiologicagents.

32. Anassociationwithpsychological(stress,
depression)andthyroiddisordershasbeen
reported.
Sometimesthisconditionbeginsasa
singlefissure nearthemidlineofthelower
lipandspreadstoproducemultiple
fissures.
Thefissuresmayultimatelydevelopa
yellow,brownwhitescaleorulcerateand
formhemorrhagiccrustsovertheentirelip.

35. Treatment
Eliminationofpredisposingfactorsor
psychologicalfactors.
Topical application of antifungal
agents.
Topical, Systemicsteriods
Mild tranquilizers, musclerelaxant.
Antidepressant

36. Perioraldermatitis
Relativelyuncommon
Usuallyyoungadultfemalesand
complain of an erythematous rash on
thefacialskinaroundthe mouth.
In some patients there is a history of
theuse ofsteriodcreams
Alsomaybe due to a contact allergy.

39. Treatment
Respondto a long-term-doseregime
oftetracyclinesas inacne treatment.
Lowdoseofsteriodcreamssuchas1
%ofhydrocortison.

40. Lickeczema
Perioralcondition.
Thepatientsareyoungandcomplainofa
sharplydelineatedzoneofirritable,scaly
skinaroundthemouth
Itistheresultoflickinghabitthatthe
patientmaystronglydeny
Thetreatmentistostopthehabit
Aremovableappliancewitharoughsurface
tointerferewiththetongueaction is
successful.

42. DevelopmentandMiscellaneous
lesions
Doneby:Dr.FahedHabash.

43. ❑Anumberofdevelopmentand
miscellaneous conditions may affect the
orofacialtissue,although mostarerare.
❑Thosethat do occurareusuallyof little
significance and do not require treatment
other than giving reassurance about the
natureof thecondition.
❑The presence of ectopic sebaceous
glands, haemangiomata or prominent
lingualpapillaecancausecancer-phobia
in somepatients.

44. ➢Sebaceousglands(fordyce’sspots):
❑Sebaceous glands may occur in the oral
mucosa membrane and present clinically
as creamy (yellowish) spots below the
epithelium.
❑Although fordyce’s spots are probably
present to some degree in all patients
morethan50%of population),some
individualsmayhavenumerous glands,
particularlyintheretromolarregionand
buccalmucosa.

45. ❑These glandsalso tend tobecomemore
prominent with age.
➢Diagnosis:
❑Prominentsebaceousglandshavea
characteristic clinical appearance and
diagnosiscanbemadeeasily.

46. ➢Treatment:
❑Oncerecognized,noactivetreatmentis
required,althoughit isnot uncommonfor
elderly patients to become concerned that
thesestructurespresentoralcancer.
❑Obviously,strongreassuranceshouldbe
giventosuchcancerphobicpatients.

47. ➢Haemangioma(vascularnaevus):
❑Neoplasia of the blood vessels is uncommon,
although there has been an increased incidence
in recent years due to the development of
Kaposi's sarcoma (malignant vascular tumor) in
HIV-positionindividuals.
❑Thevastmajorityofmalformations(hamartoma)
ofbloodvesselsarecongenitalconditions(occur
earlyinlife).
❑Morecommoninfemalesthanmales.
❑Vary in size from few milliliters to several
centimetters.
❑Haemangiomata may be divided into two forms
depending on the type and size of the blood
vesselsinvolved.

51. ❑Acapillaryhaemangiomaconsistsofamassofsmall
finecapillaryvessels,whereasacavernousangioma
containsalarge,thin-walledsinus.
❑Haemangiomamayoccuratanyintraoralsite,although
thetongue,lipsandbuccalmucosaaremostfrequently
affected.
❑Occasionalyintraoralhaemangiomasmaybeassociated
with thesturge-webersyndrome,a congenitalsyndrome
with angiomasof theface, angiomasof the
leptomeninges,intracranialcalcification,mental
retardationandepilepsy.

57. ➢Diagnosis:
❑Haemongiomataoccurringin theoral soft
tissues are similar to those occurring in the
skin and appear as well-circumscribed, flat
orraised lesions withablue/red
discoloration.
❑Blanchingofthelesionwhenpressureis
applied to it using a glass slide can help
confirm the diagnosis or contain blood on
aspiration.

59. ➢Treatment:
❑Themajorityofhaemangiomatarequireno
activetreatment.
❑However,prominentornodularregions
can become progressively traumatized
and give rise to problems or
hemorrhaging.
❑Ifsymptomspersist,smalllocalized
lesionscanbesurgicallyexcisedor
treatedwithcryosurgery.
❑More extensiveor deeplesions require
specialist management, including surgery
andthepossibleuseofsclerosingagents.

67. lymphangioma
⚫Are benign uncommonhamartomas of lymphatic
channelsthatdevelopearlyin life
⚫Theymayoccurontheskinormucous
membrane.
⚫In the oral cavity, the most common site is the
tongueandrarely lymphongiomaare diffuse and
extensivecausingmacroglossia.
⚫Small superficial have irregular projections and
varyfrompinktowhitish translusent.
⚫They may be suddenly swell and become dark
purple due to bleeding into the lymphatic
spaces.

73. Treatment
⚫Localisedlymphangiomascanbeexcised
butthisismoredifficultinthediffusetype
wheretheoperationmayhavetobedone
instages.
⚫Donotgointomalignantchange.
⚫Somelymphangiomasregress
spontanouslyduringchildhood.

74. ➢Hereditaryhaemorrhagictelangiectasia:(oslerweber-
rendusyndrome)
❑this condition is an autosomal hereditary disease which is
characterized bythe appearanceofnumeroustelangiectasiaor
angiomatousareas ofskin andoral mucosa.
❑Thelesionsare purplishor red papules,1-3mm,andblanchunder
glassslide.
❑Bleedingisaprominentfeatureofthisdiseaseandmucosallesions
are more easilytraumatizedthanskin lesionsresultinginrupture,
hemorrhageandulcerformation.
❑Somecomplicationscanoccurincludeepistaxisfromnasalmucosa,
gastrointestinalbleedingfromruptureoftelengectasiasof
gastointestinal mucosa and hematuria caused by rupture of
telengectasia withinurinarytract.
➢Diagnosis:
❑Diagnosisismadefromthefamilyhistoryandclinicalexamination.

77. ➢Treatment:
❑Treatment will depend on the extent of
symptoms, but may involve the use of
surgeryifrepeatedbleedingoccurs.
❑Ruptureoftelengectasiawhichwillcause
hemorrhage bestcontrolledbypressure
pack.

78. ➢Tonguelesions:
Fissuredtongue:
❑The fissures on the dorsal surface of the
tongue may vary considerably among
individuals.
❑Theterm ‘fissuredtongue’has beenused
to describe the occurrence of marked
fissuring.
❑The incidenceofthis conditionisuncertain
duetodifferingclinicalopinionsonwhat
constitutesa fissuredtongue.

79. ❑However,it islikelythatmanypatients
havefissuredtonguewithoutsymptoms.
❑Occasionally patientsmay complain of
discomfort on the tongue as a result of
localizedinflammationwithinthefissures.
➢Diagnosis:
❑Clinicalappearanceisdiagnostic.

80. ➢Treatment:
❑Tonguehygieneinvolvingthe use of a
topical antiseptic such as chlrohexidine
usually leadstoresolutionofany erythema
ordiscomfort.

81. ➢Medianrhomboidglossitis(superficial midline
glossitis):
❑Medianrhomboidglossitishas longbeen
considered to be a developmental
abnormalityassociatedwiththe
tuberculumimpar.
❑This belief probably arose due to the fact
that median rhomboid glossitis
characteristically presents at the junction
of the anterior two-thirds and posterior
one-thirdof thetongue.
❑However,ithasbeenshownrecentlythat
manyoftheselesions containcandida.

82. ➢Diagnosis:
❑Diagnosis can be made relatively easily from the
clinicalappearance.
❑The size and shape of the lesion vary but the
lesionappearsasawell-demarcated1-2,5 cm.
ovalorrhomboidinshape.
❑Asymptomaticlesion
❑Microbiological investigations should include oral
rinseand swab ofthetongue.
❑Biopsy is not indicated unless there is any doubt
abouttheinitialdiagnosis.

85. ➢Treatment:
❑Treatment in the past has consisted of
topical antifungaltherapyin theformof
lozenges or pastilles, dissolved on the
midline of the tongue 8-hourly for up to 3
months.
❑Lack of patient compliance with this
treatmentmayinpartexplainthepoor
therapeutic results.
❑More recently,the use of systemic
antifungalagentshas produced
encouragingresults.

86. ➢Coatedtongue(Hairytongue)
❑Thetongueof healthyindividualscommonlyhas a coatingof
desquamatedepithelialcells, mucus, microorganisms and
debris.and mainlyappearsinthosewhoareonasoftnon-abrasive
diet,thosewithpoor oralhygiene,orthosewhoare fasting.
❑The coatingappearsmore obviousin xerostomia,poor oralhygiene
and illpatient(dehydrated).
❑Hairytonguemaybedueabnormalelongationofthefilliformpapilla
thatgivesthedorsumofthetongue ahairelikeappearance.
❑Occasionally,ablackhairytonguemaybecausedbyantimicrobial
therapy,especiallywithbroadspectrumdrugsandthisisrelatedto
overgrowthofcandida.
❑Thecoatingmaybediscoleredespeciallyinpatientswhosmoke
heavily.
❑Somefoodsanddrinkssuchascoffeeandtea,andchlorhexidine
maycausethisdiscoloration.
➢Diagnosis:
❑coatedtongueisdiagnosedbyclinicalexamination.

88. ➢Treatment:
❑The awareness of a coated tongue is a
common cause of anxiety, and therefore
reassuranceisrequired.
❑Effervescent mouthwasheshavebeen
found to behelpful,althoughbest results
occurfollowingthemechanicalcleaningof
thetonguewith a toothbrush.
❑In extremecasesascalpelmay beused
toscrapeoffthehyperplastic papillae.
❑Chemicalcauterizationandcryotherapy
have also been suggested for possible
treatment, but their success has been
limited

89. ➢Geographic tongue (benign migratory
glossitis,erythemamigrans:
❑This common condition is characterized by
irregulardepapillatedareas(erythramtous
patch) surrounded by pale-demarcated margins
(pinheadwhitemargin)on thedorsalsurface
andlateralmargins oftongue.
❑Such areas appear and regress over a period of
afewdays.
❑Affectingonlythefilliformpapillae.
❑The condition is relatively common and can
affectanyageincludingyoungchildren.

90. ❑Patients are often unaware of the presence of
geographic tongue, although some individual
complain of discomfort on eating, especially hot
orspicyfoods.
❑Patientswhohavesensitivetongueshouldbe
hematologicalinvestigatedasiftheyhadnon-
specificglossitis,sincethetwoconditionsmay
coexist.
➢Diagnosis:
❑Geographic tongue can be diagnosed from
clinicalappearanceandhistory.
❑Biopsy,israrelyindicated.

93. ➢Treatment:
❑The patientshouldbe reassuredaboutthe
benignnature of thecondition.
❑Nutritionaldeficiencyshouldbeexcluded
in allpatients withsymptomatic
geographic tongue.
❑Therefore, a full blood count and an
evaluation of levels of vitamin B12,
corrected whole blood folate and ferritin
shouldbeundertaken.
❑In addition,a zinc assaymay be helpful
because symptomatic geographic tongue
hasbeen foundtorespondtozinc therapy.

94. ❑Zincshouldbe givenaszinc sulphate,
200mg 8-hourly, dissolved in water and
held inthemouthfor approximately3
minutes beforeswallowing.
❑In somepatientssymptomsof geographic
tonguemay bepsychogenic.

95. AtrophicGlossitis
⚫Glossitis is term used to describe the symptoms
oftongue discomfort.
⚫Glossopyrosis=burningtongue
⚫Glossodynia=painfultongue
⚫Atrophic glossitis occurs in deficiencies of iron,
folicacid andvitB12.
⚫There may be coexisting anemia but the atrophy
is due to nutritional deficiency rather than
anemia.
⚫Thetonguemaybepainfulbeforeatrophy

96. Clinicalappearance
⚫Thedorsumoftongueinitiallyappearpale,with
flatteningofthefiliformpapilla.
⚫Continued atrophy result in a surface devoid of
papilla and appears smooth,dry,andglassed.
⚫Theremaybeotherassociatedtissuesignsof
deficiencysuchasaphthae,angularcheilitisor
intraoralcandidiasis.
⚫Replacementtherapyretaintheappearanceof
tonguetonormal.

98. ➢Polypsandgranulomata:
❑Avarietyoflesionscanbeclassifiedunder
a heading ‘polyps’ and ‘granulomata’. And
this group forms the most common cause
of localized swellings occurring on the oral
mucosa.
❑Characteristically,theselesionspresentas
painlesssessileorpedunculatedswellings
whichcanaffectanyintraoralsite.
❑the aetiologyoftheselesionsis fully
understood,but it islikelythat chronic
minor irritationplaysanimportantrole.

99. Polypsandgranulomata:
❑Fibrousepulis.
❑Fibroepithelialpolyp.
❑Pyogenicgranuloma.
❑(pregnancyepulis).
❑Denture granuloma.
(denture-inducedhyperplasia).
❑Giantcellepulis.
❑Giantcellgranuloma.

100. Fibroepihelialpolyp(irritationfibroma)
⚫Oneofthemostcommonbenignlesionsofthe
oralcavity
⚫It result from reactive hyperplasia caused by a
chronicirritant
⚫This lesion is not a true neoplasm. True
neoplasticfibroma arearareintraoralfinding
⚫It appears as a well-defined, pale pink, slow
growingpapulethatenlarge toformanodule
⚫Firmandpainlesstopalpationbutmaybe
ulceratedbecauseofrepeatedtrauma

101. ⚫It isusuallyseenin adultsand thereis no
sexdifferentiation.
⚫Thelesionappearsessileorpedinculated.
⚫Usuallyaround1 cmindiameterbut
sometimeswecanseelarge lesion.

105. Epulides
⚫An epulis is defined as a soft-tissue swelling of
thegingivalmargin.
⚫The term is more specifically used to describe
an hyperplastic reactive inflammatory lesions
arisingfromperiodontaltissues.
⚫Three types, the fibrous epulis, the pyogenic
granuloma,andthegiantcellepulis.
⚫Most epulides are common in females than
males and usually occur anterior to the molar
teeth.

106. Fibrousepulis
⚫Presents as pedunculated or sessile
swelling on the gingiva and essensially
consists of heavily fibrosed granulation
tissue.itscontentofcollagenfibresgivesit
a firm rubbery texture and its color is
usually palepink.
⚫In a longstandinglesion,focal
mineralization or bone formation may
occur.

107. Pyogenic granuloma and pregnancy
epulis
⚫Thesearebothvascularepulis
⚫Presentclinicallyasreddishswellingon
thegingiva.
⚫Histologicallyidentical.
⚫Has atendencytobleedeasilybecauseof
its highvascularcontent.

108. ➢Diagnosis:
❑Althoughthediagnosisofall thesetypes
of polyporgranulomatacanfrequentlybe
made on clinical examination alone,
surgical removal is the treatment of
choice,and therefore clinicaldiagnosis
canbeconfirmedhistopathologically.
❑Theterms of fibrousepulis,fibro-epithelial
polyp, denture-induced hyperplasia and
pyogenic granulomaareallusedto
describe a similar reactive condition,
depending on its site, microscopic
appearance and the underlying
predisposing factor.

109. ❑Afibrousepulisreferstoapolypoccurringonthe
gingivalmargin,whereasthetermfibro-epithelialpolypis
usuallyusedwhenothersitesareaffected,suchasthe
buccalmucosa,inneraspectof thelipsorlateralmargins
ofthe tongue.
❑When involvement coincides with the periphery of a
denture,thetermdenture-inducedhyperplasiahasbeen
used.
❑Morefloridinflammatorychangesaresometimes
presentedunderthesecircumstancesthe term
pyogenic granulomaisused.
❑Richincapillariesanimmaturefibrousconnectivetissue
❑Appearsredandsoftandminormanipulationinduces
bleedingbecauseofthethinnedepitheliumandhighly
vasculartissue.
❑Aparticularexample ofthis conditioncanbeseenon
the gingivalmargin(interdentalpapilla)ofpregnant
women,whenthe lesionhasbeenreferredtoas
pregnancyepulis.
❑About1%ofpregnantwomandevelopthis lesion.

113. ➢Treatment:
❑Treatmentof thesepolypand granulomata
isbasedon removalthesourceof
irritationwithadequatesurgicalremoval.
❑Lesionsquiteconsiderablyif the
associated dentureperipheryisrelieved.
❑Following relief of the denture, any
remaining tissue can be surgically
removedafterapproximately3-4weeks.

115. ❑Giantcellepulis
❑isless common than theother irritational lesions.
❑Itisusuallyassociatedtowithahistoryoftraumaand
irritation.
❑Itonlyoccursonthealveolarprocess,usually
anterior to the first molars. (mandibular area
more)
❑Well-defined firm swelling and the base is
sessileand thecolorfrompinktodarkred.
❑Diagnosis is made on histopathological
examination and is characterized by the
presence of multinucleated giant cells in
proliferatinggranulationtissue.

118. ❑Giantcellsgranulomaariseswithinbone,but
the intraoral presentation is sometimes similar to
thatofgiantcellepulis.
❑Differentiation between the two is important
because giant cell granuloma can rapidly cause
widespreadbonedestruction.
❑In addition these lesions may arise due to
underlying hyperparathyroidism. ( brown tumor
ofhyperparathyroidism)

121. ❑If giant cell epulis or giant cell granuloma is
suspected than radiographs should be
undertaken to determine the extent of any bone
involvement.
❑In addition, haematological investigations of
serum calcium, phosphate and alkaline
phosphataseshouldbeperformed.
❑Treatmentissurgicalexcisionandcurettageof
the underlying bone. Incomplete removal may
resultin recurrence.

125. ➢Squamouscellpapilloma:
❑The squamous cell papilloma is a common
benign epithelial neoplasm which can arise at
any age and often develops on the soft palate or
mainly at the junction of hard and soft palate,
lateralmarginsofthetongueor lips.
❑The clinical appearance is classically described
as ‘cauliflower-like’ because it consists of a
discreteswellingwith numerousepithelial
projectionswhich aresometimeskeratinized.
❑Pink-white exophytic masses that are usually
lessthan 1cmindiameter.

126. ❑The cause is uncertain, but involvement of
papillomavirushasbeensuggested.
❑Support for a viral cause is provided by the
similarity in clinical appearance to the common
wart(verrucavulgaris)occurringontheskin.
❑Appeartoremainbenign.
➢Diagnosis:
❑Clinical appearance is usually sufficiently
characteristic for diagnosis, but excision biopsy
shouldbe carriedout.
❑Histological features are finger like projection
anda fibrovascularcore.

129. ➢Treatment:
❑Treatmentiscompleteexcisionincluding
thebase.Recurrenceis rare.
❑Histopathologicalexaminationwillconfirm
theclinical diagnosis.

135. Lipoma
⚫Slowgrowingbenignneoplasmcomposedofmaturefat
cellssurroundedbyathin, fibrousconnectivetissue
wall.
⚫Rare intraorally
⚫In the mouth the lipoma appears as well-demarcated,
smoothsurface,domeshapedorelevatednodulethat is
paleyellowincolor.
⚫Theyoccurmainlyonbuccalmucosa,tongue,floorof
mouthandlip.The palateisa raresiteofinvolvement.
⚫
⚫Palpationrevealssoft,movableandcompressible
submucosalmass
⚫Treatmentconsistofsurgicalremoval,whichincludes
the baseof the lesion.Lipomararelyrecur.

139. Neurofibroma
⚫Neoplasticproliferationofalloftheelementsofa
peripheralnerve.(axon,schwanncells, sheath).
⚫Neurofibromasmostcommonlyappearasfirmpink
nodules.Nontenderbut movable.
⚫May besolitaryormultiple(diffuse)
⚫Morecommonly,multiplelargeneurofibromaswhichare
associatedwithneurofibromatosis(vonRecklinghausens
disease).
⚫Thesetumorsarelocatedinskin,bones,buccalmucosa,
tongueorlips.
⚫Continuedenlargementcanleadtodeformity
⚫Skinpigmentationareassociatedwith
neurofibromatosis.

140. Management
⚫Excisionalbiopsy,histological
examination, and follow-up for malignant
transformation in cases of
neurofibromatosis.
⚫Solitaryneurofibromshavenotendency
for malignanttrasformation.

144. ➢Exostoses:
❑Bonyexostoses(benignosteomas)may
occur intraorally and present as firm
swellings.
❑The terms torus palatinus or torus
mandibularis are used respectively
whenever these exostoses occur either in
the midline of the hard palate or on the
lingualaspectof themandiblein the
premolarregion.(usuallybilateral)
❑Theselesionswhichconsistoflamellaeof
compactboneusuallyoccurinadultlife.

146. ➢Diagnosis:
❑Diagnosisison clinicalappearance.Blood
biochemistry should be undertaken to
confirm normal levels of alkaline
phosphatase,calciumandphosphate.
➢Treatment:
❑Notreatmentotherthan reassuranceis
required.
❑However,surgicalreductionoflargetori
may be necessary if the patient has to be
provided with dentures.

149. White patches and premalignant lesions
oftheoralmucosa
oralcancer
Doneby:Dr.FahedHabash.

150. ➢Whitepatchlesionsoftheoral
mucosa:
❖Developmental.
❖Infection.
❖Traumatic(frictional/smoking).
❖Dermatological.
❖Idiopathic.
❖Neoplastic.

151. ➢Developmentwhitepatches:
❖Ingeneraltheyarealluncommon.
➢Whitespongynaveus:
❖Relativelyuncommon.
❖Autosomaldominantdisorder.
❖Usually appears at birth or in early
childhoodbut persiststhroughoutlife.

152. ➢Clinicalappearance:
❖Bilateral.
❖The affected mucosa appears white,
thickenedandspongy tothetouch.
❖The most common location, buccal
mucosa.
❖Familialdisorder,several familymembers
maymanifest thedisorder.
❖The lesionmayaffecttheoralmucosa,
esophagus,rectum orvagina.
❖No treatment is required, and the lesions
areharmless.

156. Benignintraepithelialdyskeratosis
•inherited condition.
•Rare
•Theabnormalityisrestrictedtotheoralmucosa
membraneandconjunctiva,butthehistologyof
the orallesionsrevealsadegreeof dyskeratosis
thatwouldbeconsideredalarminginother
lesionsofthe oralmucosa.Inspiteofthis,
however,thecondition,asitsnameimplies,
remainessentiallybenign.

160. Pachynichacongenita
•Autosomalinheritedcondition
•White lesions of the oral mucosa and
rectum are associated with defective
formationofnailsofthehandsandfeet.

162. Tylosis,palmoplanterkeratoderma
•Discoveredinthe1950s
•Inheritedasdominantcondition
•Associated with white lesions of oral mucosa,
oesopgageal carcinoma and tylosis (hyperkeratosis of
palmsandsoles).
•It would seem likely that a wide spectrum of such
conditionsexistswithdermalandmucosal abnormalities
havefrequentlyreported.
•Recently new term palmoplanter ectodermal dysplasia
has been used. to describe the multiple ectodermal
structuresinvolvedin thisdisease

165. ➢leukoedema:
❖Isacommonmucosalvariant.
❖Associatedwithdarkpigmentedpersons
butmaybe seeninfrequentlyinlighter
pigmented persons.
➢Clinicalappearance:
❖Bilateralmainlyonthebuccalmucosa.
❖Faintwhitness(milkywhite),or grey.
❖Thelabialmucosa,softpalate,andfloor
of the mouth are less common locations of
occurrence.

167. ❖Theconditionisdiagnosedbystretchingthe
mucosa,whichcausesthewhiteappearanceto
significantlydiminishordisappearinsome
cases.
❖The causeofleukedemaisunknownanditmay
associatedbymildkeratosiswith largeswollen
cellsinthesuperficiallayersoftheepithelium.
❖Leukoedemaisnotassociatedwithepithelial
atypiaandshouldmot beregardedasa
premalignantlesion.
❖Noseriouscomplicationsareassociatedwith
thislesion,andnotreatmentisrequired.

168. ➢Infectivewhitepatches:
❖Candidosis.
❖Candidalleukoplakia.
❖Hairyleukoplakia.
❖Syphiliticleukoplakia.
➢Traumaticwhitepatches:
❖Traumatickeratosescanbeclassified on
the basisof the natureoftrauma.
❑Mechanical.
❑Chemical.
❑thermal

170. ➢Mechanical:(frictionalkeratosis)
❖Chronicirritationasaresultoflow-gradefriction
whichcan leadstohyperkeratinizationand
thickeningofepitheliumanddeveloparoughed
whitesurface(frictionalkeratosis).
❖Whenthe traumais severe,acuteandlocalized,
theepithiliumisdestroyedandanulceris
produced.
❖Itiscausedbyexcessivetoothbrushing,
movementofill-fittingdentures,sharptooth
cusporrestorationandchewingonthe
edentulousridge.
❖Painisabsent.

173. ❖Diagnosis of frictional keratosis relies on
the identificationofanobvioussourceof
chronic irritation,whichcorrelateswiththe
size and site of the lesion, and the lesion
shouldresolvefollowingeliminationof the
sourceoftrauma (reversible).
❖Norisk ofmalignanttransformation.

174. ➢Chemical:
➢Aspirinburns:
❖Resultfromplacingaspirintabletsadjacentto a
painfultooth.
❖Causesepithelialnecrosis,sloughingand
ulcerationandbleedingiftheareaistraumatized
or cancausehyperkeratosiswhichmanifestasa
whitelesionon theoralmucosa
❖Thusamixedappearanceofwhitepatchand
ulcerationmaybeseen.
❖Resolveswithin7-10days.

178. ➢Chemical-thermal:
➢Cigarettekeratosis:
❖Isaspecificrxnevidentinpersonswho
smoke non-filtered or marijuana cigarettes
toaveryshortlength.
❖Both thermals and chemical factors
contributingtotheetiology.
❖Involve the upper and lower lips at the
locationof cigaretteplacement(lateralto
midline).

179. ❖Raisedwhitepatchwith roughtexture
andfirmnesstopalpation.
❖Smoking cessation usually brings
resolution.
❖The development of ulcer and crust
formation should raisethesuspicious of
neoplastictransformation.

182. ➢Tobaccochewer’slesion,snuff
keratosis:
❖Wrinkledyellow-whitearea.
❖Locatedmainlyeitheronbuccalor
maxillaryvestibule.
❖early lesion are pale pink and the color
with time progress to white or yellow
white as hyperkeratosis and exogenous
staining occur.
❖Long term use of smokeless tobacco is
associated with periodonal alterations,
dysplastic changes and verucous
carcinoma.

185. ➢Management:
❖Toachieve resolution cessationofthe
habit isrecommended.
❖If normalappearancedoesnot return 14
daysaftercessation,biopsyisnecessary.

186. ➢Nicotinestomatitis:
❖Duetoprolongedpipeandcigar smoking.
❖Specificlesionaffectingthepalate.
❖Theirritationinitiallycausesthepalate to
becomes grayish-white secondary to
hyperkeratosis.
❖Associated with small red spots which
represent a inflamed dilated minor salivary
gland ductorifice.
❖Smoking cessation usually results in
regression.
❖NoneedforBX.

190. ➢Idiopathicwhitepatches(leukoplakia)
❖Isaclinicalterm forawhitepatch onthe
oral mucosa that cannot be scrapped off
and cannot be classified as any other
clinicallydiagnosabledisease.
❖Menmorethanwomen.
❖Oldage morethanyounger.
❖Most cases occur in men between the
ages45and65years.
❖Recentincidentfiguresindicatethatmale
tofemaleratiois decreasing.
❖Recentstudiesindicate that theincidence
Betweenyoungerage.

192. ➢Leukoplakiacauses:
❖Tobacco.
❖Alcohol.
❖Viral.
❖Syphilis.
❖Candidiasis.
❖Deficiencies(vitand iron:atrophy).
❖Chronicfriction.
❖Allof these havesomeevidence to be
considered as the cause of these lesions
but tobacco have the most important
evidence.

194. ➢Clinicalappearance:
❖Varyconsiderablyis size,locationand
clinical appearance.
➢Thepreferablesiteare:
❖Lateralandventralsurfaceof tongue.
❖Floorofmouth.
❖Alveolarmucosa.
❖Labialandbuccal mucosa.

195. ❖Softpalate.
❖retromolarpadarea.
➢Thelesions canvary in color,fromfaintly
translucentwhiteto grayor whitish in
color.

196. ➢Leukoplakia:
❖A classificationsystemofferedbythe
world health organization recommends
two divisions for oral leukoplakias:
homogeneousandnon-homogeneous.
❖Non-homogeneous leukoplakias have
been further subdivided into
erythroleukoplakia,nodular,speckled,and
verrucoid.
❖Most leukoplakias 80% are benign, and
therestaredysplastic orcancerous.

197. ❖The clinicalchallengeliesindetermining
which leukoplakias are premalignant or
malignantespeciallybecause4-6%of all
leukoplakiasprogresstosquamouscell
carcinomawithin5years.
❖High-risksitesofmalignancyincludethe
floor of the mouth, lateral and ventral
tongue,uvulo-palatalcomplex,andlips.
❖Leukoplakiaswithlocalizedredareasalso
conferahighriskforcarcinoma.

199. ❖Forexample,non-hommogeneous
leukoplakias, particularly oral speckled
leukkoplakias,representepithelial
dysplasia in about half of the cases and
havethe highest rateofmalignant
transformationamongintraoral
leukoplakias.
❖Candida albicans, a fungal organism often
associatedwithoralspeckled leukoplakias,
mayhavearolein the dysplasticchanges
seen.

201. ➢Erythroplakia:
❖Erythroplakiaisdefinedasapersistent
redpatchthatcannotbecharacterized
clinicallyasanyothercondition.
❖Thisterm like‘leukoplakia’hasno
histologic connotation however,most
erythroplakiaarehistologicallydiagnosed
as epithelial dysplasia or worse and thus
havea muchhigher propensityfor
progressiontocarcinomathanleukoplakia.

202. ❖Erythroplakias appear most prevalent in
the mandibular mucobuccal fold,
oropharynx, andfloor ofthe mouth.
❖The redness of the lesion is a result of
atrophic mucosa overlying a highly
vascularsubmucosa.
❖The border of the lesion is usually well
demarcated.
❖Thereisnosexualpredilection,and
patientsolderthanage60aremost
commonlyaffected.

203. ❖Biopsy ismandatory foralltypesof
erythroplakia because 91% of
erythroplakiasrepresentseveredysplasia
carcinoma in situ, or invasive squamous
cell carcinoma.
❖Close inspectionof theentireoralcavityis
also required because 10-20% of these
patientshaveseveralerythroplakicareas,
a phenomenon known as field
cancerization.

206. ➢Precancer:
❖Patientswiththeseconditions havea
greater risk of developing oral cancer than
individualswith apparentlynormal
mucosa.
❖However,therateofmalignantchangein
these lesions is variable being between 2
and 50% with erythroplakia having a
worseprognosis.
❖The clinical presentation of these
conditions can vary from a minimal
localizedlesionto involvementof
extensiveareasoftheoralmucosa.

207. ❖The clinical appearance has no
relationship to the presence and degree of
anydysplasia.
❖Therefore, regardless of clinical
appearance, biopsy is mandatory for all
patients presenting with leukoplakia or
erythroplakia.
❖Selectingabiopsysitecanbeaproblem
whenextensiveareasoftheoralmucosa
areinvolved.

208. ❖Aleukoplakiapatchassociatedwithan
areaoferythema isagoodchoice
❖More than one site may have to be
biopsied.
❖Atthetimeofinitialbiopsyanypotential
aetiologicalfactorsshouldbeinvestigated
andnoted.

209. ❖Thisshouldincludearecordoftobaccoand
alcoholhabits,microbiologicalinvestigationsand
haematologicalassessment.
❖Subsequentmanagementof leukoplakiawill
depend onthefindingsoftheinitialbiopsy.
❖Leukoplakiaswithverylittleorno dysplasiaare
oftenleftwithoutactivetreatmentbutall
possibleetiologicalfactorsmust beeliminated
andthehistologicalappearanceofthelesion
reassessedafteraperiod of3-6months.

210. ❖Haematologicalinvestigationsare
worthwhile in all such cases, as deficiency
states lead tomucosalatrophyand
presumably, increased susceptibility to
carcinogens.
❖Long-term review of all such cases is
mandatory and not more than 2 years
should elapsebeforefurtherbiopsy.

211. Principleofmanagementof
dysplasticlesions
•Stopanyassociatedhabits.Apartfromsurgical
treatmentitispossibletoobtainamarked
regressionofasignificantnumber oftobacco-
inducedleukoplakiasbydiscontinuingthehabit.
•Treatcandidalinfection(systemicantifungal,
fluconazole)andorirondeficiencyifpresent.
•Biopsytoassessdysplasia.
•Assessriskofmalignantchangesonclinical and
histological findings
•Considerremovalofindividuallesions
•Maintainobservationforsignsofmalignant
change.

212. Optionsformanagement(removal)
ofpremalignantlesions
•Surgicalexcisionwithgrafting,ifrequried.
•Cryotherapy (there is increasing doubt regarding the
recurrenceof cryosurgicallytreatedleukoplakia)
•Laserexcision
•currently,excisionof thelesionsusinga CO2laser is felt
to be a safer alternative. Certainly, this technique greatly
reducesthenecessityforgraftingofexcisedareas,
there is little tissue distortion and in terms of
postoperative discomfort, it is greatly preferable to
cryotherapy
•Topicalchemotherapy
•Retinoids

214. Sideropenicdysplasia
•Isalsoknownasthepaterson-kelly(or
plummer-vinson)syndromeandpredominantly
affectsmiddle-agedfemaleswhohaveiron
deficiency.
•The oralandpharyngealmucosamayappear
atrophicandshinyred.
•Oralleukoplakiaandmultiplesquamouscell
carcinomascandevelopinthiscondition.

217. Otherprecancerousconditions
•Lichenplanus,rarely(atrophicanderosive
forms)
•Discoid lupus erythromatous (few cases
reported)
•Tertiarysyphilis

220. ➢Terminologyappliedtooralcancer
and precancer:
Morbidity
Incidence:
❖The numberofnew cases of oral
cancerin adefinedpopulation
(usually100,000)ingivenperiodof
time(usuallyoneyear).
Prevalence:❖The numberof casesoforal
cancerin adefinedpopulationat a
specifiedtime.

221. Percancerous
lesions:
❖Amorphologicallyalteredtissuein
which oralcancerismorelikelyto
occurthaninitsapparentnormal
counterpart.
Leukoplakia:❖Awhitepatchorplaquewhich
cannotbecharacterizedclinicallyor
pathologicallyasanyotherdisease.
Erythroplakia:❖Abrightredvelvetpatchthat
cannotbecharacterizedclinicallyor
pathologicallyasbeing duetoany
other condition.
Mortalityrate:Thenumberofdeathsresultingfrom
oralcancerinadefinedpopulationin
aspecifiedperiodoftime

223. Oralcancer
INTRODUCTION
•Oralcancerisoneofthetenmostfrequent
cancers worldwide.Threequartersofthese
cases aroseindevelopingcountries,where itis
thethirdmostcommonformofcancerafter
stomachandcervix.Inthedevelopedworld,oral
cancer rankseighth,althoughtherankingvaries
between countrieseg, inFrance,oralcanceris
thethirdmost frequentformofcancerinmen
andthesecondcommonestformofcancer
death.

225. Epidemiology:-
•Squamouscellcarcinomaaccountfor90%of all
oralmalignantneoplasms.
•The prevalenceof oralcancervariesfrom1-2%
ofallmalignanciesinwesternEurope&Japanto
over45%inpartsofASIA(Johnson,1991).
4

226. Ageandsexdistribution
•Thereisasharplinearincreaseintheincidence
of oralcancerwithage.
•Duringrecentyearstherewasevidence of
slightlyincreasedincidence ofintraoral
squamouscellcarcinomainmenyoungerthan
40years(chenetal,1991).
•Cancerofthemouthis considerablymore
commoninmen thanwomeninmost countries.
And carcinomaofthelipisatleasteighttimes
ascommoninmenasinwomen inBritain
(Cawson&Odell,2002).

227. •The lowerlip isthe mostcommon sitefor
orofacialcancer.
•Intraorally,oralcancermayoccuronanypart
of theoralmucosa.
•Intheunitedkingdomthetongue&floorof
moutharethecommonestsites.Incontrast,in
Indiathebuccalmucosaisthemostfrequent
site,andthiscanbeduetowidespreadchewing
of betel quid (Soames& Southam,1998).
6

231. Aetiologyoforalcancer
•Tobacco(smokedandsmokeless)
andheavyalcoholintakearestillthe
dominant risk factors for oral cancer.
Alcohol and tobacco are responsible
forthemajorityoforalcancersinthe
USA(Meshbergetal,1993).
7

232. Theinfluenceoftobacco
•Thereis a4-6foldincreaseinriskamong
subjectswithmediumorhightobacco
consumptionaswellasatrendin
increasingriskwithdurationandwith
earlierageatthe startofsmoking.
•Aprotectiveeffecthasbeenfoundby
stoppingsmoking(Lewisand
Lamey,1993).
8

233. ▪Cancerofthefloorofmouthismoreassociated
withsmokingthancancer ofthegingivaand
tongue(baraschetal,1994).
Nitrosaminesintobaccohavebeenidentifiedas
themostimportantcarcinogens.Nitrosominesin
tobaccocanactsynergisticallywithherpes
simplexvirus incarcinogenesis. Smokingcan
alsoimpairthehost immuneresponse.
9

234. Theinfluenceofalcohol
•While pure ethanol have never been shown to
be carcinogenic, there is no doubt that
frequentuse of alcoholcanpotentiatethe
effectof othercarcinogenssuchas tobacco.
•The past few decades have seen an increase in
alcoholconsumption indevelopedcountries
anditislikelythatpartofincreased incidence
ofintraoralcancerindeveloped countrieswas
duetothisincreasein alcoholconsumption
(Macfarlaneetal,1992).
10

235. •In addition to the probable existence of a
carcinogenic component, alcohol might
promote carinogenesis by a localized
solventaction. Nutritional deficiencyin
alcoholics may potentiate the systemic
effectof alcoholintheetiologyof oral
cancer(binnie,1991).
11

236. Alcohol-tobaccosynergism
•Theriskoforalcancerishighamongstheavy
consumersofbothalcoholandtobacco.The
greateramountofsmokingandalcoholintakein
Scotlandincomparisonwith otherpartsofU.K
mayberesponsibleforthehigherincidenceof
oropharyngealcarcinomareportedinScotland
(LiewelynandMitchell, 1994).
12

237. Viralinvolvementinoral
cancer
•Humanpapillomaviruscontainsviralgenesand
someofthesegenes maybeinvolvedin
carcinogenesisoforalcancerbecausethey
interactwithmechanismswhichcontrolcell
growthand differentiation.Herpessimplex virus
can,undercertaincircumstances, causecell
transformationandatleastinanimalscanbe
oncogenicbutherpes simplexvirusisan
endemic virus and the presence of the virus in
oralcancertissuedoesnotproveacausal
associationwiththecancer(Scully,1993).
14

239. HostImmuneresponse
•One hypothesisof thedevelopmentof oral
cancer isthatthereisaspecific cellulardefense
mechanismactingagainstcancer development
which mightpossiblybemutatedbyvirusesand
ithasbeenshownrecentlythatthehuman
papillomavirusgeneproductsmaybeableto
actinthatwayandpossibly causederegulation
control ofcellproliferationand differentiation
(Scully,1993).
15

240. •Oral malignancy is increasingly seen in
immunosuppressed individuals due either
toinfectionwith thehuman
immunodeficiency virus(HIV)or to
systemic immunosuppression and this may
illustrate the role of immunosuppression in
the pathogenesisof oralmalignancy
(Thomasetal,1993).
16

241. Ultravioletradiation
•Sunlightisthoughttohavea roleinthe
pathogenesis of cancer of the vermillion
borderassquamouscell carcinomaofthe
lip often occurs in fair skinned individuals
who haveoutdoor occupations.
17

242. Dietandnutrition
•Adecreaseintheriskfordevelopingoralcancer
canbeachievedbyencouraginghigh fruitand
vegetableconsumption.
•Individualswhoconsumeadequatesourcesof
fruit,greenandyellowvegetablesdietaryfiber
and reduce theirconsumptionoffathavea
lowercancer risk(Doll,1992).
•Ironhasarolein maintainingoralepithelium
anditispossiblethatatrophicchangesiniron
deficiencyanaemiarenderthemucosamore
susceptible.
•Itisgenerallyconsideredthatdeficienciesof
vitamineA,CandEmaypredisposetothe
developmentoforalcancer

243. Chronic infective
considerationsinoralcancer
•Chroniccandidalinfectionisoftenassociated
withspeckled leukoplakias(chronichyperplastic
candidiasis)andmayhavesome premalignant
potential.However,otherchronicoralcandidal
infectionssuchaschronicmucocutanous
candidiosis,donotundergomalignantchanges
so theroleofcandidalinfectioninmalignant
transformationisuncertain.
19

244. CLINICALPRESENTATION:-
•The clinicalpresentationof oralsquamouscell
carcinomacantakemanyforms.Earlydiagnosis
isthe mostimportantfactorinfluencing
prognosis,andthedentistmustbesuspiciousof
anylesionforwhichnocausecanbefound.
•Earlylesionsareusuallyasymptomatic
( painless).
•Commonmodesofpresentationareawhite
patch,asmallexophyticgrowthintheearly
stagesmayshownoulcerationorerythema,a
smallulcer,oranareaoferythroplakia.
22

245. Classicalsignsofamalignant
condition
•Persistentulceration
•Induration (thickening and hardening of
the tissues)
•Proliferative growth of tissue above its
normal level, often with changes in the
surfacetextureand colorchanges.
•Fixationoftheaffectedtissuetothe
underlyingstructures.

249. •Itmaybe impossibleto differentiate
clinicallybetweenleukoplakiaor
erythroplakia and early carcinoma, and
thusbiopsyis mandatoryinthesecases.

251. •An advancedorlatelesion maypresentasa
broadbased,exophyticmasswitha rough,
haemorrhagic,or necroticsurfaceor asdeeply
crater–likeulcerwithraised,rolledeverted
edges.
•Infiltrationoftheoralmusculaturemayresultin
functionaldisturbances,particularlyifthe
tumourinvolvesthetongueorfloorofmouth.
•Painmaybeafeatureofanadvancedlesion.
•If theaffectedareaincludestheteeth,these
maybecomemobile.Thusunexplainedrapid
looseningofthe teeth shouldbecarefully
investigated.
•Metastaticspreadto regionalnodescouldoccur.

258. Spreadof oralcarcinoma
•Carcinoma spread by direct invasion of surrounding
tissues. Bone initially forms a barrier but then it is
destroyed.
•Metastaticspreadisprimarilybythelymphaticstothe
regionallymph-nodes.Thespecificsitesofmetastasis
dependonthedrainageofthetumorsites.
•Because most carcinomas arise posteriorly in the lower
mouth, the submandibular and jugulodiagastric nodes
aremostfrequentlyinvolved.
•It is certainlytruethatprognosisis morefavorableif
treatmentis donebeforethelymphareinvolved.
•Perineuralinfiltrationandvascularinvasionareless
common, bloodstream spread which occur rarely, late
featureofthe disease.

259. Preventionoforalcancer
•Thedentalsurgeonhasanessentialrolein
preventiveaspectsoforalcancer.
•Dentisthasanideal positionto giveadvice
concerning lifestyle(forexample,tobacco
cessationanddietaryadvice)andtoidentify
highriskorallesions
•Prognosisinlatestageispoorand5 year
survivalratebeingeffectivelydoubledifthe
lesionisdiscoveredearly.

263. Managementoforalcancer
Complextreatmentdependon
•Age
•Medicalcondition
•Site
•Degreeofspread
•Histologicalstage

264. Stagingsystemsfororalcancer
•The most widely used is the TNM
SYSTEM(TUMOR,NODES,METASTASIS).
•Staging systems have been found of
considerablevalueinselectingthe most
appropriatemanagementandassessing
the overallprognosis.

265. •T1lessthan2cm
•T2morethan2butless than4cm
•T3morethan4cm
•T4massivetumorwithgrosslocal invasion
•N0
•N1 single ipsilateral nodenotgreaterthan3cm diameter
•N2 single ipsilateral more than 3cm but less than 6 cm
diameter or or multiple ipsilateral or bilateral nodes
involvementnotmorethan6 cm
•N3any nodemorethan 6cm
•M0,M1 distantmetastasis

268. •Treatmentoforalcancerconsistsprimarilyofsurgery
and/orradiotherapy.
•Surgery alone is preferred for small carcinomas of the
tongue which may be easily excised, when there is a
highriskofradionecrosis,andforverrucouscarcinoma.
•The aim of surgery is to excise the carcinoma with a
wide marginaspossible,ideally1cmormore.
•In practice, most intraoral carcinoma are treated by
surgery combinedwithradiotherapy.
•Dental treatment and especially extraction should be
done before radiotherapy. Dental infection or extraction
may lead to osteoradionecrosis because of its poor
vascularity.

270. •The management of oral carcinoma should
becoordinatedbymaxillofacialsurgeon,
oncologist,radiotherapist,speech
therapistsand otherpersonnelinvolvedin
rehabilitation.
•Chemotherapy is not routinely used for
thetreatment oforalcancer

271. ➢Verrucouscarcinoma
•LowgradeSq.cellcarcinoma.
•Inthemouthitisfoundmostcommonlyinthe
mandibularbuccalsulcusandadjacentbuccal
mucosa.
•Diseaseofelderly.
•Seenparticularlyintobaccochewersandsnuff
takers.
❖Clinical appearance:
•Thick whiteplaque.
•Foldedtissuewithdeepcleftbetweenthefolds

272. •It grow slowly and spread laterally than
deeply.
•Metastasesaresaid nottooccur.
❖Pathology:
•Well-differentiated Sq. epithelium which is
heavily keratinized.
•The lower border of the lesion is well
definedbut donotinvadethe underlying
tissues.

274. ➢Basalcellcarcinoma:
•Common neoplasm of the skin of face
particularlyin elderlypatients.
•Most commonsite, midface.
•More occasionally, basal cell carcinoma
present on the lips, particularly the upper
lip.
•Thetypicalbasalcellcarcinomapresents
asaslow-growingnodulethateventually
ulceratescentrally.