ALL Oral Epithelial Tumors I and II and III (slide 7+8+9)

8/2/2019 ALL Oral Epithelial Tumors I and II and III (slide 7+8+9)

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Dent 355 Oral Epithelial Tumors, Melanocytic

Nevi, and Melanoma I

HPV-Associated Lesions

Squamous Cell Carcinoma

Premalignant Lesions and Conditions

Basal Cell Carcinoma Melanocytic Nevi and Melanoma

Dr. Rima Safadi


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Human Papilloma Virus-Associated Lesions

HPV: DNA virus of >75 types.

At least 16 types isolated from oral lesions.

Associated with a number of benign lesions of skinand mucosa.

Role in leukoplakia and SSC?

May be present in normal epithelium.


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Human Papilloma Virus-Associated Lesions:Squamous Cell Papilloma

Common benign tumor of oralmucosa.

Most occur in adults.

Variable size, may be sessile orpedunculated.

Presents as a warty orcauliflower-like growth with a

white or pink surface.

No reports of malignanttransformation, treated byconservative excision.


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Squamous Papilloma


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Histopathologic Features:

Finger-like epithelial

proliferation supported bythin fibrovascular cores.

Variable keratosis.

Mitotic figures in basallayer, no dysplasia.


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keratin

Fibrovascular core
http://images.google.com/imgres?imgurl=http://ajoupath.ajou.ac.kr/slides/hn3_2.jpg&imgrefurl=http://ajoupath.ajou.ac.kr/slides/hn3.htm&h=330&w=504&sz=58&tbnid=GuPX-RCfT3oJ:&tbnh=83&tbnw=127&start=29&prev=/images%3Fq%3Dsquamous%2Bpapilloma%26start%3D20%26hl%3Den%26lr%3D%26sa%3DN


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Human Papilloma Virus-Associated Lesions:Verruca Vulgaris (Common Wart)

Similar clinically to squamous papilloma;sessile or pedunculated.

May be single or multiple.

White due to hyperkeratosis.

Common on fingers in children.

Autoinoculation from fingers to lips.

Treated by surgical excision, cryosurgery orchemical cautery.

HPV types 2 or 4.


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Verruca Vulgaris


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Human Papilloma Virus-Associatedlesions:Condyloma Acuminatum (Venereal Wart)

Occur in the anogenitalarea, may be seenintraorally.

Multiple pink noduleswhich grow and coalesceto form soft, pink,pedunculated or sessilepapillary lesions.

One of the oralmanifestations of HIVinfection.

HPV types 6, 11, and 16.


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Condyloma Acuminatum


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Human Papilloma Virus-Associated Lesions:Condyloma Acuminatum


Prominent acanthosis with

marked broadening andelongation of rete ridges.

Koilocytosis.

Keratinization is not aprominent feature.
http://rds.yahoo.com/S=96062857/K=koilocytosis/v=2/SID=w/l=II/R=1/SS=i/OID=dab8643b2d2383a4/SIG=1h899sa61/EXP=1113798032/*-http%3A//images.search.yahoo.com/search/images/view?back=http%3A%2F%2Fimages.search.yahoo.com%2Fsearch%2Fimages%3Fp%3Dkoilocytosis%26ei%3DUTF-8%26fr%3Dsfp%26fl%3D0%26x%3Dwrt&h=460&w=675&imgcurl=www.mef.hr%2FPatologija%2Fch_9a%2Fc9a_koilocytosis.jpg&imgurl=www.mef.hr%2FPatologija%2Fch_9a%2Fc9a_koilocytosis.jpg&size=167.4kB&name=c9a_koilocytosis.jpg&rcurl=http%3A%2F%2Fwww.mef.hr%2FPatologija%2Fch_9a%2Fc9a_koilocytosis.html&rurl=http%3A%2F%2Fwww.mef.hr%2FPatologija%2Fch_9a%2Fc9a_koilocytosis.html&p=koilocytosis&type=jpeg&no=1&tt=22http://rds.yahoo.com/S=96062857/K=condyloma+acuminatum/v=2/SID=w/l=II/R=57/SS=i/OID=3a2a460aa84a815c/SIG=1h2f0mt2f/EXP=1113797938/*-http%3A//images.search.yahoo.com/search/images/view?back=http%3A%2F%2Fimages.search.yahoo.com%2Fsearch%2Fimages%3Fei%3DUTF-8%26p%3Dcondyloma%2Bacuminatum%26imgsz%3Dall%26fr%3Dsfp%26b%3D41&h=299&w=452&imgcurl=ajoupath.ajou.ac.kr%2FFGT%2Flecture%2FFgt09.jpg&imgurl=ajoupath.ajou.ac.kr%2FFGT%2Flecture%2FFgt09.jpg&size=38.5kB&name=Fgt09.jpg&rcurl=http%3A%2F%2Fajoupath.ajou.ac.kr%2FFGT%2Flecture%2Faccuminatum.htm&rurl=http%3A%2F%2Fajoupath.ajou.ac.kr%2FFGT%2Flecture%2Faccuminatum.htm&p=condyloma+acuminatum&type=jpeg&no=57&tt=109


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Squamous Cell Carcinoma: Epidemiology

Accounts for 90% of all oral malignancies.

Variable incidence worldwide:

- Oral cancer: UK & USA: < 4% of all cancers.

- Oral Cancer: India & SE Asia: up to 40% of allcancers.

Regional and ethnic variation in largecountries.
http://images.google.com/imgres?imgurl=http://www.suck.com/daily/99/01/14/harmonic.gif&imgrefurl=http://www.suck.com/daily/99/01/14/daily.html&h=88&w=171&sz=4&tbnid=LG_RkeM8_uoJ:&tbnh=48&tbnw=93&start=29&prev=/images%3Fq%3Dreverse%2Bsmoking%26start%3D20%26hl%3Den%26lr%3D%26sa%3DN


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Oral Cancer:

4th commonest cancer in men and 6th in womenon a global basis, 6th for both combined.

8th in incidence in developed, but 3rd indeveloping countries.
http://images.google.com/imgres?imgurl=http://www.suck.com/daily/99/01/14/harmonic.gif&imgrefurl=http://www.suck.com/daily/99/01/14/daily.html&h=88&w=171&sz=4&tbnid=LG_RkeM8_uoJ:&tbnh=48&tbnw=93&start=29&prev=/images%3Fq%3Dreverse%2Bsmoking%26start%3D20%26hl%3Den%26lr%3D%26sa%3DNhttp://images.google.com/imgres?imgurl=http://www.suck.com/daily/99/01/14/harmonic.gif&imgrefurl=http://www.suck.com/daily/99/01/14/daily.html&h=88&w=171&sz=4&tbnid=LG_RkeM8_uoJ:&tbnh=48&tbnw=93&start=29&prev=/images%3Fq%3Dreverse%2Bsmoking%26start%3D20%26hl%3Den%26lr%3D%26sa%3DN


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Incidence in developed countries is on theincrease despite previous decrease in incidenceand mortality rates.

Most cases occur above age 40 years, but age ofaffected patients is declining.

More common in men than in women but ratio ischanging.


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Geographical variations in oral sites particularly atrisk reflect different etiological factors. Tongue in UK while buccal mucosa in India

Geographical variation in mortality rates: 30-40% inWestern societies.

Despite advances in treatment, mortality rates havenot significantly changed.

5-year survival rates have increased significantly.


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Squamous Cell Carcinoma:Etiological Factors, Tobacco

Main carcinogenic agents in tobacco, regardless of howit is used are nitrosamines derived from nicotine.

Tobacco smoke also has polycyclic aromatichydrocarbons.

Carcinogens in tobacco smoke may dissolve in salivaand collect in areas where saliva tends to pool,increasing risk in FOM, dorsal and ventral tongue, andsoft palate.


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Etiological Factors, Tobacco

Risk factor is: number of cigarettes per day

Type of tobacco, curing and method influence

the relative risk. Pipe and cigar lip cancer

Reverse smaoking palate cancer

Relative risk of reverse smokers is 40 times more

than non smokers Regular smokers: FOM, tongue, soft palate


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Squamous Cell Carcinoma:

Etiological Factors, Tobacco

Tobacco and alcohol arethe two most importantfactors.

Evidence linking tobacco tooral cancer is firmlyestablished regardless ofits type.

Heavy smokers (40+cigarettes/day) are at 10-20 times increased risk.
http://images.google.com/imgres?imgurl=http://www.winehub24.com/wine/images/cigars.gif&imgrefurl=http://www.winehub24.com/wine/cigars.asp&h=194&w=150&sz=11&tbnid=hoMAK3ua2NMJ:&tbnh=97&tbnw=75&start=5&prev=/images%3Fq%3Dcigars%26hl%3Den%26lr%3D%26sa%3DG


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Squamous Cell Carcinoma:Etiological Factors, Tobacco Smokeless tobacco:

snuff dipping, tobaccosachets, tobacco

chewing.
http://images.google.com/imgres?imgurl=http://www.drkimberly.com/snuffers.jpg&imgrefurl=http://www.drkimberly.com/smokeless.html&h=167&w=275&sz=37&tbnid=XfjLnYhG5scJ:&tbnh=66&tbnw=109&start=9&prev=/images%3Fq%3Dchewing%2Btobacco%26hl%3Den%26lr%3D%26sa%3DGhttp://images.google.com/imgres?imgurl=http://images.clinicaltools.com/images/wasinother_putinrightfolder/snuff.jpg&imgrefurl=http://images.clinicaltools.com/images/wasinother_putinrightfolder/&h=204&w=173&sz=36&tbnid=OdUX-xNi_44J:&tbnh=98&tbnw=83&start=24&prev=/images%3Fq%3Dsnuff%26start%3D20%26hl%3Den%26lr%3D%26sa%3DNhttp://images.google.com/imgres?imgurl=http://www.finckcigarcompany.com/finck/assets/product_images/ts.finck.premium.jpg&imgrefurl=http://www.finckcigarcompany.com/finck/brand.asp%3Fdept_id%3D40%26brand_id%3D2457&h=216&w=223&sz=12&tbnid=VedcDefG4RIJ:&tbnh=98&tbnw=101&start=8&prev=/images%3Fq%3Dchewing%2Btobacco%26hl%3Den%26lr%3D%26sa%3DG


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Etiological Factors,Betel Quid & Other Chewing Habits

Betel quid (pan), chewinghabits, areca nut (submucousfibrosis).

Leukoplakia where the pan isheld

Development of papilliferousand ulcerated mass

Possible interactions betweencomponents of pans


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Chewing Habits

In India: Betel nut and lime and tobacco inbetel leaf:

Alkaloids are released from the nut

Alkaloids are carcinogenic

In Malysia: without tobacco

Tobacco increase the risk when placed in the pan

Areca nut chewing: increase the risk ofsubmucous fibrosis


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Etiological Factors, Alcohol

All Forms of Alcohol consumption are DANGEROUS

Second major factor.

Dose/time relationship.

Pure ethanol has not been shown to be carcinongenic, butother chemicals in the beverage, congeners, may beresponsible for increased cancer risk.

Increasing incidence of oral cancer, especially in youngergroups, may be linked to increased alcohol consumption.


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Close association with tobacco since most heavy drinkers areheavy smokers, too.Synergistic effect

Mechanism of Alcohol Possible carcinogenic effect of chemicals other than ethanol Alcohol may enhance transport of carcinogens across mucosal

barrier. Nutritional deficiencies in alcoholism may impair mucosal barrier

function.

Alcohol and tobacco usage have been associated with mucosalatrophy.

Chronic alcohol intake may impair ability of liver to detoxifycarcinogens, and can suppress immune responses needed to fightcancer.


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Concerns about high alcoholcontent in some mouthwashes?


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Etiological Factors, Diet and Nutrition

Increased risk foresophageal, pharyngeal,and oral cancer in primarysideropenic anemia(Plummer-Vinson orPatterson-Kellysyndrome).

Epithelial atrophy: Iron defeciency lichen planus and

tertiary syphilis Render mucosa more

susceptible tocarcinogens.
http://rds.yahoo.com/S=96062857/K=iron+deficiency+anemia/v=2/SID=w/l=II/R=8/SS=i/OID=dffa640880c5fd52/SIG=1ijt6ohp8/EXP=1113740063/*-http%3A//images.search.yahoo.com/search/images/view?back=http%3A%2F%2Fimages.search.yahoo.com%2Fsearch%2Fimages%3Fp%3Diron%2Bdeficiency%2Banemia%26rs%3D0%26ei%3DUTF-8%26fl%3D0%26fr%3Dsfp%26vf%3D&h=275&w=252&imgcurl=www.infocompu.com%2Fadolfo_arthur%2Fimages%2Fglositis_a.jpg&imgurl=www.infocompu.com%2Fadolfo_arthur%2Fimages%2Fglositis_a.jpg&size=18.1kB&name=glositis_a.jpg&rcurl=http%3A%2F%2Fwww.infocompu.com%2Fadolfo_arthur%2Fingles%2Fglositis_a.htm&rurl=http%3A%2F%2Fwww.infocompu.com%2Fadolfo_arthur%2Fingles%2Fglositis_a.htm&p=iron+deficiency+anemia&type=jpeg&no=8&tt=383


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Squamous Cell Carcinoma:Etiological Factors, Diet and Nutrition

Vitamin A is also important inmaintenance of oral epithelium.

A diet high in the antioxidant vitamins A, C,& E is believed to lower the risk of oralcancer.


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Squamous Cell Carcinoma:Etiological Factors, Occupational Risks

High exposure to UV lightis important in SCC of skin,including lips.

Lip cancer is morecommon in lower lip in fair-skinned males withoutdoor occupations.

SCC of the lip may bepreceded by solar keratosis(actinic cheilitis).
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Etiological Factors, Viruses

HSV can be carcinogenic or co carcinogenic in laboratoryexperiments.

It only rarely produce tumors


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Squamous Cell Carcinoma:Etiological Factors, Viruses

HPV HPV types 16 & 18important factors in SCC of uterine cervix.

Evidence for role of HPV in some oral premalignant andmalignant lesions increasing.

HPV 16 is the most common isolate, but it has also beendetected in normal mucosa.

Some HPV proteins : inactivation of tumor-suppressor genes p53 and Rb. significant step in development of oral cancer.

HPV is likely to be an important cofactor in at least some oral cancers.


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Squamous Cell Carcinoma:Etiological Factors, Viruses

EBV is important in development of somenasopharyngeal carcinomas and lymphomas, but asimilar role in oral cancer has not been established.

EBV is probably an incidental passenger virus foundin some lesions.


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Squamous Cell Carcinoma:Etiological Factors, Immunosuppression

Increased risk oflip cancerreported following renal andother transplants linked toimmunosuppressive therapy.

Increased incidence of oralcancer with AIDS.

Inconclusive evidence ofincreased risk in HIV-positivepatients.

Smoking, alcohol, and irondeficiency may impair cell-mediated immunity, butsignificance of this role is not

established.


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Squamous Cell Carcinoma:Etiological Factors, Chronic Infections

Chronic candidal infection associatedwith some speckled leukoplakias, andchronic hyperplastic candidosis(candidal leukoplakia) have relatively

high malignant transportation rates.

However, other chronic oral candidalinfections are not associated withmalignant transformation.

Role of candida therefore is uncertain.
http://images.google.com/imgres?imgurl=http://www.nohic.nidcr.nih.gov/pubs/detect/pages/images/s18.jpg&imgrefurl=http://www.nohic.nidcr.nih.gov/pubs/detect/pages/page10.html&h=367&w=400&sz=30&tbnid=Kk6MzJdX2K8J:&tbnh=110&tbnw=120&start=10&prev=/images%3Fq%3Dleukoplakia%26hl%3Den%26lr%3D%26sa%3DGhttp://images.google.com/imgres?imgurl=http://www.primer.ru/std/gallery_std/images/candida.JPG&imgrefurl=http://www.primer.ru/std/gallery_std/candida.htm&h=272&w=350&sz=32&tbnid=4tIBdzrqtuoJ:&tbnh=90&tbnw=116&start=9&prev=/images%3Fq%3Dcandida%26hl%3Den%26lr%3D%26sa%3DG


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Squamous Cell Carcinoma:Etiological Factors, Chronic Infections

Historically, tertiary syphilis has beenlinked to oral cancer, especiallyanterior 2/3rds of dorsal tongue.

Epithelial atrophy in late stages mayrender mucosa more susceptible tocarcinogens.

Syphilitic leukoplakia may precede

invasive carcinoma.

However, late stage syphilis is rarenow.


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Squamous Cell Carcinoma:Etiological Factors Summary

1. Tobacco smoking: pipes, cigars, cigarettes, bidis, reverse smoking.

2. Smokeless tobacco: snuff dipping, tobacco sachets, tobacco chewing.

3. Betel chewing, betel quid, areca nut.

4. alcohol: spirits, wines and beers, alcohol and tobacco synergism.

5. Diet and nutrition: iron deficiency, vitamins A & C, nutritionaldeficiencies & alcoholism.

6. Dental factors.

7. Ultraviolet light.

8. Viruses: HSV, HPV, HIV.

9. Immunosuppression.10. Chronic infections: candidosis, syphilis.

11. Occupation.


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Oncogenes and Tumor-Suppressor Genes

Cellular proliferation:

1. growth-promoting proto-oncogenes

2. growth inhibitory tumor-suppressor genes.

Oral cancer has a multifactorial etiology and is the result of

damage to these genes allowing uncontrolled cellularproliferation.

Carcinogenesis is a multistep process

multiple sequential mutations which accumulate within thecell.


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Model for genetic progression

The development of oral cancer involves progressiveaccumulation of genetic changes:

Model for genetic progression based on loss ofheterozygosity (LOH):

( loss of genetic material from specific locations onchromosomes)

1. normal mucosa, LOH at 9p: predysplastic

2. predysp, additional loss LOH at 3p, 17p:

dysplasia 3. dysplasia:- additional LOHat 13q, 11q, 14q:

carcinoma in situ (CIS)

4. CIS: LOH at p, 8, 4q: invasion


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During carcinogenesis:

a. proto-oncogenes may undergo mutationand become activated oncogenes, or:

b. tumor suppressor genes may be mutatedand their products inactivated.

The result in both cases leads toderegulation of cell proliferation and tumorformation.


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Overexpression and mutations of the oncogenesc-

myc, ras, and erb B-1 has been reported in oral SCC.


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Abnormalities in the tumor-suppressor gene p53 areinvolved in many human cancers, including oral cancer.

The p53 is essential for normal cell growth and division sinceits product blocks the cell cycle in the G1 phase.


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Clinical Presentation

Clinical presentation of oral SCCcan take many forms.

Early diagnosis is themost important factorinfluencing prognosis.

Clinicians must be

suspicious of any lesionfor which no cause canbe found or which doesnot respond asexpected whenputative causes are

eliminated.


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Clinical Presentation, Early Lesions

Early lesions are usuallyasymptomatic.

Many forms ofpresentation, mostcommonly:

1. White patch.

2. Small exophytic growthwhich in early stagesshows no ulceration orerythema
http://www.usc.edu/hsc/dental/opfs/SC/20bb.html


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3. Small indolent ulcer. 4. Erythroplakia.


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Squamous cell cracinoma


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S C ll C i


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Suspicious clinical featuresfor early carcinoma:

1. Persistent ulceration.

2. Induration.

3. Fixation to underlyingstructures.

4. Destruction of underlyingbone in alveolar ridge lesions.

5. Enlarged reactive regional

lymph nodes.6. Carcinoma of vermilion

border of lip: slightly raisedswelling, or crusty, lesionresembling delayed healing of

herpes labialis.

S C ll C i


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Clinical Presentation, Advanced Lesions

Advanced lesions maypresent as:

1. Broad-based, exophyticmass with rough, nodular,warty, hemorrhagic, ornecrotic surface.

S C ll C i


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2. Deeply destructive, crater-like ulcer with raised, rolledeverted edges.

S C ll C i


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3. Infiltration of musculature may result in functionaldisturbances including impaired speech and difficultswallowing.

4. Pain may be a feature.

S C ll C i


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5. Radiographic evidence ofbone destruction.

6. Mobility of teeth.

7. Altered sensation overdistribution of mentalnerve.

8. Pathologic fracture ofmandible.
http://www.usc.edu/hsc/dental/opfs/SC/24bb.htmlhttp://www.usc.edu/hsc/dental/opfs/SC/25bb.html


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S C ll C i


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S C ll C i
http://www.usc.edu/hsc/dental/opfs/SC/16bb.htmlhttp://www.usc.edu/hsc/dental/opfs/SC/15bb.html


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S C ll C i


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S am C ll Ca in ma


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Pathology

Considerable variation.

Invasion and destruction of localtissues accounts for induration

and fixation detected clinically.

Cytologically malignantsquamous epithelium with

variable degrees ofdifferentiation.

Keratinization varies with degree

of differentiation.



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Pathology

Well-differentiated tumors:

- Obvious squamousdifferentiation.

- Masses of prickle cells with

limiting layer of basal cellsaround them.

- Recognizable intercellularbridges.

- Central keratin pearlformation.

- Nuclear and cellularpleomorphism is notprominnemt.

- Relatively few mitotic figures.



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Pathology

Moderately differentiatedtumors:

- Less keratinization.

- More pleomorphism of cellsand nuclei.

- Abundant and atypicalmitotic figures.

- Still readily identified assquamous type.



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Pathology

Poorly differentiated tumors:- Keratinization usually absent.

- Marked atypical features.

- Cells may be hardly recognizable as

epithelial.

- The need for immunohistochemistry

- Subjectivity and overlap in grading.


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Poorly differentiated SCC stained for

cytokeratin

Brown stain: epithelial cells positive for cytokeratin



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Pathology

In general:

- variable lymphocytic and plasma cell infiltration insupporting stroma, probably an immune reaction totumor antigens, necrosis and ulceration.


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Pattern of infiltration affects prognosis:

Cohesive invasive fronts: Broad front ofinvasion:

Better prognosis

Non- Cohesive:

Separate islands

Individual malignant cells


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Different patterns of invasion

immunostaiuned for Cytokeratins


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Pathology

Variable pattern oflocalinfiltration and destruction:

- lymphatic permeation

- Vascular invasion

- Sarcolemmal spread- perineural spread

- bone invasion,edentulous/dentate.- Through alveolar crest

- Through PDL- Extent of bone invasion may

be greater than that seen onradiographs


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Verrucous Carcinoma

A variety of low-grade SCC.

thick white warty plaque ofheaped up folds of tissuewith deep cleft-like spacesin between.

prognosis is good.

Some cases transform intoa regular SCC with

metastasis.*



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Verrucous Carcinoma

In the mouth, mostcommon location ismandibular buccal sulcus

and adjacent buccalmucosa.*

Mainly affects the elderly.*

Particularly seen in tobaccochewers and snuffdippers.*

http://images.google.com/imgres?imgurl=http://www.drkimberly.com/snuffers.jpg&imgrefurl=http://www.drkimberly.com/smokeless.html&h=167&w=275&sz=37&tbnid=XfjLnYhG5scJ:&tbnh=66&tbnw=109&start=9&prev=/images%3Fq%3Dchewing%2Btobacco%26hl%3Den%26lr%3D%26sa%3DG


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Verrucous Carcinoma


Very well differentiated, heavilykeratinized SCC with little or nocytological atypia.

Slowly pushing cohesive front

Local destruction but no mets

Mitoses are rare.



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Verrucous Carcinoma


Although it is an exophytic tumor, it also has a slowlyadvancing, pushing, cohesive invasive front causing local

destruction.



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Verrucous Carcinoma

Strict criteria for diagnosis shouldbe employed, and it

Must be differentiated from:i. Well-differentiated SCC with a

papillary component.

ii. Leukoplakias with warty surfaces

variously called verrucoushyperplasia or verrucousleukoplakia.



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Carcinoma-In-Situ

A term used todescribe severeepithelial dysplasia inwhich the whole, oralmost the wholethickness of epitheliumis involved, but

basement membraneis intact and there is noinvasion of laminapropria.


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Carcinoma-In-Situ

Field cancerization:dysplasia or carcinoma-in-situ

in epithelium surroundingan invasive carcinoma,which may suggest a fieldchange in a wide area ofmucosa

It is probable that some

carcinomas thought to berecurrent tumors,represent new primarylesions arising in such afield change.

Oral Premalignant Lesions and Conditions


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g

Premalignant lesion: amorphologically altered tissue inwhich cancer is more likely to occur than in its normalcounterpart,

e.g. leukoplakia, i.e. the lesion itself undergoes malignanttransformation.

Premalignant condition: a generalized disorder associatedwith a significantly increased risk of cancer developingsomewhere in the mouth, e.g. submucous fibrosis.

However, relatively few oral SCCs are preceded by arecognizable premalignant lesion or condition.



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The following may be consideredpremalignant lesions orconditions:

1. Precancerous lesions:

a) Leukoplakia- homogeneous,non-homogeneous, nodular, andspeckled types, including chronichyperplastic candidosis andproliferative verrucousleukoplakia.

b) erythroplakia

c) carcinoma in situ.

http://images.google.com/imgres?imgurl=http://www.nohic.nidcr.nih.gov/pubs/detect/pages/images/s18.jpg&imgrefurl=http://www.nohic.nidcr.nih.gov/pubs/detect/pages/page10.html&h=367&w=400&sz=30&tbnid=Kk6MzJdX2K8J:&tbnh=110&tbnw=120&start=10&prev=/images%3Fq%3Dleukoplakia%26hl%3Den%26lr%3D%26sa%3DG


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2. Precancerousconditions:

a) oral submucous

fibrosis.b) lichen planus.

c) actinic keratosis orcheilitis.

d) other conditionsassociated with oralepithelial atrophy, e.g.

sideropenic dysphagia.

Basal Cell Carcinoma (Rodent Ulcer):
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( )Clinical Features

Common neoplasm of skin,especially face.

Affects old people with

chronic exposure to UVradiation.

Occasionally presents onlips, particularly upper lip.

Many may be skin tumorsspreading to involvevermilion border.



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Typically presents as aslow growing nodulethat eventually

ulcerates centrally, andmay cause extensivedamage if not treated.

http://rds.yahoo.com/S=96062857/K=basal+cell+carcinoma/v=2/SID=w/TID=I034_83/l=II/R=33/SS=i/OID=f891bcdb6be92f90/SIG=1il2n0mdb/EXP=1114585583/*-http%3A//images.search.yahoo.com/search/images/view?back=http%3A%2F%2Fimages.search.yahoo.com%2Fsearch%2Fimages%3Fp%3Dbasal%2Bcell%2Bcarcinoma%26ei%3DUTF-8%26fl%3D0%26imgsz%3Dall%26fr%3Dslv1-%26b%3D21&h=334&w=334&imgcurl=www.ghorayeb.com%2Ffiles%2Fbasal_cell_carcinoma_temple_gg_sq234.jpg&imgurl=www.ghorayeb.com%2Ffiles%2Fbasal_cell_carcinoma_temple_gg_sq234.jpg&size=124.5kB&name=basal_cell_carcinoma_temple_gg_sq234.jpg&rcurl=http%3A%2F%2Fwww.ghorayeb.com%2FBasalCellCa.html&rurl=http%3A%2F%2Fwww.ghorayeb.com%2FBasalCellCa.html&p=basal+cell+carcinoma&type=jpeg&no=33&tt=2,109


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Multiple basal cellcarcinomas arising atyounger age and onnon-sun-exposed sitesare a feature of basalcell nevus syndrome.



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( )

Histopathologic Features

Histologically consistsofmalignant basaloidcells arranged invarious patterns ,invading adjacenttissues.

Melanocytic Nevi and Melanoma
http://www.meei.harvard.edu/shared/ophtho/pathlab4.html


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Melanocytic Nevi and Melanoma

Melanocytes are dendritic cells ofneuroectodermal origin.

They are located mainly in the basal layer of epidermis andsome mucous membranes.

They are widely distributed and present in large numbers inoral mucosa of clinically pigmented and non-pigmentedraces, the difference being of activity and not number.

Their function is to produce melanin which they pass toadjacent keratinocytes.

Acquired Melanocytic Nevi:


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Clinical Features

Nevus: any developmental on skin ormucosa, from Latin naevus = birthmark.

Acquired melanocytic nevi or moles, arevery common, particularly on skin of head

and neck.

Most present in childhood andadolescence.

The average person may develop 20-30nevi.

Malignant change can rarely occur in nevi.

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Clinical Features

Melanocytic nevi are rare inthe oral mucosa.

Most reported intraoralnevi present in adult life asslightly elevated,pigmented lesions on thehard palate or buccalmucosa.

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Melanocytic nevi areconsideredhamartomatous lesionsformed by proliferation of

melanocytes or theirprecursors, with variablemelanin pigmentproduction.

There are different stagesin the natural history ofmelanocytic nevi.



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Histopathologic Features They are separated histologically based on location of nevus cells

relative to epithelium:

1. Junctional nevus.

2. Compound nevus.

3. Intramucosal (intradermal). Most oral nevi are of this type.



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Junctional Nevus Compound nevus

Nevus cells

Nevus cells


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Malignant Melanoma:


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Clinical Features

ABCD Clinical Features:

1. Asymmetry (uncontrolledgrowth pattern)

2. Border irregularity

3. Color variation

4. Diameter greater than 6mm

Malignant Melanoma:


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Highly pleomorphic neoplasms.

Variable melanin production,may be absent (amelanoticmelanoma).

Immunohistochemical studiesusing specific markers formalignant melanocytes (S-100and HMB-45) are useful.

Ultrastructural examination toidentify immature melanosomescan be used.

Oral Malignant Melanoma


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Oral melanoma is rare.

Slightly more common inmales than females.

> 70% involve posteriormaxillary alveolar ridgeand hard palate.

In about a third of cases,there is history of previouspigmentation in the area.

Oral Malignant Melanoma


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Oral melanomas present as darkbrown or bluish black slightly raisedlesions with an uneven nodular orpapillary surface.

Amelanotic lesions tend to appearreddish.

Growth may be rapid with extensivedestruction of bone and loosening ofteeth.

Most are advanced at presentation,with both regional lymph node andblood-borne metastases common.

Documents

ALL Oral Epithelial Tumors I and II and III (slide 7+8+9)