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Carcinoma of Tongue
DR. T YASASWI 2nd YR POST GRADUATE DEPARTMENT OF ENT
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INRODUCTION
• Oral carcinoma is fifth most common malignancy in head and neck globally.
• Oral cavity malignancies account for 20 per 100,000 population in India, out of which carcinoma tongue has a 4.6 in 100,000 and 1.8 in 100,000 incidence in males and females respectively.
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Distribution of cancer in oral cavity
Occurrences
Buccal mucosaTongueLower lipPalateVestibuleAlveolusFloor of mouthGingivaUpper lip
32%
22% 11%
11%
8%
5%
5% 3% 3%
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• Carcinoma of the tongue has a higher risk of metastases to the regional lymph nodes and subclinical nodal metastases are found up to 30 % of T1 and T2 .
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ETIOPATHOGENISIS
• Tobacco abuse- dose dependent.(risk factor 4to5) • Alcohol ( risk factor 2)has synergistic effect( risk
factor 15). • In India tobacco chewing along with betel nut,
lime contributes to 25 % of cancers in oral cavity. • Pooling of carcinogen contaminated saliva in the
oral cavity is the main cause in these patients.
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Etiology
• Tobacco contains a number of known
carcinogens, e.g. polynuclear aromatic hydrocarbons and nitrosamines which cause DNA damage leading to gene mutations.
• Oral tobacco is mixed with betal leaf, slated lime and areca nut to form a quid called ‘paan’.
• The lime lowers the pH which accelerates the release of alkaloids from both the tobacco and areca nut.
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• Alcohol causes DNA damage and gene mutation by a number of mechanisms.
These include: • Alcohol act as a solvent increasing the cellular
permeability of tobacco carcinogens through the mucosa .
• The immediate metabolite of ethanol is acetaldehyde and this have a locally damaging effect on cells.
• Chronic alcohol use up regulates enzymes of the cytochrome P450 system which result in the activation of pro-carcinogens into carcinogens.
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• Alcohol also decreases the activity of DNA repair enzymes resulting in increased chromosomal damage
• Alcohol impairs immunity due to a reduction in T cell number, decreased mitogenic activity and
macrophage activity. • Alcohol is high in calories, which suppresses
appetite in heavy drinkers. Metabolism is further damaged by liver disease resulting in nutritional deficiencies and therefore lowered resistance to cancer.
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OTHER CAUSES
• Poor oral & dental hygiene. • Chronic irritation from sharp tooth, oral
sepsis, spices • Syphilis. • Vit. A deficiency • Marijuana - increasing incidence of tongue
cancer seen in western world .
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• HPV 16, 18, 31, 33, 35, 39 are associated with premalignant lesions and squamous cell Ca.
• HPV 16 and 18 are the most common types associated with squamous cell carcinoma.
• HPV bind to and inactivate tumour suppressor genes p53 and Rb.
Fresh fruit, vegetables, antioxidants, vitamins A, C and E are protective
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Site: 1. Lateral border of the anterior 2/3 of tongue - 25% each side. 2. Tip of tongue - 10% 3. Dorsum of tongue- 10% 4. Posterior 1/3 - 20% 5. Ventral surface of tongue - 5% 6.Tonsilolingual sulcus - 5%
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Pathological relevance to surgeons
• Pathologically, Depth of infiltration is measured from the level of the basement membrane of the closest adjacent normal mucosa.
• A “plumb line” is dropped from this plane to the deepest point of tumor invasion
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Prognostic factors • Primary tumor-depth of infitration -perineural infitration • Nodes – volume - extranodal extension
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Extranodal Extension (ENE)
• Pathological ENE is defined as extension of metastatic carcinoma from within a lymph node through the fibrous capsule and into the surrounding connective tissue, regardless of the presence of stromal reaction.
• Metastatic carcinoma that stretches the capsule but does not breach it does not constitute ENE
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Premalignant lesions • High Risk Lesions:
– Erythroplakia – Chronic Hyperplastic Candidiasis
• Moderate Risk Lesions: – Oral submucous fibrosis – Syphilitic glossitis – Sideropenic dysphagia (Paterson – Kelly Syndrome)
• Low Risk: – Oral lichen planus – Discoid lupus erythematosus – Discoid keratosis congenita
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Leukoplakia:
• Oral leukoplakia is defined by the WHO as “a white patch or plaque that cannot be scrapped off and also characterized clinically or pathologically as any other disease”.
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Clinical forms of Leukoplakia
Homogenous Non Homogenous
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Malignant Transformation Potential
• Overall - 1 – 5% • Homogenous - 0% • Non Homogenous - 26%
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Erythroplakia: • Any lesion of the oral mucosa that presents as a
bright red plaque which cannot be characterized clinically or pathologically
• lesions are irregular in outline and separated from normal mucosa
• Incidence of malignant changes is 17 times higher than leucoplakia
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• Chronic Hyperplastic candidiasis: - -Produces dense plaques of leukoplakia
– High incidence of malignant transformation – Believed to be invasion of Candida Albicans
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Oral submucous fibrosis
• Progressive disease with fibrous bands beneath the mucosa contracture limited mouth opening restricted tongue movement.
• Epithelium also shows dysplasia • Mainly associated with areca nut usage than
tobacco.
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SPREAD
• Direct: to surrounding stucutres like floor of mouth, gums and mandible. • Lymphatic: (rapid, early & very common) • Perineural spread leads to direct spread
along cranial nerves. • Angioinvasion Distant metastasis.
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CLINICAL FEATURES • Painless long standing ulcer Later becomes painful
d/t infection or lingual nerve involvement – bleeds to touch – Induration present more than the ulcer area – Edge may be raised and everted.
•Excessive salivation: due to pain and inability to swallow •Ankyloglossia: inability to protrude tongue with deviation to the affected side due to infiltration of muscles of the tongue, XI cranial nerve and / or floor of mouth.
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• Dysphagia • Dysarthria • Halitosis • Referred Otalgia • Palpable Neck nodes
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INVESTIGATIONS
• All lesions of the tongue and floor of mouth that last for longer than two to three weeks require biopsy to confirm the diagnosis.
• Similarly, all areas of leukoplakia and erythroplakia require a biopsy / excision(toludine blue).
• FNAC of suspicious/enlarged/palpable lymphnodes.
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• CECT scan – for primary , cervical metastasis and infiltration of mandible.
• MRI – investigation of choice for imaging soft tissue infiltration and to detect perineural invasion.
• X-ray chest –for pulmonary metastasis. • Routine investigation and immunological
screening.
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• Positron emission tomography (PET) is useful
in improving the detection of distant metastasis in cases with large tumor volume and also for recurrent disease.
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TNM Classification • TX-Primary tumor cannot be assessed • Tis-Carcinoma in situ • T1-Tumor ≤2 cm, ≤5 mm depth of invasion (DOI) (DOI is
depth of invasion and not tumor thickness) • T2-Tumor ≤2 cm, DOI >5 mm and ≤10 mm or tumor >2
cm but ≤4 cm, and ≤10 mm DOI • T3-Tumor >4 cm or any tumor >10 mm DOI • T4- involvement of floor of mouth. Reference –Head and Neck cancers – major changes in
American Joint Commiteeon Cancer ,8th Edition ,January 2017.
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T1Lesion T2 LESION
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T3 LESION T4 LESION
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REGIONAL LYMPH NODES PATHOLOGIC CATEGORY CRITERIA
• Nx- Regional lymph nodes cannot be assessed • N0-No regional lymph node metastasis
• N1- Metastasis in a single ipsilateral lymph
node, 3 cm or less in greatest dimension and ENE-negative
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• N2a- Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest dimension and ENE-positive;
Or More than 3 cm but not more than 6 cm in greatest dimension and ENE-negative;
• N2b-Metastases in multiple ipsilateral lymph nodes, none more than 6 cm in greatest dimension and ENE-negative;
• N2c- Metastasis in bilateral or contralateral lymph nodes, none more than 6 cm in greatest dimension, ENE-negative
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• N3a- Metastasis in a lymph node more than 6
cm in greatest dimension and ENE-negative; • N3b-Metastasis in a single ipsilateral lymph
node more than 3 cm in greatest dimension and ENE-positive; (or)
Metastasis in multiple ipsilateral, contralateral, or bilateral lymph nodes, with any ENE-positive
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DISTANT METASTASIS
• Mx – can not be assessed • M0 – no detectable distant metastasis • M1 – distant metastasis present
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Stage 0 Tis N0 M0
Stage I T1 N0 M0
Stage II T2 N0 M0
Stage III T1, T2 N1 M0
T3 N0, N1 M0
Stage IVA T1, T2, T3 N2 M0
T4a N0, N1, N2 M0
Stage IVB Any T N3 M0
T4b Any N M0
Stage IVC Any T Any N M1
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Types of TNM STAGING
• cTNM – clinical • pTNM- pathological • rTNM-(recurrent) • RTNM-(residual)
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Treatment- EARLY STAGE
• Stage 1 and 2- T1,N0,M0 -T2,N0,M0 • SINGLE MODALITY TREATMENT: 1) Surgery: Wide local excision (1.5 to 2cm
unstretched normal mucosa all around the tumour) and Selective Neck Dissection (level I to III) OR
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2) Teleradiotherepy + Brachytherepy • total of 6000 to 7000rads in a period of 6 to 7
weeks.
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TREATMENT -Advanced Stage
• Stage III - T1,2,3 N1 M0 T3 N0 M0 • Stage IV –T1,2,3 N2,3 M0 T4 N0 M0 COMBINED MODALITY TREATMENT: Surgery +Postoperative Chemoradiation 1)Wide local excision with Reconstruction + Radical
neck dissection followed by post operative Chemoradiation.
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• Reconstruction: • Pectoralis Major Myocutaneous FLAP-
PEDICAL flap - Forearm free flap - Fibular free flap, if mandible is also excised. • Chemoradiation: • radiation 5000 to 6000 rads for 5 days/week. • On 6th day – chemotherapy
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Management of neck nodes:
• Clinically node negative : – Cervical nodes may have occult metastasis upto
30% even if clinically node negative – Hence Selective Neck dissection “Supraomohyoid
dissection”(levels 1,2,3) as a sampling procedure to be done.
– If nodes are positive – completion neck dissection or radiation therapy given.
• Clinically node positive:- radical neck dissection .
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SURGERY • Advantages:
– Short period treatment – Control of margins – Specimen available for HPE/ DOI – Helps in planning adjuvant treatment – No radiation sequelae
• Disadvantages:
– Tissue and functional loss – Disfigurement – Bleeding & infection
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Rehablitation
• Swallowing Therapy • Speech Therapy • Jaw stretching exercise after radiotherapy.
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Radiotherapy
RT & surgery have equal success in early lesion. RT can be given:
• Brachytherpy • Tele therapy – EBRT • Combination therapy • RT help in organ preservtion but long term
complication are significant
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• Post operative RT is preferred over pre operative because of effect on wound healing
• Per operative RT: inoperable, unfit for surgery & down staging
• Post RT is indicated in patients with – T3/T4 primary – positive surgical margins – perineural, perilymphatic vascular invasion – microscopic gross residual tumor – extra capsular spread
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• Disadvantage – no specimen for HPE • Altered taste,xerostomia and the protracted
nature of treatment course. • Requires atleast 6 weeks of treatment. • Osteonecrosis of mandible. • Newer technique of IMRT and brachytherapy
reduces above side effects. • ADVANTAGE-Provide better functional result
with speech .
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CHEMOTHERAPY
-As a adjuvent to RT
• Palliative – Recurrence – Metastatic disease
• Drugs: Cisplatin, MTX,5FU
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Follow up
• Every 2 months- for 6 months • 3 monthly- upto 2 years • 6 monthly-upto 5 years • Yearly – after 5 years Look for- -Recurrence , -2nd primary -Hypothyroidism due to postop radiotherapy -Rehablitation
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Predictors of Poor prognosis:
Past Increasing tumor
thickness(>4mm) -Poorly differentiated -High grade tumors -Perineural,Vascular and
lymphatic invasion. -DNA ploidy status such as
aneuploid carry worst prognosis
-Verrucuous Ca has better prognosis
Latest • Depth of infiltration • Perineural,Vascular and
lymphatic invasion • Human papilloma virus
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PROGNOSIS
• Stage 1: 80 – 90 % • Stage 2: 70 – 80 % • Stage 3: 30 – 50 % • Stage 4: 20 – 30 %
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PREVENTION
• Primary prevention is better. • Secondary prevention: -Cancer screening regularly for early detection -Regular follow up to decrease morbidity.
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THANK YOU
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Examination
• General EXAMINATION : • Examination of oral cavity:
• Site ,size,margins, • Colour , texture,
• mobility of tongue
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• Homogenous: Uniform flat appearance that may exhibit shallow
cracks and has a smooth, plaque like, wrinkled or corugated surface with a consistent texture throughout
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Non Homogenous (speckled
• A predominantly white or white and red lesion (erythroleukoplakia).
• Area of redness and ulceration • Irregularly flat, nodular thickening and exophytic • Nodular lesions have raised, rounded red and or white
excrescences