Premalignant Malignant Lesions of Oral Cavity

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Premalignant

and MalignantLesions of Oral

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The palate forms theroof of the mouth andintervenes between

the nasal and oralcavities.

It consists of the

palatine process of themaxilla, the horizontalplates of the palatine

bone.

Anatomy


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Incisive Fossa Slight depression

posterior to centralincisor teeth

Nasopalatine nerve Greater palatine foramina

Medial to 3rd Molar Greater palatine

vessels and nerve

Lesser palatine foramina Lesser Palatine nerves

and vessels to softpalate

Three foramina open on the oral aspect of the hard palate


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Greater palatine artery

Superior Alveolar Arteries

The Greater Palatine arteryis a branch of the third partof the maxillary artery. Thegreater palatine arterydescends with itsaccompanying nerve in thepalatine canal.

The superior alveolararteries are terminalbranches of thenasopalatine artery

Blood Supply


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The greaterpalatine emerges

on the hard palatefrom the greaterpalatine foramenruns forward in agroove on theinferior surface ofthe bony palatealmost to theincisor teethsupplies the gumsand the mucosaand glands of thehard palate.4


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The venousdrainage is to thepterygoid plexus

and subsequentlyto the internaljugular venoussystem.

Venous Drainage


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The nasopalatine nerves Greater Palatine Nerves

The nasopalatine nervesare branches of themaxillary division of thetrigeminal nerve.

They enter the palate atthe incisive foramensupply the anterior part

of the hard palate behindthe incisor teeth.5

Innervation


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Greater (and Lesser)Palatine run through

the palatine canaland exit at the Greatand Lesser PalatineForamens,respectively.

Parasympatheticpostganglionicsecretomotor fibresfrom the

pterygopalatineganglion run with thenerves to supply thepalatine mucousglands.


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Tumors spreadingby perineuralextension can bediscovered by

radiographicenlargement of thepalatine foraminaor widening of thepalatine canals or

the foramenrotundum.6

Perineural Spread


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Oral submucous fibrosis (OSMF)

OSMF is a high risk precancerouscondition that predominantly occursamongst Indians.

Factors implicated in the pathogenesis ofsub mucous fibrosis:

Chillie consumption

Areca-nut chewing, autoimmunity

Genetic predisposition

Now there is convincing epidemiologicevidence implicating areca nut as a

causative factor in its pathogenesis.


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Epidemiology

The prevalence of OSMF in randomsamples of the population in Indiais up to 0.4%.

Although hard data are notavailable, indications are that this

disease is increasing rapidly inIndia

Submucous fibrosis occurs inboth

sexes over a wide age range


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Definition

OSMF is a chronic mucosal conditionaffecting any part of the oral mucosa.

Mucosal rigidityof varying intensitydue to fibroelastic transformation ofthe juxtaepithelial connective tissuelayer.

The presence of palpable fibrousbands is a diagnostic criterion for

submucous fibrosis.


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When the tongue is affected, it is

devoid of papillae and its mobility,especially the protrusion, is impaired

The opening of the mouth is restricted

In severe OSMF, the patient cannotprotrude the tongue beyond the incisaledges and there is a progressive

closure of the oral opening OSMF must be diagnosed only if

palpable fibrous bands are present


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Clinical aspects

The most common initialsymptoms:

Burning sensation of theoral mucosa aggravated byspicy food followed byeither hypersalivation ordryness of the mouth.


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The most common and initial

clinical sign as well as a regularfeature:

blanching i.e., marble-like

appearance of the oral mucosa.In advanced cases, the mucosabecomes tough and leathery,with numerous vertical fibrousbands


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Natural History

Unlike precancerous lesions OSMF isnot known to regress, eitherspontaneously, or with the cessation

of the areca-nut chewing habit The most serious aspect of this

disease is the high risk for the

development of oral cancer The epithelium is atrophic in this

condition which renders it susceptible

to the action of carcino ens


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OSMF and coexistent leukoplakia:

Leukoplakia is a precancerous !lesion; its coexistence with OSMFimplies the high risk for oral cancer.

OSMF and coexistent oral cancer: Notuncommonly (in 5% to 42% of thecases), submucous fibrosis and oralcancer coexist

Malignant transformation: Long-termpopulation based studies haveconfirmed its precancerous nature.


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No definitive and widely accepted

treatment is currently available. Some temporary relief from the

symptoms and improvement in the oral

opening with medicinal treatment suchas local injections of cortisone andplacentrex.

It is essential to follow-up the patientsregularly.

Patient education to discontinue the use

of areca nut and tobacco in any form.


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LEUKOPLAKIA


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Leukoplakia is the most common

premalignant or "potentiallymalignant" lesion of the oralmucosa

It is a predominantly white lesionof the oral mucosa

The incidence and prevalence ofleukoplakia vary in different partsof the world


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In general the reported

prevalence ranges from 0.2to 5% (India 0.2-4.9%)

It is seen most frequently inmiddle-aged and older men.

Gender distribution is alsovariable. Men are more

affected in some countries.


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Clinical presentation

Leukoplakia can be eithersolitary or multiple

It may appear on any site of theoral cavity, the most commonsites being: buccal mucosa,alveolar mucosa, floor of themouth, tongue, lips and palate


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Classically two clinical types of

leukoplakia are recognised Homogeneous leukoplakia is defined as a

predominantly white lesion of uniform flat

and thin appearance that may exhibit shallowcracks. This type is usually asymptomatic.

Non-homogeneous leukoplakia has beendefined as a predominant white or white-and-red lesion ("eritroleukoplakia") that may beeither irregularly flat, nodular ("speckledleukoplakia) or exophytic ("exophytic or

verrucous)


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Homogeneous leukoplakia on the dorsum and left

lateral margin of the tongue


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Non-homogenous Leukoplakia


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Verrucous Leukplakia


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Aetiopathogenesis

The aetiologyof leukoplakia is stillunclear

Tobacco seems to be the major inductor

factor, its association cannot bedetermined in all cases

A variety of smokeless tobacco habits

have been reported as leukoplakiainductors: e.g. snuff, chewing. Theselesions have shown to have a low

malignant transformation risk


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Other factors such as:

Alcohol Inadequate diet

Vitamin deficiency (e.g. vitaminA and C), areca nut (betel)

Chronic traumatic irritation

Poor oral hygienePoor socio-economic status.


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Treatment

There are different treatments for leukoplakia. However, the risk of malignant transformation is

not completely eliminated by any of the currenttherapies.

Initial treatment of a white oral lesion is theelimination of the possible aetiological factors. Complete surgical removal (leaving free-lesion

borders) is recommended in cases with epithelialdysplasia.

Apart from surgical excision, other treatmentmodalities available include cryosurgery, lasersurgery, retinoids, beta-carotene, bleomycin,calcipotriol, photodynamic therapy.


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Prognosis and complications

The malignant transformationrate of oral leukoplakia varies

from 0 to 33%.Regular check-up of these

patients is essential, probablyevery 3, 6 and then 12 months,both in treated and untreated

patients


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Oral Cancer


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Oral Cancer is the sixth leading cause ofcancer worldwide

The survival rate was 52%.

Oral cancer generally are socially deriveddiseases.

Tobacco and alcohol have synergisticeffect

Treatment of early oral cancer is surgery.

Locally advanced T3/4 are best treatedwith combined surgery and Radiotherapy.

High risk of second primary cancer


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EPIDEMIOLOGY

The Oral cavity extends from vermilion borderof lips to the plane between junction of the hardpalate and soft palate.

Include: Lips and oral cavity(buccal mucosa,tongue, ginggiva, retromolar trigone, flour ofmouth, hard palate)

The incidence of oral cancer varies throughout

the world.High incidence in India, France, SE Asia.

40% of HN cancer

Age onset 50 yrs. Sex ratio 3:1


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Risk factors

Heavy tobaccoAlcohol.

Syphilis

Viruses (EB, HSV, HPV, HIV) Neglect of oral dental hygiene(chronic

infection, unfit dentures)

Lichen planus, Plummer Vinson sy.

Immunosuppression, malnutrition


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Those who use tobacco and alcoholsimultaneously are thought to have asignificantly increased risk of oral cancer relativeto using either one alone, likelybecause thecombined use of nicotine and ethanol (knowncytotoxins) significantly increases thepenetration of N-Nitrosonornicotine (NNN), a

known carcinogen found in tobacco, across theoral mucosa.

N-Nitrosonornicotine (NNN),


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Distribution of Oral Cancer

According to Locations

Tongue

34%

Retromolar

2%Ginggiva Max

12%Ginggiva Mand

7%

Buccal

24%

Lower Lip16%

Palatum

5%


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Pathology

90% SCC:Well/Moderate/Poorly/Undiff

Exophytic, Ulcerative, Infiltrative,verucous

Other: Adeno Ca / from malignant minor

salivary gland tumors, Melanoma, Sarcomas. Premalignant lesions:

Leucoplakia, hyperplasia, Erythroplakia, anddysplasia

Regional Lnn meta related to size and thicknessof primary tumor


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Clinical presentation

Non healing ulcersInduration

Verucous/cauliflowerHot potato chewing

TrismusLnn enlargement


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Tumors of the softpalate

similar to othertumors of the oral

cavity 90% of all oral

cancer issquamous cell1

69.7% of soft palatetumors aresquamous cellcarcinoma2

Tumors of the hard palate Squamous:Non-Squamous is

1:2 to 1:4

Varied histology with non-

squamous cell tumors, minor salivary gland

tumors

rare cases of melanoma3

sarcoma malignant lymphomas.4

Soft Palate vs. Hard Palate


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Diagnosis

Clinical: History

Detail clinical examination (used headlamp, mirror)

Bimanual palpation Cervical Lnn examination

Endoscopy (searching the second primary)

Biopsy

Staging: Panoramic photo, thorax,USG liver, orCT/MRI/PET Scan


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TREATMENT

Treatment Goals:To eradicate of the primary tumor and LNmetastasis, to maintain the function, andcosmetic reconstruction.

Factors affecting choice of treatment:Tumor factors

Patient factors

Resource factors


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TREATMENT SURGERY:

Early stage T1/2No tumor: Wide excision +/ - NDHigh risk of locoregional recurrent (40%)

Management ofNo Neck:High incidence of occult metastasis in the clinicallyNo Neck (15-43%)

Controversy : Observation or Surgery/RadiationDepend on primary site.Should have minimal morbidityELND if risk of occult meta >20%. (SND/SOHND).

Sentinel Lymph Node Biopsy (SLNB)? Locally advanced tumor: Combined modality treatment


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6 Levels of Lymph-Nodes


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Selective Neck Dissection


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Classification of ND

1991 Classification:

RND

Modified RND

Selective ND:SupraomohyoidLateralPosterolateralAnterior

Extended ND

2001 Classification:

RND

Modified RND

Selective ND (SND):SND (L.I-III/IV)SND (L.II-IV)SND (L.II-V)SND (L.VI)

Extended ND

Proposed by American HN Society and AAOHNS


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Selective Neck Dissection


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Modified RND 123


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SURGICAL APPROACHES

Trans-oral approach

Lower cheek approach

Upper cheek approach

Swing mandibulotomy

Visor flap


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RECONSTRUCTION Single-stage immediate reconstruction is

recommended.

The technique:Skin graftsPedicle flapsAlloplastic meterialsAutografts

Free flaps


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Adjuvant treatment Radiothrepy (External beam/Interstitial)

Chemotherapy

Concomittant Radio+Chemotherapy(Neoadjuvant)

Palliative Chemotherapy for advanced diseases


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PROGNOSIS Location/thickness/depth of primary tumor Staging

Type of histology

Grading Presence of perineural spread

Mandibular invasion

Lnn extention (Level, size, extracaps of meta)

Molecular markers (?)


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Summary The main problem of oral cancer is early

detection Surgery is still the most important modality in

management of oral cancer. Better understanding of molecular biology of

HNSCC. Bio-molecular markers can be used in the

management of SCC oral cancer. High risk of second primary cancer,

Chemoprevention?


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Premalignant Malignant Lesions of Oral Cavity

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