Oral cavity malignancy.pptx

UNIT -3 SYMPOSIUM-ORAL CAVITY MALIGNANCY
1. ANATOMY OF ORAL CAVITY – R. BHUVANESHWARI
2. RISK FACTORS’ CLINICAL FEATURES AND PREMALIGNANT
LESIONS OF ORAL CAVITY – N.K.CHERAN
3. EXAMINATION OF ORAL CAVITY MALIGNANCY –P.M.CHURNIKA
4. CLASSIFICATION,STAGING AND INVESTIGATION OF ORAL
CAVITY MALIGNANCY – E.DEEPAK KUMAR
5. SURGICAL MANAGEMENT ORAL CAVITY MALIGNANCY –
R.DEEPAK RAJA
6. NON-SURGICAL MANGEMENT OF ORAL CAVITY MALIGNANCY –
B.DHANALAKSHME

ANATOMY OF
ORAL CAVITY
HOD MAM:
DR.BANUREKHA M.S.,D.G.O
R.BHUVANESHWARI
3rd UNIT

ORAL CAVITY
It extends from the lips to
the oropharyngeal isthmus
i.e upto the level of anterior
pillar of tonsil.
DIVISIONS
- Outer part,vestibule
- Inner part,oral cavity proper

VESTIBULE
● Narrow space bounded externally by lips and
cheeks, and internally by the teeth and
gums.
● It communicates
- With the exterior through the oral fissure
- With the mouth open , it communicates with
oral cavity proper.

ORAL CAVITY PROPER
It is bounded
● anterolaterally : teeth , gums and alveolar arches
of the jaws
● Floor : tongue
● Posterior:communicates
with pharynx through
Oropharyngeal isthmus

LIPS
Lip is composed of
● Skin
● Superficial fascia
● Orbicularis oris muscle
● Submucosa
● Mucous membrane
Frenulum of lips : mucous membrane forms median folds
that pass from lips to gums.
Philtrum:median vertical groove on outer surface of upper lip.

Each cheek is composed of
● Skin
● Superficial fascia
● Buccinator covered by buccopharyngeal fascia
● Submucosa
● Mucous membrane
Parotid duct : opens on the inner surface of the cheeks
opposite to the crown of the upper second molor tooth.
Buccal pad of fat:lies on the buccinator

● The cheeks are supplied by buccal branches of the
maxillary artery.
● Innervated by buccal branches of the mandibular
nerve.
● The lymphatics of the cheek drain chiefly into
submandibular and preauricular lymph nodes and
partly into buccal and mandibular nodes.

GUMS ( GINGIVAE )
● The gums are the soft tissues which envelop the
alveolar processes of the upper and lower jaws and
surround the necks of the teeth.
● These are dense fibrous tissue covered by startified
squamous epithelium.
● Each gum has two parts :
- Free part
- Attached part

NERVE SUPPLY OF GUMS
UPPER GUMS
● Labial side
● Lingual side
LOWER GUMS
● Labial side
● Lingual side
Posterior, middle and anterior superior alveolar nerves.
Anterior palatine and nasopalatine nerves.
Buccal branch of mandibular and incisive branch of
mental nerve.
Lingual nerve

LYMPHATIC DRAINAGE OF GUMS
● Upper gums drains into submandibular nodes.
● Anterior part of lower gums drains into the
submental nodes.
● Posterior part of lower gums drains into the
submandibular nodes.

RETROMOLAR TRIGONE
Triangular area
overlying anterior
ramus of mandible.
Apex: maxillary
tuberosity
Base: posterior most
Molar.

HARD PALATE
Forms roof of the oral cavity.
● Anterolateral margins : continuous
with the alveolar arches and gums.
● Posterior margin: gives attachment
to soft palate.
● Superior surface : forms floor of the
nose.
● Inferior surface : forms roof of
the oral cavity.

SOFT PALATE
● It is a movable, muscular fold, suspended from
the posterior border of the hard palate.
● It separtes nasopharynx from the oropharynx.
● The soft palate has two surface
- anterior surface
- posterior surface

● Two borders:
- Superior border
- inferior border
● Muscles of soft palate

Dorsum of the tongue
It is divided into
● Oral part
● Pharyngeal part

Inferior surface of the tongue

Extrinsic muscles Actions
● Genioglossus
● Hyoglossus
● Styloglossus
● Palatoglossus
Protrudes the tongue.
Depresses the tongue.
Retracts the tongue.
Elevates the tongue.

Intrinsic muscles of the tongue

Intrinsic muscles Actions
● Superior longitudinal
● Inferior longitudinal
● Transverse
● Vertical
● Shortens the tongue makes its dorsum
concave.
● Shortens the tongue makes its dorsum
convex.
● Makes the tongue narrow and elongated.
● Makes the tongue broad and flattened

Taste buds
The bud is formed by two kinds of cells
- supporting cells ( form an outer envelope
for the bud )
- Gustatory cells which are chemoreceptors
occupy central portion of the bud.
The taste receptors are located around the
papillae found on upper surface of the tongue.
These structures are involved in taste
perception.

MINOR SALIVARY GLANDS
Around 450 minor salivary glands in the oral cavity.
They contribute 10% of the salivary volume.
Sites :
Cheek
Palate
Floor of the mouth
Lips
Retromolar area
Upper aerodigestive tract
. oropharynx
. Larynx
. Trachea
. Sinuses

OROPHARYNX
Anterior : oral cavity
Above : nasopharynx
Below: Hypopharynx
Extent: soft palate to upper
border of epiglottis.

Subsites
● Palatine tonsil
● soft palate
● Base of tongue

HOD MAM: DR.BANUREKHA M.S, DGO
Risk factors ,
Clinical features,
Premalignant lesions
of oral cavity
N.K.Cheran
3rd unit

Risk factors.
••increase in age
•Tobacco
•smoking
•alcohol
•areca nut /pan masala
•Epstein Barr Virus
•Human papilloma virus
•Plummer Vinson syndrome
•poor nutrition

● AGE: M/c in old age - due to low immunity
● SEX: males affected twice than females
( Due to smoking & tobacco use )
● SMOKING: cigarettes contain nicotine - carcinogenic
● OCCUPATION: persons who work under uv exposure
⬇️
Lip cancer
● Poor oral hygiene – leads to oral lesions
Risk factors of oral lesions

ALCOHOL: dehydrating effect
⬇️
on oral mucosa
⬇️
increases permeability,DNA damage
⬇️
Allowes carcinogens easily
⬇️
Precancerous to cancerous lesion formation

ARECA NUT / PAN MASALA:
3 Alkaloids -Arecoline,arecaidine,Guvacaine
⬇️
Increased collagen synthesis,fibroblast formation
⬇️
oral submucosal fibrosis

TOBACCO - indigenous- smoking or snuff - bidi ,hookah etc
Oral chewable form - betel quid
⬇️
Polycyclic aromatic hydrocarbon , nitrosamine,etc
⬇️
Carcinogenic effect ,Chronic irritation
⬇️
Inflammation - cytokines release + activation of TGF growth factor-beta
⬇️.
Cancerous lesion formation

NUTRITION:
● Vitamin c - blocks the conversion of nitrites to nitrosamine
which has carcinogenic effect.
● Vitamin A,B Complex , antioxidants,Cu ,Zn- have protective
effect on cancer
● Red chillies,spices - causes chronic irritation and results in lesion
formation

HUMAN PAPILLOMA VIRUS:
HPV 16,HPV 18,HPV 31,HPV 45
⬇️
Abnormal alteration & growth lining the infected mucosa in
the oral cavity
⬇️
Dysplasia - leads to cancer formation

EPSTEIN BARR VIRUS :
In Immunocompromised individuals it causes oral
hairy leukoplakia

Premalignant lesions of oral cavity
High risk
● Erythroplakia
● Speckled
erythroplakia
● Chronic
hyperplastic
candidasis
Medium risk
● Oral submucosal
fibrosis
● Syphilitic glossitis
● Sideropenic
dysphagia
Low risk
● Oral lichen planus
● Discoid lupus
erythematous
● Discoid keratosis
congenita

Premalignant lesions of oral mucosa &
oropharyngeal mucosa present as…..
● Leukoplakia
● Speckled leukoplakia
● Erythroplakia

Premalignant lesion:
● It is defined as morphologically altered tissue in which cancer is more likely to develop than its
apparently normal counter part.
● Premalignant condition:
It is a generalised state assosiated with a significantly incresed risk of cancer.

Premalignant lesions premalignant conditions
 Leukoplakia
 Erythroplakia
 Leukokeratosis nicotina
palatinae
 Candidiasis
 Carcinoma in situ
 Oral submucosal fibrosis
 Oral lichen planus
 Actinic keratosis
 Syphilis
 Discoid lupus erythematosis
 Sideropenic dysphagia

Leukoplakia
● A White patch / plaque that cannot be characterized clinically or
pathologically.
● Varies from small well circumscribed to an extensive lesion.
3 - types
↙️ ⬇️️ ↘️
Homogeneous nodular speckled
Uniform white Fine nodules arises from an
Patches. on surface erythematous base

Predisposing factors ..
7S
•syphilis -Sharp tooth
•smoking -Sunlight
•spirit -UV radiation
•sepsis
•spices

5 stages ..
Stage 1 - mild thickening of the surface with hypertropy
of the papillae & hyperkeratosis
Stage 2 - Tongue is covered with smooth paint.
Stage 3 - surface becomes irregular like dried paint
Stage 4 - warty projections appears with cracks&
fissures( precancerous)
Stage 5 - desquamation leads to red glazed tongue (
progress to carcinoma )

Clinical features …
Gross morphology
● Occurs anywhere in oral cavity ( buccal mucosa ,floor of mouth
, ventral surface of tongue ,palate ,gingiva).
● Solitary / multiple patches
●
● Thickening,smooth /wrinkled/ fissured.
● Palpation - induration -suggestive of malignant change.

Investigation…
● Biopsy and histological examination is the key to define the
nature and relative risk of leukoplakia.
● Molecular,biological and immunohistochemical techniques(p53
antigen,HPV 16,18,33)are important for detection of
leukoplakia with high risk of malignant transformation.

Differential diagnosis…
● Lichen planus
● Discoid lupus erythematous
● Candidiasis
● Hairy leukoplakia
● Uremic stomatitis

Histopathology..
● Hyperkeratosis
● Mild Dysplasia - nuclear
hyperchromasia ,
Increased nuclear to
cytoplasmic ratio
● Severe dysplasia - nuclear &
cellular pleiomorphism
,numerous mitotic figures

Treatment:
● Stop pan masala & smoking –homogenous leukoplakia without
epithelial dysplasia may disappear or diminish in size with in 2-
3months after cessation of habit.
● Surgical excision ( skin graft if required)
● In wide spread or multiple leukoplakia oral administration of 13-
cis retinoic acid (1mg/kg of body weight daily for 2-
3months)maybe used with limited success.
● Topical application of retinoic acid has been used in the
treatment of selective cases.
● Co2 laser excision

Erythroplakia
(erythroplasia of queyrat)
● Bright red plaque,which cannot be characterized clinically or
patholologically as any other recognisable condition.
● More malignant .
● Can be
Homogenous
Speckled
Erythroleukoplakia

Clinical features ..
Gross morphology
● More common in lower alveolar mucosa ,gingivobuccal sulcus,floor
of mouth, tongue & vestibule
● Bright red plaque
● Slightly depressed than surrounding mucosa.
● Surface - nodules
● Red color - decreased keratin
↙️ ↘️
Shining vasodilation + subepithelial Inflammatory reaction

Investigation: Differential diagnosis
1.Speckled leukoplakia
2.Erythematous candidiasis
3.Early squamous cell carcinoma
4.Local irritation
5.Drug reaction.
 History and examination.
 Biopsy-exfoliative cytology
 Fluorescence staining
 Toluidine staining

Histopathology
● Lack of keratin
● Subepithelial
Inflammatory reaction
● Vasodilation

Treatment :
1. Surgical excision
2.Interventional laser surgery is an alternative
treatment for oral erythroplakia.
3.Topical 5% imiquimod cream and 5-aminolevulinic
acid has been used with for success of treatment.

Potential risk of malignant transformation…
Increases with ……
● Increase with age of the patient
● Increase with age of the lesion
● Higher in smokers
● Increase with alcohol consumption
● Depends on anatomical site of Premalignant lesion
● Higher for leukoplakia in floor of mouth ,ventral surface of
tongue, particularly in younger women.

Chronic hyperplastic candidasis
● Dense plaques of leukoplakia.
● Caused by Candida albicans.

Immunocompromised individuals
⬇️
Easily acquires fungal infection- Candida albicans
⬇️
Produces oral lesion -chronic hyperplastic candidasis high risk for malignant
transformation
⬇️
Dense plaques of leukoplakia
⬇️
M/C -around commissures of mouth
⬇️
Can extend to vermilion & facial skin
Chronic hyperplastic candidiasis

Clinical features:
● White patches over buccal mucosa ,commisures of mouth ,
Vermilion border ,facial skin .
● Painless
● Lesions are adherent to the surface
Investigation
Biopsy

Histopathology
Invasion of candidia in epithelium
Elongation of epithelial ridges
Inflammatory infiltrate

Treatment:
Medical
Topical antifungals 6 weeks
Systemic antifungals 2 weeks
Surgical
● Surgical excision
● Laser vaporization

Oral submucosal fibrosis:
Fibrous bands beneath the oral mucosa
⬇️
Scarring
⬇️
Contracture
Progressive
disease

Causes..
● Prolonged irritation by chillies, tobacco ,areca nut
● Dietary causes - vit A,B complex,iron - deficiency
● Localised collagen disorder
● Common in indian & Asian population - middle age
M/c - soft palate ,faucial pillars,buccal mucosa

Clinical features:
● Trismus - limited mouth opening
● Difficulty in protruding the tongue
● Soreness & burning in mouth during food

Histopathology
Hyperplasia of overlying epithelium
Atrophied epithelium replaced with
fibroblasts

Treatment..
Medical
● Avoid precipitating factors- chillies , tobacco, areca.
● Maintain orall hygiene.
● Restricted mouth opening - intralesional steroid
(Local injection- dexamethasone 4 mg with Hyalase 1500 units)
biweekly for 10 days
● Vitamin and iron deficiency- treat with supplements.
Surgical
Surgical excision+ skin graft

Sideropenic dysphagia
● As known as Plummer Vincent / Patterson Kelly syndrome
Triad
↙️ ⬇️ ↘️
Iron deficiency. Beefy. Oesophageal web
Red tongue

Iron deficiency
⬇️
Epithelial atrophy of oral mucosa
⬇️
Oral mucosa vulnerable to carcinogens
⬇️
Development of oral cancer

Treatment..
Iron supplements- correct iron deficiency
Reduces atrophy of epithelium
& Risk of malignant transformation

HISTORY AND EXAMINATION OF
ORAL CAVITY MALIGNANCY
HOD MAM- DR.BANUREKHA M.S.,D.G.O.
BY,
P.M.Churnika,
3rd unit.

HISTORY OF PRESENTING ILLNESS:
H/O pain, referred to ear
H/O Halitosis, foul smelling discharge from mouth
H/O dysphagia
H/O ulcer
H/O excessive salivation
H/O alteration in voice, difficulty in speech, difficulty in swallowing
H/O difficulty in opening mouth
H/O swelling in upper part of neck
H/O fever
H/O loss of weight, loss of appetite
H/O trauma
H/O recent falling of tooth
H/O hemoptysis, pleuritic chest pain

HISTORY:
AGE AND SEX-
cleft lip, cleft palate-birth
mucous retention cyst, stomatitis-any age
carcinoma lip and tongue-Males above 50 yrs.
OCCUPATION:
Outdoor activities-countryman’s lip
RESIDENCE:
White causians in Australia-more susceptible
negroes –less susceptible
INCIDENCE- MC in India- CARCINOMA GINGIVOBUCCAL SULCUS
MC in west – CARCINOMA TONGUE.

SWELLING/ULCER:
mucous retention cyst –inner side of lip or cheek,
very slow growth, long time
cancer of lip, tongue-short history
though slow growing

PAIN:
Site of pain: dental ulcer --side of tongue
late Carcinoma tongue –referred to ear of affected side(lingual, auriculotemporal
nerve)
PAINFUL PAINLESS
Aphthous ulcer Carcinoma
Dental ulcer Syphilitic ulcer
Tb ulcer Systemic diseases
Smoker’s ulcer Monilial ulcer
Herpetic ulcer Leucoplakia
Ictal ulcer Mucous retention cyst

SPECIFIC COMPLAINTS:
o excessive salivation-carcinoma tongue
o inability to protrude tongue –tongue tie,
late stage of carcinoma tongue
o difficulty in speech-cleft lip, cleft palate, carcinoma tongue
o deviation of tongue tip to side of lesion –carcinoma tongue.
o alteration of voice-1st symp of carcinoma posterior 1/3 tongue

PAST HISTORY:
H/O DM,TB,AIDS,any immunocompromised state
H/O ill fitting dentures
H/O tooth removal with delayed healing of socket
H/O sexually transmitted diseases

PERSONAL HISTORY:
smoking, alcohol leucoplakia
Tobacco ,spicy food
Clay pipe smoking- carcinoma Tongue
Exposure to sunlight- carcinoma lip
betel nut ,Pan chewing- carcinoma cheek
Supari/khaini
Eg: betel quid kept in inner aspect of left cheek for 30 mins each
time and spits it out. Uses it 6times/day.
Reverse smoking- carcinoma hard palate
Diet – vit A, (Iron Deficiency Anemia-squamous cell
carcinoma of oral cavity, hypopharynx)

GENERAL EXAMINATION:
Cancer-anemia, cachexia, tb ulcer-primary focus in lungs
gummatous-syphilitic lesions
EXAMINATION OF ORAL CAVITY:
LIPS
HARD AND SOFT PALATE
BUCCAL MUCOSA(CHEEK)
RETROMOLAR TRIGONE
TONGUE
FLOOR OF MOUTH
GUMS/ALVEOLUS

PHYSICAL EXAMINATION
INSPECTION:
1.Lips,
2.cheek-retract outwards
3.Gums,
4.floor of mouth,
5.Posterior 1/3rd OF TONGUE -push tongue to one side
6.Anterior 2/3rd Tongue-mouth opened fully,
protrusion of tongue
7.Fauces,tonsil,beginning of pharynx-depress tongue
with spatula
8.Dental formula :2123 2123
2123 2123

INSPECTION
1.LIPS:
Cleft lip
Cleft palate
Facial cleft
Pigmentation of lip and buccal mucosa-Addison’s disease
Small bluish black spots-Peutz jegher’s syndrome
Chancre of lip-painless ulcer, dull red
Cracked lips-midline of lower lip(cold weather)
Ectopic salivary neoplasm-upper lip, slow growing,lobulated

CA lip-erosion in early stage
red granular appearance with whitish flecks,
Yellowish crusting in middle of erosion
ulcerated centre, everted margin
skin –red, vascular
Macrocheilia-thickening (upper lip)

2.TONGUE:
Volume
Macroglossia--lymphangioma,hemangioma,
neurofibroma,muscular macroglossia(cretins)
Colour
white – leucoplakia(chronic superficial glossitis)
Red glazed tongue-desquamated leucoplakia,
Blue-venous hemangioma
Black,hairy-antibiotics,hyperkeratosis in smokers (aspergillus Niger)
Crack/fissure
Syphilitic-longitudinal

INCIDENCE SITE of carcinoma in tongue
25% ANTERIOR 1/3RD LATERAL *2
(ON EACH=50%)
10% TIP
10% UNDER SURFACE
5% DORSUM
25% POSTERIOR 1/3RD

Swelling/ulcer:
 Dental ulcer-lateral margin of tongue
 Traumatic ulcer
 Aphthous ulcer-small, multiple
 Tb ulcer -tips and sides
 Gummatous ulcer-midline ant2/3rd dorsum of tongue,
 Carcinomatous ulcer-scc MC SITE:MIDDLE 3RD OF LATERAL MARGIN OF TONGUE
 Angioma like swelling –lingual thyroid (at foramen caecum)
Mobility of tongue:
Inability to protrude completely-ankyloglossia
Deviate(impaired nerve supply)- advanced CA tongue
Impaired speech ,not protrude-tongue tie

3.PALATE:
Congenital cleft
Perforation of hard palate-syphilis
ulcer-
Most Common-MINOR SALIVARY GLAND TUMORS

4.GUMS:
Healthy gums-bright pink
Pyorrhoea alveolaris-deep red line along free edge of gum
Vincent stomatitis-ulcer,pseudomembrane,bad smell.
Cancrum oris-painful, purple red papule on molar/premolar area
Dental abscess-swollen gums
Lead-blue line

5.FLOOROF MOUTH:
ranula-unilateral, bluish translucent cyst
Sublingual dermoid-opaque, midline, submental region
Plunging ranula-cervical prolongation to
submandibular region
Wharton’s duct opening
Leucoplakia of floor of mouth and
ventral surface of tongue: high
incidence of malignant change .

6.CHEEK:
Pigmented patches-Addison’s disease, Peutz jegher’s syndrome
Mucous cyst-buccal mucosa of cheek at bite of teeth
Stenson’s duct opening
Cyst
Salivary tumour
Ulcer

PALPATION:
1.LIP:
Benign-firm, lobulated
carcinoma lip-stony hard, always fixed
Hunterian chancre-rubbery hard
Mucous retention cysts-inner surface of lower lip
Fluctuation, transillumination –positive in large cysts
Squamous cell carcinoma
most common in lower lip

2.TONGUE:
ULCER TB SYPHILITIC APHTHOUS
ULCER
TRAUMATI
C
MALIGNANT
Pain PAINFUL Painless Painful Marked Painless---
painful,iceberg like
Shape Oval/circular Round Any shape Irregular
Number Multiple Single Single/multi Single Single
Edge Undermine
d
Punched out - Edematous Everted, rolled out
Floor Pale
granulation
tissue
Wash
leather
slough
White
floor,yellowish
border,
Slough Necrotic debris,dirty
grey
Discharg
e
Thin
,watery
Greyish
white
- Purulent BLEED ON TOUCH,
Thick,purulent,offensiv
e
Induratio
n
- Slight - slight Marked

3.PALATE:
Alveolar abscess-tender, fluctuating swelling
Gumma-soft, swelling in middle of hard palate
Mixed tumour of ectopic salivary gland.
4.GUMS:
Scurvy-bleed, swollen, tender
Uremia-bleed
Epulis-swelling of alveolar margin of gum

5.FLOOROF THE MOUTH:
Ranula-fluctuating ,brilliantly transilluminant.
Sublingual dermoid-not translucent,tense
fluctuant in midline.
Carcinoma of floor of mouth-fixed, indurated base

6.CHEEK:
Mucous cyst-smooth surface, mobile ,fluctuate
Papilloma-solid tumor,irregular surface,mobile
Carcinoma-fixed, indurated
Most common carcinoma IN CHEEK-
SQUAMOUS CELL CARCINOMA

EXAMINATION OF JAW:
Upper jaw(maxilla)
Swelling/ulcer-epulis
Tenderness in maxillary antrum without distension-empyema
TEETH-count, dental cyst, dentigerous cyst

Lower jaw(mandible):(carcinoma tongue,
floor of mouth, lip)
thickening /irregularity, alveolar abscess
Fracture of mandible(mostly at the
region of canine tooth)
Body, angle, inferior part of ramus of mandible-accessible
For temporomandibular joint:
Ask patient to open and close his mouth-trismus, ankylosis
Place fingers over temporomandibular joint just below and in front of tragus –
crepitus(osteoarthritis)/clicking jaw(loose meniscus/disarticulated articular cartilage)
Little finger inserted into external ear with pulp directed forwards-dislocation

EXAMINATION OF CERVICAL LYMPH NODES
LEVEL PRIMARY CANCER SITES
1 Anterior tongue,floor of mouth,anterior alveolar
ridge,lip,salivary gland
2 Oral cavity,oropharynx,nasopharynx,salivary
gland,larynx
3 Oral cavity, lateral tongue,
oropharynx,hypopharynx,thyroid,
larynx
4 Oral cavity,hypopharynx,larynx, thyroid, cervical
esophagus
5 Git,lungs,testis,scalp,external ear,
6 Thyroid
7 CARCINOMA TONGUE- SKIP METASTASIS

OTHER SYSTEM EXAMINATION:
Head and neck
Cranial nerves-7,8,9,10,11,12
Ear,nose,throat.
Thyroid
Central nervous system
Cardiovascular system
Respiratory system
Abdomen

COMMON MODES OF PRESENTATION:
Anterior 2/3rd of tongue-ulcer
Posterior 1/3rd of tongue-pain, dysphagia, dysarthria
Dentate patient-swelling of gums, tooth extraction which fails to heal
Numbness over distribution of mental nerve
Pathological fracture of mandible

CLASSIFICATION,STAGING
AND INVESTIGATIONS OF
ORAL CAVITY
MALIGNANCIES
- E.DEEPAK KUMAR
- UNIT 3
HOD MAM: DR.BANUREKHA
M.S.,D.G.O.

SPREAD OF SQUAMOUS
CELL CARCINOMA
• Local infiltration
◦ Invasion of local soft tissues
◦ Invasion of perineural space
◦ Invasion of vessels
◦ Invasion of bone
• Lymphatic spread
• Hematogeneous spread (distant
metastasis)

NECK NODE LEVELS
• IA- Submental nodes
• IB- Submandibular nodes
• II - Upper jugular nodes
• III- Middle jugular nodes
• IV- Lower jugular nodes
• VA &VB- Posterior triangle
nodes
• VI- Anterior compartment
nodes
• VII- Upper mediastinal
nodes

CARCINOMA OF LIP
Most common location of oral cancer.
90% on lower lip,common in old age.
90% 5-year survival if <2 cm
90% squamous cell carcinoma (Rules of 90's)
Basal cell carcinoma is more common on upper lip
2-15% regional metastasis (for all stages)

CLINICAL FEATURES
• Non-healing progressive
ulcer, painless to begin with
• Everted edge with
indurations
• Growth moves with the lip
• Fungation, bleeding, halitosis
is present
Red granular appearance with whitish
flecks.
Yellowish crusting in the middle of erosion
The centre becomes ulcerated and margin
becomes everted

SPREAD OF CARCINOMA LIP
• Lower lip has bilateral and
ipsilateral lymphatic
drainage into level I-Ill
nodal groups
• Upper lip has ipsilateral
lymphatic drainage into
level I-Ill nodal groups (no
contralateral drainage due
to embryological fusion
plates).

CARCINOMA TONGUE
GROSS
1. Papillary.
2. Ulcerative or
ulceroproliferative 60%.
3. Fissure with induration.
4. Lobulated, indurated
mass—frozen tongue.

CLINICAL FEATURES
Painless ulcers/ swelling in tongue.
Excessive salivation ( often blood
stained)
Dysphagia
Inability to articulate
Ankyloglossia
Halitosis
Bronchopneumonia
SITES OF CARCINOMA
1.Lateral margin (47-50%)
2.Posterior third (20%)
3.Dorsum (6.5%)
4.Ventral surface (9%)
5.Tip (10%)

SPREAD OF CARCINOMA TONGUE
LOCAL SPREAD:
• In case of anterior two-thirds of tongue, the spread
occurs to genioglossus muscle, floor of the mouth,
opposite side and mandible.
• In case of posterior third of tongue it spreads locally
to tonsil, side of pharynx, soft palate, epiglottis, larynx
and cervical spine.

Lymphatic spread:
• From tip of tongue it spreads to
submental nodes.
• From lateral margin it spreads
to submandibular lymph nodes
and later to deep cervical
lymph nodes.
• From posterior third it spreads
to pharyngeal nodes and upper
deep cervical lymph nodes.
• All oral cavity malignancies spread to level I and II
sometimes level III
• Tongue malignancy follows skip metastasis and spread
to level III and IV

CARCINOMA
CHEEK/BUCCAL MUCOSA
Clinically, there are three distinct types: exophytic, ulcerative, and
verrucous.
The patient may present with pain or bleeding, trismus,halitosis.
Posterior extension may result in involvement of the lingual or dental
nerves, which may cause ear pain.
Extension behind the pterygomandibular raphe into the pterygoid
muscles or into the buccinator and masseter muscles may cause trismus.
Involvement of retromolar trigone indicates an advanced disease.
Death usually occurs as a result of poor nutrition and general debilitation

SPREAD OF CARCINOMA BUCCAL
MUCOSA
LYMPHATIC SPREAD
The submandibular lymph nodes are most frequently
involved; involvement of the upper cervical and the
parotid lymph nodes is less common.
LOCAL SPREAD
Infiltrating lesions of the buccal mucosa can invade the
buccinator muscle, extend to the buccal fat pad, and
invade the subcutaneous tissue.
Carcinomas of the buccal mucosa frequently spread by
direct invasion into the gingivobuccal sulcus, the upper
and lower alveolar ridges, the hard palate, the maxilla,
and the mandible.

OTHER CARCINOMAS
CARCINOMA OF HARD PALATE:
• Minor salivary gland tumours(adenoid cystic) are more common in
palate.
• Malignant tumours may spread to periosteum, bone, maxilla,sinus,
or nose.
• Upper deep cervical nodes are involved in 25% of patients.
CARCINOMA OF ALVEOLUS
• It is squamous cell carcinoma arising from gums
• There will be invariable bone involvement by direct extension
• Nodal spread is also common

As posterior third tongue has got abundant lymphatics which cross
communicates on either side, lymph node spread is common (70%).
Bilateral nodal spread is common.
Remains asymptomatic for long time —> Early symptoms mimic sore
throat —> Late symptoms dysphagia and change in voice.
Infiltration into the tongue muscles like genioglossus, epiglottis, pre-
epiglottic space, tonsillar pillars and hypopharynx are common.
Hematological spread is common,carry poor prognosis.
CARCINOMA FLOOR OF
MOUTH

SECONDARIES WITH UNKNOWN
PRIMARY
Primary may be very small to be detected
clinically in places like fossa of Rosenmuller,
pyriform fossa, nasopharynx, posterior third
tongue but present clinically as hard lymph
node secondaries in neck called as secondaries
with unknown primary.
Hard secondaries in neck confirmed by FNAC
but all investigations including blind biopsies,
CT head and neck region and endoscopies could
not identify primary lesion creates a situation
called as secondaries in neck nodes with an
occult primary (30%).

QUIZ
A 58-year-old man presents with discomfort in his mouth. He
denies any trauma to his oral mucosa. He has smoked
cigarettes daily for the past 38 years. He drinks 2 beer daily.
His heart rate is 94 beats/minute, blood pressure is 142/74
mmHg, and temperature is 37°C (98.6°F). On physical
examination, the physician notices a plaque in the oral
mucosa.
Which of the following findings would most likely indicate the
plaque is a premalignant lesion?
a) A white deposit on the tongue that can be easily scraped off
b) A white, rough patch on the lateral tongue
c) A white plaque that cannot be scraped off
d) A clear base surrounded by erythema

CLINICAL FEATURES OF ORAL
CANCER THAT WARRENT
INVESTIGATION
Persistent oral swelling for >3 weeks
Mouth ulceration for >3 weeks
Sore tongue
Difficulty swallowing
Jaw or facial swelling
Painless neck lump
Unexplained tooth mobility
Trismus

BIOPSY
When a clinical diagnosis of
oral cancer is suspected,a
tissue diagnosis, typically by
way of incisional biopsy(edge
biopsy), is essential.
The biopsy must include the
most suspicious area of the
lesion, as well as normal
adjacent tissue.

Biopsy has to be taken from the edge as it contains active
cells; not from the centre as it is the area of necrosis.
Malignant squamous cells with epithelial pearls (Keratin
pearls) are the histological features.

MAGNETIC RESONANCE IMAGING-
Staging
It provides excellent visualisation of
soft tissue infiltration of the tumour.
Ideally it should be performed
before diagnostic biopsy as biopsy
frequently distorts the image of the
primary tumour.
It can detect the cervical node
metastasis

COMPUTED TOMOGRAPHY- Staging
CECT Head and neck is useful when bony invasion is
suspected.
CT of the thorax and abdomen is now indicated for all
patients and not just those with proven cervical lymph
node metastasis and large-volume disease.
CT is much more widely available than MRI but its
utility may be restricted by artifact degredation of
images by dental restorative materials.

ULTRASOUND
It is useful in evaluation of undiagnosed
neck lumps or presumed cervical
metastasis.
Used alongside fine-needle aspiration
cytology (FNAC), ultrasound is capable of
delineating and sampling cervical
lymphadenopathy and both thyroid and
salivary gland lesions/masses.

abnormal nodes include shape
(round), absent hilus, intranodal
necrosis, reticulation, calcification,
matting, soft-tissue edema,low or
mixed echogenecity and peripheral
vascularity.
sonograms of patients with
metastatic nodes. Image of 70-year-
old man with carcinoma of tongue
and with bilateral metastatic upper
cervical lymph nodes shows one of
metastatic upper cervical nodes is
hypoechoic, round, and without
echogenic hilus (arrows). Lymph
node also shows multiple areas of
intranodal cystic necrosis
(arrowheads).

FINE NEEDLE ASPIRATION CYTOLOGY
FNAC is useful for the assessment and
pathological diagnosis of enlarged cervical
lymph nodes.
It involves the use of a fine-needle puncture
into the mass and immediate aspiration for
cytological examination. It has few
complications and there is no evidence of
tumour seeding along needle tracts.
It requires no specialist equipment other than a
21G or 23G needle and a 10 mL syringe.

POSITRON EMISSION TOMOGRAPHY
COMBINED WITH CT
• Positron esmission tomography combined with CT
(PET-CT) of the whole body uses the anatomical
capability of CT scanning in concert with radiolabelled
tracers capable of localising to specific tissues.
• The most widely used tracer is 18 fluoro-dexoyglrucose
(FDG), which is transported and trapped within
hypermetabolic tissues (typically cancerous or
inflammed tissues, or those that are predictably
physiologically active).

ORTHOPANTOMOGRAM
To access the state of dentition and potential gross
mandibular invasion.

OTHER INVESTIGATIONS
Direct and Indirect laryngoscopy
Endoscopy
Dentist opinion
Complete blood count
Blood grouping
Liver function tests
Hiv/HbsAg
Chest x-ray
ROUTINE BLOOD INVESTIGATIONS

TNM STAGING OF
ORAL CAVITY
CANCER
By American Joint
Committe on Cancer
(8th edition,2018)

T- STAGING
Tx- Primary tumour cannot be assessed
Tis- Carcinoma in situ
T1- Tumour ≤2cm
with depth of invasion ≤5mm
• T2- Tumour ≤2cm
with depth of invasion >5mm and ≤10mm OR
Tumour >2cm and <4cm

T3- Tumour 2cm-4cm
with depth of invasion >10mm OR
Tumour >4cm
• T4- Tumour moderately advanced local disease or very
advanced local disease

T-STAGING OF CARCINOMA OF
TONGUE

T4a (lip) - Invading through cortical bone, inferior alveolar nerve, floor of
mouth or skin of face(chin or nose).
T4a (Oral cavity) - Invading adjacent structures eg, cortical bone, deep extrinsic
muscle of tongue, maxillary sinus or skin of face.
T4b - Invading masticator space, pterygoid plates, skull base or encases
Internal carotid artery (Superficial erosion alone of bone/ tooth socket by
gingival primary is not T4)

N- Nodal spread
Nx - Nodes cannot be assessed.
NO - No regional lymph node spread.
N1 - Regional single node <3 cm with no Extranodal extension
N2 - N2a: Single ipsilateral node <3 cm with Extranodal extension OR
single ipsilateral node 3-6 cm with no Extranodal extension

• N2b: Multiple ipsilateral nodes <6 cm in size and no Extranodal extension
• N2c: Bilateral or contralateral nodes <6 cm with no Extranodal extension
N3 - N3a: Single ipsilateral node >6 cm with no Extranodal extension
N3b: single ipsilateral node >3 cm with Extranodal extension OR multiple
ipsilateral or contralateral or bilateral any sized nodes with Extranodal
extension OR single contralateral node of any size with Extranodal extension

M- DISTANT METASTASIS
cM0- Distant metastasis not present
cM1- Distant metastasis present
pM1- Distant metastasis,microscopically confirmed

STAGING GROUPS
Stage 0 - TIS NO MO
Stage I - T1 NO MO
Stage II - T2 NO MO
Stage III - T3 NO MO; T1, T2, T3 N1 MO
Stage IV - IVA: T4a NO/N1 MO; T1, T2,T3, T4a N2
MO.
IVB: Any T N3 MO; T4b any N MO.
IVC: Any T Any N M1

Surgery for Oral
Cavity
Malignany
HOD MAM : Dr.BANUREKHA.MS.,DGO
-By
R.Deepak Raja
IIIrd UNIT

Management
Treatment of oral cancer is based on staging of cancer
*STAGE 1&2:-
-Early stage oral Cancer
[Single Modality Treatment]-(Surgery or RT)
*STAGE 3&4a:-
-Locally advanced & Operable cancers
[Combined Modality Treatment]
*STAGE4b&4c:-
-palliative [RT or CT] or Symptomatic Treatment

Criteria for Inoperability
 Fixed Neck Nodal Adenopathy
 Recent onset of trismus
(Gross Infratemporal Fossa Invasion)
 Base skull involvement
 Extensive Soft Tissue Invovement
 Distant Metastasis

Neck Dissection
 Incision-Modified Schoebinger Incision
 Modified Radical Neck Dissection[MRND]
Level I-V lymph nodes are Removed
+ At least One of the 3 Extra
Lymphatic structures are saved
(*Spinal Accessory Nerve
*Sternocleidomastoid
*Internal Jugular Vein)

MRND Classification
 MRND 1-Spinal accessory Nerve is saved
 MRND 2-Spinal accessory Nerve and Internal jugular
Vein is saved
 MRND 3-All 3 are saved
(Functional neck Dissection)

Other Methods
 Radical Neck Dissection(Crile’s Operation)
Level I-V Lymph Nodes are Removed+ All 3 extra Lymphatic Structures are Removed
 Selective Neck Dissection:
1.Central neck dissection(CND)-Level VI lymph nodes are removed
2.SupraOmohyoid Neck Dissection(SOHND)-levels I,II,III are removed
3.Extended SOHND-Levels I-IV are removed

Principles Of Management of NECK

Primary Reconstructive Options In Oral Cancers
Anatomical Site Primary
Reconstructive
Options
Alternative
Reconstruction
Floor of mouth
Buccal Mucosa
Tongue Base
Lateral Tongue
Radial forearm free flap For Tongue : PMMC Flap
Total Tongue AnteroLateralThigh OR
Rectus Abdominis flap
PMMC flap
Maxillary Tumors Iliac crest graft** is the
method of choice for
Maxillary Reconstruction
Fibula

Survival and Prognosis
Stage I & II Disease have Better Prognosis
(5 Years survival 31-100%)
• Stage III & IV Disease-Advanced have Poor Prognosis
(5 Years survival 7-41%)

Content
I. LIP CANCER
II. TONGUE CANCER
III. BUCCAL MUCOSA CANCER
IV.FLOOR OF MOUTH
V. RETROMOLAR PAD
VI.HARD PALATE

I. Lip Cancer
It usually arises as an ulcer on the vermilion border.
⮚ 95% - On the lower lip,
⮚15% -On central one-third and commissures.
⮚Squamous cell carcinoma- M/C in lower lip,
⮚Basal cell carcinoma- M/ C in upper lip

•Initially starts as
*Occasionally it occurs at the angle of mouth
a red granular dry lesion
ulcerated
ulcero-proliferative lesion.

A.Small Tumors
⮚Small tumours (<2 cm) of the lip
-either a V- or W-shaped excision under
local or general anaesthesia.
⮚The defect,
(which should be no larger than one-third of
the total lip size),
is closed in three layers – mucosa, muscle and
skin
– with particular attention paid to the correct
alignment of the vermilion border
Skin markings for
wedge excision of
the lower lip.
Primary closure.

B.Intermediate tumours
⮚Larger tumours,
(defects of between one-third and two-thirds the size of the lower lip)-require local
flaps for reconstruction.
⮚V or W excision —>microstomia.
⮚Large central defects can be managed using local flaps —the Johansen step
technique.
⮚This allows closure of the defect by symmetrical advancement of soft-tissue
flaps, utilising the excess skin in the labiomental grooves.
⮚Alternative techniques include the Bernard or the Karapandzic advancement
flaps.
Skin markings for Johansen
step reconstruction.
Closure of lip and labiomental
steps.

C.Total lip reconstruction
▪Extensive tumours of the lower lip, which invade adjacent tissues
(T4), have a high incidence of neck node metastasis.
▪Patients with such advanced disease require surgery, which may
include
- unilateral or bilateral selective neck dissection,
- total excision of the lower lip and chin,
- with or without adjacent mandibular resection
(rim or segmental mandibulectomy ).
Skin markings for total excision of the lower
lip,chin and left selective neck dissection

▪The lower lip soft-tissue defect can be reconstructed with a variety of
free flaps including the
- radial forearm flap potentially suspended with palmaris longus
tendon (or)
- perforator flaps such as the anterolateral thigh(ALT) flap (or)
- The medial sural artery perforator (MSAP) free flap.
*the scapula free flap provides exceptional flexibility and tissue
variability. Postoperative view of the
reconstructed lower lip using a
radial artery forearm flap.

Methods of Reconstruction
1. Abbe-Estlander's rotation flap used for either upper or lower lip lesions (of less than ½ of lip)
located at the angle based on labial artery.

2. Fries' modified Bernard facial flap
-reconstruction using lateral
facial flaps.
- It is used when defect is more
than ½ of lip and midline.

II. Tongue Cancer
▪ The tumors may present as ulcerations or as exophytic
masses.
▪ The regional lymphatics of the oral cavity are to the
submandibular space and the upper cervical lymph nodes.
▪ The lingual nerve and the hypoglossal nerve may be directly
invaded by locally extensive tumor
▪ Involvement can result in
- ipsilateral paresthesias,
-deviation of the tongue on protrusion with fasciculations &
eventual atrophy.
Ulcerative squamous cell
carcinoma of the right lateral
border of the tongue.

•Tumors on the tongue may occur on any surface, but are most commonly seen on the lateral
and ventral surfaces.
•Primary tumors of the mesenchymal components of the tongue include
-leiomyomas,
-leiomyosarcomas,
-rhabdomyosarcomas &
-neurofibromas.

Access
 Access for oral cancer
-allow accurate assessment
-clear visualisation to enable tumour clearance to be achieved.
 Access techniques include:
❖Transoral – small –moderate sized anterior oral tumours;
❖Lip-split technique and paramedian or median mandibulotomy.
❖Visor incision with or without drop down.
Skin markings for lip split and
mandibulotomy in continuity with
neck dissection
Visor approach to the anterior
mandible/floor of the
mouth and tongue.

Surgery
• Tumour less than 1 cm in size
or in carcinoma insitu
-Wide excision with 1 cm
clearance in margin and depth is
done in Laser (CO2/diode) can be
used.
• Tumour between 1-2
cm in size
-partial glossectomy is done
with 2 cm clearance from
the margin with removal of
1/3rd of anterior two-thirds
of the tongue.
• Tumour larger than 2
cm,
-Hemiglossectomy is done
with removal of anterior
2/3rd of tongue on one
side up to sulcus terminalis

•Wide excision - growth is in the tip of the tongue.
Same side palpable, mobile lymph nodes - radical neck block dissection.
Bilateral mobile lymph nodes - One side radical block & Other side modified radical block dissection
with essentially retaining internal jugular vein (on opposite side) to maintain the cerebral venous
blood flow.
( Other option is doing same side radical neck dissection and on opposite side Supra Omohyoid block
dissection.)
• Posterior third growth - lip split and mandible resection, so as to have total glossectomy- Kocher's
approach
( When mandible is involved hemimandibulectomy is done.)

Reconstruction
▪ Small defects of the lateral tongue
-primary closure or be allowed to heal by secondary intention with little or no functional
impariment.
▪ Larger defects (e.g.T2, T3 and T4 resections) require formal reconstruction to
encourage good speech and swallowing.
[Free tissue transfer of suitable tissue (e.g. a radial forearm flap, or ALT), utilising
microvascular anastomosis in most instances,gives a good functional result]
▪ Large-volume defects, including total glossectomy, may require more bulky flaps
such as the rectus abdominus free flap or ALT depending on patient body habitus..
Radial artery forearm flap
raised before division of a
vascular pedicle and
cephalic vein

Carcinoma Of Posterior One-Third Of Tongue
•Carcinoma posterior third of the tongue is often poorly differentiated and so caries poor prognosis.
•T1, T2, N0 and N1 diseases
surgical wide excision or often by total glossectomy
+midline mandibulotomy incision (mandible split)
+neck dissection on both sides (MRND one side).

III.Carcinoma Of Buccal Mucosa
• Squamous cell carcinoma is the most common type of carcinoma of the
cheek.
• Occasionally it can be adenocarcinoma arising from the minor salivary
glands or mucous glands. Rarely it can also be melanoma.
• Carcinoma is common in posterior half of cheek than anterior.
• It spreads outwards to involve the skin causing fungation, ulceration,
orocutaneous fistula formation.
Exophytic squamous cell carcinoma of
the right buccal mucosa.

Indication for Surgery
Early tumour
Tumour spreading to mandible bone/alveolus
Fungation, haemorrhage due to erosion
Recurrence of tumour after RT
Multiple sites
Soft tissue spread
Locally advanced but amenable to surgical resection

Surgery
1.Wide excision
-wide excision with 1-2 cm clearance.
-Often, the approach to the tumour is by raising the cheek flap (outside).
-After the wide excision, the flap is placed back-Patterson operation
2. Hemimandibulectomy
3.Neck lymph nodes block dissection.

•SCC of the buccal mucosa should be excised widely,
including the underlying buccinator muscle.
•Access for buccal carcinoma can be achieved either
-Transorally for smaller lesions (T1, T2) or
-Lip-splitting technique for larger lesions (T3, T4).
•Reconstruction of the buccal mucosa prevents scarring and trismus.
•Options include the radial artery forearm flap or a temporalis muscle flap.
-Raw temporalis muscle inset into the buccal mucosal defect will epithelialize spontaneously over several weeks.

•Growth with mandible involvement:
wide excision of the primary tumour+ hemimandibulectomy or segmental resection
of the mandible or marginal mandibulectomy (using rotary electric saw) is done.
•Operable growth with mandible involvement and mobile lymph nodes on the
same side (confirmed by FNAC):
wide excision of the primary tumor
+Hemimandibulectomy
+radical neck lymph node dissection is done
(like commando operation).
-It is called as composite resection.

IV.Floor of Mouth
• Surgical excision may include a Partial Anterior Glossectomy and Anterior mandibular resection.
• Only very small tumours of the floor of the mouth can be managed by simple excision.
• Management of the adjacent mandible/mandibular rim may be necessary where the tumour abuts the
mandible.
• this may be by way of a rim resection or segmental mandibulectomy.

Reconstruction After Surgery
•Reconstruction will depend on the defect size (and its constituents) and
ranges from healing by secondary intention to use of the
- thin, pilable radial forearm free flap for small defects,
- to ALT and composite flaps for larger resections.
•If a patient is unfit for microvascular free-flap surgery or the facilities
are limited,
-bilateral nasolabial flaps tunnelled into the mouth and interdigitated
provide an acceptable alternative

V. Retromolar Pad
•Tumours occurs at this site frequently, but not always,
invade the ascending ramus of the mandible.
•They also spread medially into the soft palate and the
tonsillar fossa.
•Access for excision may necessitate additional access
(e.g. a lip split and mandibulotomy).

•Small defects are managed ideally with
a microvascular free flap, such as
-a radial artery forearm flap
-with a temporalis muscle flap
( where pedicled options are preferred)
•Abundant soft tissue capable of modification and flexible at inset, to suit larger defects.

VI.Carcinoma of hard palate
•Squamous cell carcinoma is ulcerative with raised and
everted edge.
•Upper deep cervical lymph nodes are involved in 25% of
patients.
•wide excision with removal of the underlying palatal bone.
•Often Partial or Total maxillectomy ( Weber-Ferguson
incision) may be required.

•Myocutaneous flap with dental prosthesis is essential to
reconstruct after surgery.
•Postoperative radiotherapy and neck block dissection are
often required.

NON- SURGICAL
MANAGEMENT OF
ORAL CAVITY
MALIGNANCY
-B.Dhanalakshme
3rd unit

 RADIOTHERAPY
 CHEMOTHERAPY
 LASER SURGERY
 CRYOTHERAPY
 COBLATION
RECENT ADVANCES IN TREATMENT
OF MALIGNANCY

RADIOTHERAPY
Cellular death
Free radical reaction
Apoptosis
Cell cycle arrest
• Curative
• Palliative
MODALITIES OF APPLICATION:

INDICATIONS:
 early growth
 no bone involvement
 patients who refuse surgery
 inoperable/ advanced cases
METHODS OF APPLICATION:
external beam radiotherapy
brachytherapy

TYPES OF RADIOTHERAPY
Conventional
Three dimensional conformal radiation therapy
Intensity modulated radiation therapy
Image guided radiation therapy
Streotactic body radiation therapy
Adaptive

TREATMENT MACHINES
 Cobalt 60 – emits gamma rays
 Linear accelerator
 Proton beam radiotherapy-deep seated
tumours
[bragg peak effect]
 Gamma knife
 Cyberknife
 Tomotherapy

Low / linear energy transfer- X-rays, gamma rays
High energy transfer- electron, protons, neutrons
PRINCIPLES:
Penetrated into deep seated tumour
Building of radiation under skin of the tumour to reduce skin reactions
Precise targeting towards tumour
Efficacy of the radiation therapy
depends on the patient ‘s health condition, tumour grading, lymphatic invasion

PREOPERATIVE RADIOTHERAPY
ADVANTAGES:
Downstage the tumour and
reduce the tumour bulk
Vascularity is not affected
Blockage of lymphatics
Decreases microscopic spread
Allows time for supportive
therapy for subsquent
surgery{cariac , nutrition,
pulmonaryn
DISADVANTAGES:
Impaired healing process
Delays definitive surgery
Flap necrosis
Fistula formation ,
Carotid blow out

POSTOPERATIVE
RADIOTHERAPY
Resected tumour margin is positive
Extracapsular nodal spread
Multiple lymph nodes
DISADVANTAGES:
Pathologically cure cannot be assessed
Flap necrosis, dehiscence

CARCINOMA OF CHEEK
SCC- radiosensitive
Early tumour
Fixed primary tumour/ advanced secondary
Nart

ADVANTAGES
No anasthesia complications
No surgical mutilation
Surgery is avoided
Cosmetically acceptable
preservation of organ and its function
80to90 % cure

DISADVANTAGES
Infection
Hypothyroidism
Soft tissue fibrosis
Dryness , xerostomia
Skin excoriation , hair loss
Osteoradionecrosis

CARCINOMA OF TONGUE
ADVANTAGES:
Pre- operative , post
operative
Posterior one third of
tongue
DISADVANTAGES:
Loss of taste
sensation
Trismus,
ankyloglossia
Dermatitis, sepsis
Pharyngeal oedema

CARCINOMA OF LIP
Size [<2cm],- curative
Postoperative – large tumour/ fixed lymph nodes
CARCINOMA OF HARD PALATE:
postoperative radiotherapy
SECONDARY METASTASIS WITH
UNKNOWN PRIMARY
Definitive radiotherapy is given
Surgery and post operative radiotherapy
[advanced disease]
Biopsy of the node and radiation of all
suspected areas

RADIOSENSITIZERS
Hyperbaric oxygen , nicotinamide, carbogen
Nimorazole and tirapamazine
Chemotherapeutic agents[concomitant
radiotherapy]
• Antioxidants
• Lipoic acid
• cysteine
RADIOPROTECTORS

DOSAGE:
 Definitive- Daily dosage of 180-200cGy/ day- 5 days /week
6 to7 weeks
Postoperative therapy – 6000cGy{ for 6 weeks} daily- 5 days
/ week
 T3,T4 TUMOURS
 N2,N3 NODES
 MULTIPLE NODES
PALLIATIVE:

FRACTIONATION
Hyperfractionation: smaller doses{110-120cGY}, given in multiple
doses
Better locoregional control , delayed side effects
Accelerated fractionation:180-200cGY , dose is steadily increased,
Duration of treatment is shortened , side effects are more
Hypofractionation:600-800cGY, fraction delivered several days apart
duration of treatment is shortened, low total radiation

CARE OF THE PATIENT
DURING RADIOTHERAPY
 Skin: avoid exposure to sun, chemical irritants ,
lotion/ ointments{ don’t rub/ scratch skin
 Oral cavity and dentition:
gargle several times [salt , bicarbonate] mild
antiseptic lotion, fluoride gel
Preirradiation extraction of loose teeth
 Infection: antibiotic
 Thyroid profile

 Nutrition :
High protein diet with vitamins and minerals
Blended/ semisolid diet
Ryle tube/ percutaneous gastrotomy
 Psychological support
 Severe Complications –hospitalization
 CT scan and MRI SCAN – for evaluation and
follow up
 18-FDG-PET Scan

BRACHYTHERAPY
•Sealed radiaton inside or close to the tumour,
delivered via catheters, implants
•Gold[198],pallidium[103],caesium[13], iridium[197]
•Radiation material placed in the cavity- intracavity
radiotherapy
•Radiation material inserted into the tissue-
interstitial radiotherapy
•Combined with external beam radiotherapy

•Implants can be kept either temporarily or permanently
•Low dose brachytherapy - 40-200cGY /hr
•High dose brachytherapy - 1200cGY/hr

Advantages:
 Localised , deeper,
 less side effects,
 adjacent tissues are
spared
 avoiding surgeries
 High dose rate with short
duration
 Curative and effective
Disadvantages:
Non availability of the facility
Technically difficult
local : displacement ,
erosion

CHEMOTHERAPY
Neoadjuvant chemotherapy:Anterior[induction]
High response rate, less toxicity, provides prognostic information
Delays locoregional treatment,
Adjuvant chemotherapy:Posterior
No delay in locoregional treatment
Cannot be tolerated, effect of chemotherapy on the disease cannot be
assessed
Palliative
concurrent

EVALUATION BEFORE CHEMOTHERAPY
 History and clinical examination
 Hematological
 Liver and renal function test
 X-ray chest
 ECG
 PET CT Scan
 Audiogram

DRUGS DOSAGE SIDE EFFECTS FOLLOW UP
METHOTREXATE 40mg/m2, i.v
weekly
Bone marrow
suppression,
hepatotoxic ,
nephrotoxic
Liver function
test before use
5- FLUOROURACIL 10-15mg/kg , i.v.
daily
Myelo
suppression,
Mucositis,
Skin changes
Not gven in
poorly nourished
CYCLOPHOSPHAMIDE 60-90mg/m2,
i.v. daily
Heamorrhagic
cystitis,
Neutropenia,
alopecia
Adequate
hydration
BLEOMYCIN 10-20/m2 twice
weekly, i.v,
Pulmonary fibrosis,
Anaphylaxis
alopecia
X-ray chest

ADRIAMYCIN 60-90mg/m2, iv
every 30weeks
Cardiotoxic,
Alopecia
Neutropenia,
styomatitis
ECG evaluation
Red coloured
urine
CISPLATIN 80-120mg/m2, i.v.
infusion every 3
weeks
Nausea , vomiting,
Peripheral neuropathy,
Hematologic, nephrotoxic
Renal function
test,
Adequate
hydration
VINCRISTINE 1.5mg/m2 , i.v. twice
monthly,
Neurotoxic, constipation hydration
PACLITAXEL 135-150mg/m2,
as3h infusion every
3 weeks
Neutropenia, infection ,
peripheral neuritis
Correcting
neutropenia

CHEMORADIOTHERAPY
Increased locoregional control
Decreased risk of metastasis
Improved survival
Commonly used regimen:
Cisplatin and 5- fluorouracil on
day 1 and day22 of radiotherapy
paclitaxel , docetaxel, ifosamide

CONCOMITANT
CHEMOTHERAPY
Single agent chemotherapy+ continuous course
radiotherapy
Combination chemotherapy +split course
radiotherapy
Alternating chemotherapy and radiotherapy
Amelioration of side effects:
Amifostine - free radical scavenging mechanism
pilocarpine

LASER SURGERY
Given via flexible endoscopes, straight or curved tubes.

Preferred in oropharyngeal and premalignant
conditions of oral cavity, carcinoma of tongue{CO2
LASER}

Precise
hemostasis
Minimal post operative pain
Rapid ablation of tissues
High cost
Special precautions
Requires trained personnel
ADVANTAGES DISADVANTAGES

PRECAUTIONS
Display “lasers in use”
No entry or exit permitted
Protective glasses
Wet saline pads on eyes
Wet soaked towels to cover the
exposed areas
Endotracheal tubes should be
covered
Evacuation of smoke

CRYOSURGERY
•Open method
•Closed method
•Dehydration
•Denaturation
•Thermal shock
•Vascular stasis
•Cryoimmunization

Anasthesia is not required
Used for premalignant lesions
Bleeding disorders/ coagulopathy
Minimal postoperative pain and scarring
Op procedure
Multiple cancers, palliation of secondary
cancers
No tissue is available for biopsy
No control on depth of freezing
Skin changes and destruction of
hair follicles
Not possible to assess the margins
of tumour
Advantages:
Disadvantages:
Benign vascular tumours
Premalignant lesions
Malignant lesions

COBLATION
Controlled or cold ablation
Radiofrequency energy passed through saline
Ionisation of high energy ions
Create plasma field energy
Breaks molecular bonds soft tisssue
Tissue dissolution at low temperatures

Oral cavity malignancy.pptx

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