White lesions in the oral cavity can have various causes and presentations. Keratotic white lesions include focal keratosis, white sponge nevus, lichen planus, hairy leukoplakia, leukoplakia, and candidal leukoplakia. Non-keratotic white lesions include leukodema, candidiasis, and mucosal burns. Leukoplakia is a premalignant white patch or plaque that cannot be characterized as another disease, with possible causes including tobacco, alcohol, trauma, and infections. Histopathology of leukoplakia typically shows hyperkeratosis and acanthosis.

1. Whitelesionsinoralcavity

2. White lesions in oral cavity
.Definition
lesionsappearaswhitepatchesinoral
.cavity
:-Causes of white lesions
Increaseinthicknessof oneormoreof-1
.epithelial layers
.Abnormalcharacterofkeratin-2
.Abnormalpermeabilityof epithelium-3

3. :-Classification
:-A) KeratoticWhitelesions
.Focal (frictional) keratosis.1
.Whitesponge nevus.2
.Lichen planus.3
.Hairy leukoplakia.4
.Leukoplakia.5
.Candidal leukoplakia.6
.Discoidlupus erythromatosis.7
:-B) Nonkeratoticwhitelesions
.Leukodema.1
.Candidiasis.2
.Mucosal burns.3

5. :-Focal (frictional) keratosis( 1
:-Etiology
chronicrubbingof frictionagainstanoral-1
. mucosa
Itrepresentsa protective actionagainst -2
lowgrade,longtermtraumaas
. habitualliporcheekbiting

6. :-Clinically
.Age: 5-6 decades
.Sex: male>female
Site:mandibularmucosa,cheek,
palate,floorof themouth,
maxillarymucosa, tongue,
buccalmucosaalong occlusal
.line, edentulous ridges
Shape: focalkeratosisclinically
showoutlinedwhitepatches, not
indurated,havenored
.margin, painless

7. Histopathology
hyperkeratosis or-1
.hyperparakeratosis
thickeningof granular cell-2
.layer
acanthosisbutthe-3
individualcells are
.normal
afewchronic-4
inflammatorycellsin
adjacent connective
.tissue

8. :-Diagnosis
.Carefulhistorytaking.1
.Carefulexamination. 2
Biopsymustbetakenif noexactcause. 3
. is known
:-Treatment
Removalof thecause,thelesionmay
.disappearin2-3 weeks

9. White sponge nevus
((faamiilialwhite folded gingivostomatitis
:-Etiology
.Itisahereditary disease
:-Site
Cheekmucosaalongocclusalline
bilaterally,ventralsurfaceof tongue,floor
of mouth,esophagus, rectum,
.vagina,larynx

10. :-Shape
Themucosaappears
thickened,folded,
corrugated(velvety),with
aspongytextureanda
peculiarwhite opalescent
.hue
Itisbilateraland
symmetrical

11. :-Histopathology
Theepitheliumisirregular,-1
thickened,showingboth
hyperparakeratosis and
.acanthosis
Thesuperficialepithelialcellsfail-2
totakeanystain(washedout
(.appearance
Thesevaculatedcellsmayshow-3
pyknotic nuclei
Theconnectivetissueshowa mild-4
.inflammatorycell infiltration
Intra-cellularand inter-cellular-5
.odema

12. .D.D
.hereditarybenginepithelialdyskeratosis-1
(.Lichenplanus(hypertrophic type-2
.Cheek biting-3
.Leukodema-4
:-Treatment
.No specific treatment
.Topical tetracycline

13. :-Lichen Planus
:-Def
Itisachronicinflammatorydisease,not
.infectious
Itisoneof themostcommon
dermatologicaldiseasetomanifestitselfin
oralcavity
,inwhichorallesions precede
.theskin lesions

14. :-Itsimportancerelates to
.itsdegreeof frequencyof occurrence-1
itsoccasionalsimilaritytoothermucosal-2
.diseases
.itsoccasionalpainfulnature- 3
.itspossibleconnectiontomalignancy-4

15. :-Etiology
:-Unknown,itmaybe
emotionalstress,overwork,trauma,(1
.infection, malnutrition
.Psychosomaticin origin(2
:Auto-immune disease(3
theepithelialcellsaretheprimarythe*
.target cells
The mechanismof basal celldamage is*
related to cell mediated immune process
involvingLangerhanscells, T-
.lymphocytes, Macrophages

16. activatelangerhanscells
,Stimulus
macrophages Interleukin1
-attractT
&lymphocytes
stimulatethemto
produceInterleukin
2

17. T-cellproliferation
.Interleukin2
.T-cell activation
Activatedlymphocytes
.toxicforbasalcells
SecreteGamma
interferon
Gammainterferoninducekeratinocytesto express
.HLA-DR class2histocompatibility antigen
.Lymphocytesnormallyexpress HLA-DR
Linkageof theseHLA-DR occurwhichresultin
inappropriateepithelialantigenic information
.passedto lymphocytes
So, self antigenmayberecognizedasforeign,by
hostT-lymphocytesresultinginauto immune
.response

18. :-Clinically
.Age: middleage,rarein children
.Sex: male=female
:-Site
skin lesions:anywhere, bilateral, symmetrical ( 1
onflexorsurfaceof wrist,inneraspectof
.thighs,trunk,nails,vulvar mucosa
,Oral lesions:gingiva,cheek,lips,tongue( 2
.palate

19. :-Oral lesions
:-Lichenplanushaspatternsinoral cavity
.Reticularlichenplanus-1
.Hypertrophiclichenplanus-2
.Atrophiclichenplanus-3
.Erosivelichenplanus- 4
.Bullouslichenplanus- 5

20. :-ReticularLichenplanus
.The mostcommontype
Site:posteriorbuccal
mucosabilaterally
, lips,
.palate, gingiva
Shape:radiatingwhite,
velvety,threadlike
papulesinalinear,
annularor retiform
.arrangement
Atinywhiteelevateddots
ispresentatthe
intersectionof whitelines
knownas(striaeof
(.wickham

21. :-ErosiveLichenPlanus
Site:posterior-inferior
aspectof buccalmucosa
adjacentto mandibular
.molar teeth
Shape:atrophic,
erythematousareaswith
centralulceration,the
peripheryof atrophic
regionsisborderedby
fine,white radiating
.striae

22. :-AtrophicLichenplanus
.Site: attached gingiva
Shape: smoothred,
poorlydefined
atrophiczones, atits
marginsthereare
whitishkeratoticstriae
radiatingperipherally
andblending into
.surrounding mucosa

23. :-Hypertrophiclichenplanus
Site:dorsumof tongue
.and buccal mucosa
Shape: well
circumscribedwhite
lesions(plaquelike)
whichrangefrom
slightlyelevatedand
smoothtoslightly
.irregular

24. :-Histopathology
.Hyperorthokeratosisor hyperparakeratosis-1
.Variabledegreeof acanthosis-2
Destructionof basalcelllayerof epithelium- 3
(hydropicdegeneration)withvacuolization of
.basal cell layer
Reteprocessmaybeabsent,hyperplasticor- 4
.saw-toothed shape
.tearingbetweenepitheliumandC.T- 5
presenceof colloid(civatte,hyaline,cytoid-6
bodies) as discrete eosinophilic ovoid bodies at
.basal cell layer

25. Lichen planus

26. Atrophic Lichen Planus
Erosive Lichen Planus

27. .D.D
.candidiasis- 1
.leukoplakia-2
.squamouscell carcinoma-3
.drug eruption-4
.discoidlupus erythromatosis-5
:-N.B. Grinspan`s syndrome
.Lichen planus
.Diabetes mellitus
. Vascular hypertension

28. :-Treatment
.No specificsystemicorlocal therapy
(.Corticosteroids(topical,intralesional ,systemic
.Antifungal therapy
.Retinoids

29. :-Prognosis
Itisabenignlesion, itwasnotconsidereda
premalignantconditionButalargenumber
of casesof epidermoidcarcinoma
.developinginorallesionsof lichen planus
Themajorityof casesof cancer have
.occurredinerosiveandatrophic types

30. :-Hairy leukoplakia
.:-Def
Itisanunusualwhitelesionwithahairyappearanceor
corrugatedsurfacethatoccurredonthelateralborderor
.dorsumof tongue
:-Etiology
.In male homosexuals-1
.An opportunisticinfectionrelatestoEpstein-Barr virus-2
.ItisrelatedtoAIDS patients-3
N.B. Viralparticlesarepresentandreplicatedwithintheepithelial
cellsof tongue.Humanpapillomaviruspresentin co-existence
.withEBV

31. :-Clinically
Site:lateralsurfaceof
tongue,dorsumof
tongue,floorof mouth,
.palate
Shape:unilateralorbilateral
surfacewhichisfoldedor
corrugatedor
(.papillary( hairy
Noassociatedsymptoms
unlessitissuperimposed
.by candidal infection

32. :-Histopathology
.Epithelial hyperplasia-1
.Markedhyperparakeratosis-2
Formationof keratoticsurface- 3
.irregularitiesand ridges
Spinouscelllayers show-4
.koilocytosis
Alterationasof nuclearchromatinin-5
.formof viral inclusions
Candidalalbicanshyphae extend-6
.intosuperficialepithelial layers
Noinflammatorycellinfiltrationin- 7
.C.T

33. :-Diagnosis
Immunohistochemical staining technique ( 1
. usinganti-viral antibodies
Ultrastructuralstudyusingelectron( 2
.microscope
.Southernblothybridizationprocedure( 3

34. .D.D
.idiopathic leukoplakia-1
.leukoplakiaassociatedwithtobacoo use-2
.lichen planus-3
.chronichyperplastic candidiasis-4
.frictionalkeratosis-5
keratoticreactionassociatedwith-6
.electrochemical interactions

35. :-T
reatment
Acyclovir
.Topicalcorticosteroids

37. (Candidiasis(Moniliasis
.Def
Thisisatermthatencompassesagroupof mucosal and
cutaneousconditionswithacommonetiological agent
.fromtheCandidagenusof fungi
:-Etiology
.The causativeorganismisCandida Albicans
:-The predisposingfactors are
.topical corticosteroids-1
.malabsorption, malnutrition-2
.poororal hygiene-3
.xerostomia-4
.systemicantibiotic therapy-5
.Cancer chemotherapy-6
.AIDS- 7

38. :-ClassificationofOral Candidiasis
:A) Acute Candidiasis
(.pseudomembranous(Thrush-1
(.atrophic(antibioticsore mouth-2
:B) Chronic Candidiasis
(atrophic(denturesoremouth&angular chelitis-1
hypertrophic(candidalleukoplakia&median-2
rhomboidglossitis&chronicmultifocal
(.candidiasis
:C) Mucocutanous forms
.localized-1
.familial-2
.syndrome-associated-3

39. Thrush

40. :-Laboratoryfindings
remavalof aportionof the-1
.candidal plaque
Itissmearedona-2
microscopicslide,
maceratedwith 20%
.potassium hydroxide
Thenexamination for-3
.typical hyphae
Cultureidentificationand-4
quantificationof
organismsmay be
performedwithavariety
of mediaasbloodagar or
.cornmeal agar

41. :-Histopathology
Histologicalsectionisstainedwith
periodicacidSchiff reagentPAS
willshowpresenceof yeastcells
andhyphaeinthesuperficial and
deeperlayersof involved
epitheliumgivebright magenta
.color
:-Histologicalfeatures include
.hyperparakeratosis-1
chronicinflammatorycell-2
infiltrationin CT
collectionsof neutrophils (micro--3
.abscess)inparakeratin layer
Thecandidalhyphae embedded-4
.in parakeratin layer

42. .D.D
.sloughassociatedwithchemical burns-1
.traumatic ulcerations-2
.mucouspatchesofsyphilis-3
.whitekeratotic lesions-4
:-Treatment
.Nystatin( 1
.Imidazole agents(2
.Triazole agents(3

43. :-Leukodema
.Def
Itisanabnormalityof thebuccalmucosaof
.unknowncause
Itmaybeconsideredasvariationof thenormalrather
.thana disease
:-Etiology
.Causativefactorsas: smoking,alcohol,bacterial infection

44. Site: buccalmucosa,
labialmucosa,floor of
.the mouth
Shape: bilateral,
symmetricalfilmy
opalescencemucosa
becomegrayishwhite
inlatestage with
.corrugated surface
.Race: blacks>whites

45. :-Histopathology
.The epitheliumisacanthotic,parakeratotic-1
Theenlargedcellsinthesuperficialpartof-2
stratumspinosumappearvacuolated because
.theycontain glycogen
.The reteridgesarebroadand enlarged-3

46. :-Diagnosiis
gentlestrokingwithagauzepadwillnotremove-1
(it ( notruboff
Withstretchingof buccalmucosa,the opaque-2
.changeswill dissipate
.D.D
.leukoplakia-1
.whitesponge nevus-2
.responsetochroniccheekbiting-3
:-Treatment
.No treatmentisnecessary

47. :-Mucosal burns
:-ChemicalBurns
Topicalapplicationsof
chemicalsasaspirin
tabletswhichisusedin
self medicationandheld
locallyagainstapainful
toothandallowedto
. dissolve slowly
:-Thermal Burns
Commoninhardpalatal
mucosacausedby hot,
.stickyfood

49. :-Premalignant lesion
Itisabenign, morphologicallyaltered
tissuethathasagreaterthannormalrisk
.of malignant transformation
.Ex. 1-leukoplakia
.erythroplakia-2
.sublingual keratosis-3
.candidal leukoplakia-4
.stomatitis nicotina-5

50. :-Premalignant condition
Itisadiseaseorpatienthabitthatdoesn`t
necessarilyaltertheclinicalappearanceof local
tissuebutisassociatedwithagreaterthan
normal risk of precancerouslesion or cancer
.developmentinthattissue
.Ex. 1-Oral submucous fibrosis
.Paterson-Kelly syndrome-2
.lichen planus-3
.Discoidlupus erythematosis-4

51. :-Leukoplakia
.Def
Itisawhitepatchorplaquethatcannotbe characterized
.clinicallyorpathologicallyasany otherdisease
.Itisaclinicalterm
:-Etiology
:-Exactetiologyisunknown,itmay be
.tobacco-1
.alcohol-2
.ultraviolet radiation-3
.trauma-4
.nutritional deficencies-5
micro-organisms(treponemapallidum, candidaalbicans,-6
(.human papilloma virus

52. :-Clinicallly
.Age: middleage4-6 decades
.Sex: male> female
Site: Tongue,floorof mouth,buccal mucosa,
.palate,lowerlip,retromolar sites
:-Shapes
.mild( thin)leukoplakia-1
.Homogenous(thick) leukoplakia-2
.Granularornodular leukoplakia-3
.Verrucous leukoplakia-4
.Proliferativeverrucous leukoplakia-5
.Erythroleukoplakiaorspeckledleukoplakia- 6

53. Leukoplakia

54. Proliferative verrucous leukoplakia

55. Speckled Leukoplakia

56. :-Histopathology
:-It variesas follow
Hyperkeratosis:thickenedkeratinlayerof-1
surfaceepitheliumeitherhyperparakeratosisor
.hyperorthokeratosis
.Acanthosis:thickenedspinouslayer-2
Surfacehyperkeratosisbutshowatrophyor-3
.thinningof surface epithelium

57. :-epithelial dysplasia- 4
Itisatermtosumupvariousdisturbancesofepithelial
:-growth as
.drop-shaped epithelial ridges-1
.basal layer hyperplasia-2
.lossof basalcellpolarity-3
.lossof normal stratification-4
.cellular pleomorphism-5
.nuclealpleomorphismand hyperchromatism-6
.increasednuclear/cytoplasm ratio-7
.lossof intercellular adherence-8
.individualcell keratinization-9
incrasednormalandabnormalmitosisinshape, site,-10
.number

58. Epithelial dysplasia

59. Epithelial dysplasia is classified according to the
:-severity as follow
Mild:whenalterationslimitedtobasaland
.parabasal layers
Moderate:whenalterationsinvolvefrom basal
.layertomidportionof spinous layer
Severe:whenalterationsinvolvefrombasal layer
.toalevelabovemidpointof epithelium

60. :-Carcinoma in situ
.Def
Dysplasticepithelialcellsthatextendfrom
basallayertosurfaceof mucosa (Top-to-
.Bottom)changes
(.It iscalled(intra-epithelial carcinoma

61. .D.D
.frictionalkeratosis-1
.galvanickeratosis-2
.verrucous hyperplasia-
3
.lichen planus-4
.leukodema-5
.whitesponge nevus-6

62. :-T
reatment
 Identificationoft
heetiologicalfactor-1
 . discontinuation
 Ifnodysplasticchangesarefound,periodic-2andcarefulfollow-upisneeded
every6
 . m
o
n
t
h
s
 R
emovalofdysplasticchanges: surgically
,-3
 .cryosurgery
,electrodessication
 .Incaseofextensivelesions,graftingisneeded-4

63. :-Candidal Leukoplakia
Age:adult
:-Histopathology
mitoticactivityis4timeshigherthanthatof-1
.idiopathic leukoplakia
heavlyinfiltrationof surfaceepitheliumwithhyphae-2
.of Candida
.chronicinflammatorycellsaremore numerous-3
Treatment:antifungaltherapymayimprove the
.condition

64. :-Nicotinic Stomatitis
.Def
Itisthemostfrequentlyleukoplakiclesion
.of the palate
:-Etiology
.pipe andcigar smoking-1
.long termuseof extremelyhot beverges-2
.reverse smoking-3

65. :-Clinically
.Age: morethan45 years
.Sex: male> female
.Site: palatalmucosa
:-Shape
Erythematouspatchesovertime
increasein keratinization
,opacification.Reddotsare
seeninposteriorportionof
.hard palate
Thesedotsaresurroundedby
whitekeratoticring, these
dotsrepresentinflammationof
ductalelementsof underlying
.minorsalivary gland

66. :-Histopathology
.epithelial hyperplasia-1
.acanthosis-2
.hyperkeratinization-3
chronicinflammatorycell-4
infiltrationof sub epithelial
.connective tissue
minorsalivaryglandshow-5
moderatedegrees of
.inflammation
excretoryductsshow-6
.squamous metaplasia

67. :-Treatme
en
nt
t
.Stop smoking-1
Itisacompletelyreversiblehabit,the-2
palatereturntonormalwithin1-2 weeksof
.smoking cessation

68. :-Erythroplakia
.Def
Itisaclinicaltermrepresentsaredpatchthat
can'tbeclinicallyorpathologicallydiagnosed as
.any other condition
:-Etiology
Unknown,Someetiologicalfactorsas:tobacco,
.alcohol,nutritionaldefects,chronicirritation
N.B. Erythroplakiaislesscommonbut more
.dangerousthan leukoplakia

69. :-Clinically
.Age: 50-70years
.Sex: male> female
Site: floor of mouth,
retromolararea ,
.tongue,soft palate
:-Shape
homogenous:red-1
patch,velvety,well
demarcated, soft
.maculeor papule
spkeled:associated-2
.withfocalwhitearea

70. :-Histopathology
of casesshow90%
.severe dysplasia
of casesshow50%
invasive squamous
.cell carcinoma
of casesshow40%
.carcinomain situ

71. .D.D
.atrophic candidiasis-1
.macularformof Kaposisarcoma-2
.vascular malformation-3
.contactallergic reaction-4
.psoriasis-5

72. :-Treatment
.careful examination-1
.biopsytakingisnecessary-2
.surgicalexcisionisnecessary-3
postoperativehistopathological-4
.examinationis necessary

74. Oral submucous fibrosis
.Def
Itisachronic, progressive,scarringhigh
.precancerousconditionof oralmucosa
:-Etiology
.chronicchewingof arecaandbetel nut-1
.generalnutritional deficiency-2
hypersensitivitytovariousdietaryconstituents as-3
.spicy

75. :-Clinically
.Race: NorthAmerica, Pakistanis
.Age: widerange,20-40years
Site: buccalmucosa,retromolararea, soft
.palatemayextendintopharynx,esophagus
Shape: Whiteyellowishlesion,theoralmucosa
losesitsresilienceandelasticity
,theprocess
progressesfromlaminapropriato underlying
.musculature

76. :-Histopathology
.hyperkeratosiswithepithelialatrophy-1
.variabledegreesof dysplasticchanges-2
superficialportionsof lamina propria are poorly-
3
.vascularizedand hyalinized
submucosaldepositionof extremelydenseand-4
avascularcollagenousC.T
. withvariable
.numbersof chronic inflammatory

77. .D.D
.radiatingrelatedsubepithelialfibrosis-1
mucosalscarringsecondarytothermalor-2
.chemicalburn
:-Treatment
.stopthe habit-1
.stretching exercises-2
.introlesionalinjectionof corticosteroids-3
surgical excision of fibrous bands and sub-4
. mucosalplacementof placentalgrafts

78. Paterson-Kelly syndrome.
(:-(Plummer-Vinson Syndrome
:-It Includes
.glossitis-1
.hystrical dysphagia-2
.hypochromicmicrocytic anemia-3
:-Etiology
.micro-organisms:CandidaAlbicans, Staph-1
.xerostomia-2
.nutritional deficiencies-3
.anamias-4
.mechanical trauma-5
.neurologic abnormalities-6

79. :-Clinically
.Age: middleage40-50 years
.Sex: female
.Site: softpalate,buccal mucosa
Symptoms:pain,burningsensation,altered taste
.and xerostomia
Shape: lemon-tintedpallorskin,angularcheilosis,
.smoothglazypainfultongue.koilonchia

80. :-Histopathology
.atrophyof the epithelium-1
.completeabsenceof reteprocess-2
.hyalinizationof lamina propria-3
.narrowingof blood vessels-4
:Treatment
.replacementnutritional therapy-1
.identificationof thecauseandtreat it-2
.high protein diet-3

82. Nevus
.Def
Itisacongenitalordevelopmentalmalformationof skin
andmucosaleadstopigmentedlesioncomposedof
.nevus cells
:-Nevus cell
Origin: melanoblastsoriginatesfromneuralcrestcellsin
dorsalregionof embryoandmigratestoskinand
mucousmembranealongthecourseof peripheral
.nerves
: Shape
.Oval, roundorpolygonal* (.Tend
tomakenests(Theques*
.Produce melanin in superficial areas of lesion*

83. :-Clinically
.Age: childhood
.Sex: female> male
.Race: whites>blackes
:-Site
.In skin: inanysitemostcommonabovewaist
Intra-orally:palate,buccalmucosa,labial mucosa,
.gingiva,alveolarmucosa, vermilion
Colour:rangefromtantoblackdependingonthe
amountof melaninproducedandthedepthof
.the lesion

85. :-Histopathology
Itischaracterizedbyabenignunencapsulated
proliferationof nevuscellswhichhasa
characteristicfeatureisthatthesuperficialnevus
cellstendtobeorganizedintoroundaggregates
(.(Theques
:-There are3 types
.junctional nevus-1
.compound nevus-2
.intradermal nevus-3

86. :-junctionalnevus- 1
Theques of vevus cellsare found only along thebasal cell
.layerof epithelium,especiallyattipsof rete ridges
Itpresentsatjunctionalzone betweenepitheliumand
.C.T

87. :-Compound nevus-2
Groupsof nevuscellsproliferatetodropoff into
.underlyingdermisorlaminapropria
Nevus cells present both along junctional area
.and withinunderlyingC.T

88. :-Intradermal(intramucosal) nevus-3
.Nevus cellsarefoundonlywithinunderlying C.T

89. :-OralNevi
Themostcommontypeisintramucosal*
.nevus
Thelesionmayormaynotshowsome*
.degreeof melanin pigmentation

90. Malignanttransformationof nevus
(:-(dysplastic nevus
:-Clinically
.varies pigmentation-1
.irregular margins-2
.distortedsurface architecture-3
:-Histopathology
disordedproliferationof nevuscells atdermal--1
.epidermal junction
nuclearatypiaasnuclearpleomorphism,-2
.hyperchromatism

91. :-Bluenevus
.Def
Itisabenignproliferationof dermal
melanocytesusuallydeep within
.subepithelialconnective tissue
:-Types
.commonblue nevus-1
.cellularblue nevus-2

92. :-Commonbluenevus-1
.Site: dorsaof hands,feet,palate
.Age: children
.Sex: female
.Shape: macularlesion,blueorblack
.Size: < 1cm
:-Histopathology
Itiscomposedof collectionof elongated,
slendermelanocyteswithbranching
dendriticextensionslocatedwithindermis.
Thesecellsalignthemselvesparallel to
.surface

93. :-Cellularbluenevus-2
.Site: buttock region
.Age: 2-4 decades
.Size: > 2cm
Shape: slow-growingblue-blackpapuleor
.nodule
:-Histopathology
Wellcircumscribed,highly cellular
aggregationof plump,melaninproducing
spindlecellswithindermisorsubmucosa,
moretypicalpigmenteddendriticspindle
cellsareseenattheperipheryof the
.lesion

94. .D.D
.Kaposi sarcoma-1
.Haemangioma-2
.Early melanoma-3
:-Treatment
.Conservativesurgical excision