Introduction
Epidemiology
Etiology
Manifestations
TNM staging
Squamous cell carcinoma is defined as malignant epithelial neoplasm exhibiting squamous differentiation as characterised by the formation of keratin and/or the presence of intercellular bridges.
( Pindborg et al, 1997).
3. DEFINITION
Squamous cell carcinoma is defined as malignant epithelial
neoplasm exhibiting squamous differentiation as characterised by
the formation of keratin and/or the presence of intercellular
bridges.
( Pindborg et al, 1997).
4. REASONS FOR DELAYED DETECTION AND TREATMENT
1. The public is generally unaware of oral cancer and its risk factors.
2. Approximately 50% of the public does not have routine dental or oral examinations and care.
3. Most early oral cancers are symptomless.
4. In the cancers that do produce symptoms, the symptomsare common to those produced by
common dental diseases.
5. A significant number of oral clinicians may not perform a thorough systematic oral, face, and
neck examination.
6. A significant number of oral clinicians are not able to recognize premalignant lesions or early oral
cancer
5. EPIDEMIOLOGY
• Oral and oropharyngeal cancer is the sixth most common cancer
in the world.
• Oral cancer constitutes about 10% of all cancer cases in India.
• In India, the age standardized incidence rate of oral cancer is 12.6
per 100 000 population.
6. • Oral cancer ranks number one among men and number three among
women in India.
• Oral cancer constitutes 12% of all cancers in men and 8% of all
cancers among women.
• Oral cancer is one of the 10 most common causes of death.
• There is a slight Male predilection, with a male to female ratio of
1.7:1.
7. • Squamous cell carcinoma is the most common, representing 90–
95% of all oral malignancies.
• The overall 5-year survival rate for oral cancer has increased from
45-53% from 1960 s.
• Factors which influence are stage at diagnosis, access to
treatment, and the success of treatment.
9. I. Smoking of cigarettes, cigars, and pipes
2. Use of smokeless tobacco: snuff and chewing tobacco
3. Drinking of 3 ounces or more of ethanol per day
4. Smoking and ethanol (highest risk)
5. Betel nut
6. Age over 40 years
7. High accumulation of x-irradiation over the years
10. 8. Previous history of oral cancer
9. Infection with human immunodeficiency virus and other
immunosuppression conditions
10. Ethnic or family history
11. Mouth rinse with a significant alcohol content?
12. Chronic mechanical irritation?
13. Poor oral hygiene?
14. Candidal infection?
11. Smokeless Tobacco
• Smokeless tobacco / spit tobacco / chewing tobacco.
• Mainly two forms: snuff and chewing tobacco .
• Snuff – users ; between their lower lip and gum.
• Chewing tobacco - users put between their cheek and gum.
• The tobacco juice is sucked and chewed - nicotine -absorbed
into the bloodstream through the oral tissues.
13. T Y P E S O F S M O K E L E S S T O B A C C O
• Gutkha
• Khaini
• Mainpuri tobacco
• Mawa
• Mishri
• Paan
• Snuff
• Zarda
14. G U T K H A
• Main component - arecanut along with tobacco .
KHAINI
• Paste of tobacco + slaked lime & is used with arecanut.
• Mixed with the thumb to make the mixture alkaline-premolar
region of mandibular groove.
Z A R D A
• Tobacco leaves + lime+spices – boiled in water.
• Residual tobacco –dried & coloured.
15. M A I N P U R I T O B A C C O
• Tobacco+ slaked lime + finely cut arecanut + camphor + cloves.
• Mainly-Uttar Pradesh.
• High incidence of oral cancer & leukoplakia.
M A W A
• Gujarathi preparation made from shavings of arecanut, tobacco and
slaked lime.
• Mixed & chewed excessively and kept in mandibular groove- causes
oral cancer.
16. M I S H R I
• Prepared by roasting tobacco on a hot metal plate-black-
powdered-used with catechu.
• Used to clean teeth.
P A N ( B E T E L Q U I D ) W I T H T O B A C C O
• Most common-ancient habit.
• Betel leaf + arecanut + slaked lime + catechu.
• Arecanut-vital component-drastically affects oral health.
• Contains nitrosamines-carcinogenic.
• Pan masala - mainly contains tobacco - causes oral cancer.
17. S N U F F
• Finely powdered air-cured & fire-cured tobacco leaves.
• Used orally/nasally.
• Carried in a metal container-a twig is dipped into it-placed in oral
vestibule.
• Causes oral squamous cell carcinoma.
18. CONTENTS
TOBA C C O
• Nitrosamines
• Polycyclic aromatic
hydrocarbons
• Nitrasoproline
• Polonium
TOBACCO SMOKE
CONTAINS
• Carbon monoxide
• Thiocyanate
• Hydrogen cyanide
• Nicotine
19. R O L E O F C O N S T I T U E N T S O F T O B A C C O
• Polycyclic aromatic hydrocarbons
• Nicotine carcinogenesis
• Nitrosamine
• Phenol tumour promotion& irritation
• Benzopyrene
• Carbon monoxide - impaired oxygen transport
• Formaldehyde & oxides of N - toxicity
20. • Alcohol: synergistic effect
• Radiation
- U. V Radiation
- Ionizing Radiation
• Oncogenic viruses
• Trauma
21. P H E N O L I C A G E N T S
• Recent studies have shown that wood products industry
workers are exposed to chemicals such as phenoxyacetic
acid .
• Causing nasal and nasopharyngeal carcinoma
22. R A D I AT I O N
• Uv radiation exposure can cause mutations in p53 gene
• Mutation in telomerase gene resulting in delayed apoptosis.
23. I R O N D E F I C I E N C Y
• Iron is required for normal functioning of epithelial cells….
• In iron deficiency , due to impaired cell mediated immunity . The
epithelial cell turn over more rapidly producing atropic immature
mucosa
• Susceptible for malignant transformation.
24. V I TA M I N A
• Reduced blood levels of retoinic acids,betacarotene
• Produces excessive keratinization
• May lead to dysplasia
25. S Y P H I L L I S
• Arsenical agents ,heavy metals contain
carcinogenic properties
26. C A N D I D A L I N F E C T I O N
• Nitrosamines producd by certain candidal strains have been
implicated in carcinogenesis.
• Experiments have also shown that certain strains produced
hyperkeratotic lesions on tongue of rats on dorsal surface.
27. O N C O G E N I C V I R U S E S
• HPV – human papilloma virus… 16,18,31,33
• Proteins E7 AND E7 promote degradation of P53 and RB gene respectively
• Immortalization of host gene facilitating malignant transformation.
• Herpes simplex virus:2.
28. I M M U N O S U P R R E S I O N
• Decrease in immunosurveillence the produced
malignant cells cannot be detected and destroyed at
early stage
• Causing carcinoma
29. P A T H O G E N E S I S
M o l e c u l a r b a s i s o f C a n c e r
• It is characterized by a progression of changes on cellular and genetic level that
ultimately reprogram a cell to undergo uncontrolled cell division, thus forming a
malignant mass.
30.
31.
32. There are 4 regulatory genes:
• Growth promoting proto oncogenes.
• Growth inhibiting cancer suppressor genes antioncogenes.
• Genes that regulate programmed cell death /apoptosis.
• Genes that regulate repair of damaged dna
33. H A L L M A R K S O F C A N C E R
• Self-sufficiency in growth signals
• Insensitivity to growth-inhibitory signals
• Evasion of apoptosis
• Limitless replicative potential (i.e., overcoming cellular senescence and avoiding mitotic
catastrophe)
• Development of sustained angiogenesis
• Ability to invade and metastasize
• Genomic instability resulting from defects in DNA repair
38. M A N I F E S TAT I O N S
• Rapid proliferation / growth of long standing, innoculous lesion.
• Unexplained colour change.
• Growth / ulceration of pigmented area.
• Ulceration / erosion in otherwise.
• Homogenous white/red lesions.
• Longstanding ulcers with areas of sharp tooth or appliances insult.
• Induration in / around ulcer.
39. • Unexplained mobility, exfoliation of teeth.
• Unexplained paresthesia.
• Unexplained dysphagia, hoarseness of voice.
• Unexplained restriction of tongue movements.
• Pain in ear.
• Rapid enlargement of lymph nodes.
• High risk patients.
40. T N M S TA G I N G O F O R A L C A N C E R
• The tumor-node-metastasis (TNM) staging system was first reported by pierre denoix in the
1940s.
• The international union against cancer (uicc) eventually adapted the system and compiled
the first edition of the tnm staging system in 1968.
• The classification system is recognised worldwide and the latest 6th version was published
in 2002.
41. O B J E C T I V E S
1. To aid the clinician in treatment planning
2. To provide prognostic value
3. To evaluate the results of treatment
4. To facilitate exchange of information between surgical teams
5. To contribute to the continuing investigation of human cancer.
42. T T U M O U R S I Z E
TX - Primary tumor cannot be assessed
T0 - No evidence of primary tumor
Tis - Carcinoma in situ
T1 - Tumor 2 cm or less in greatest dimension
T2 - Tumor more than 2 cm but not more than 4 cm in greatest
dimension
T3 - Tumor more than 4 cm in greatest dimension
43. T4a - Lip tumor invades through cortical bone, inferior alveolar nerve, floor of mouth, or
skin of face (ie, chin or nose)*
oral cavity tumor invades through cortical bone, into deep [extrinsic] muscle of tongue
(genioglossus, hyoglossus, palatoglossus, and styloglossus), maxillary sinus, or skin of
face.
T4b - Tumor involves masticator space, pterygoid plates, or skull base and/or encases
internal carotid artery
AJCC Cancer Staging Manual, Sixth Edition (2002)
44. N : N O D A L M E TA S TA S I S
• 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
• N2 - Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than 6 cm in
greatest dimension; or in multiple ipsilateral lymph nodes, none more than 6 cm in greatest
dimension; or in bilateral or contralateral lymph nodes, none more than 6 cm in greatest
dimension
45. • N2a Metastasis in a single ipsilateral lymph node more than 3 cm but not more than 6 cm
in greatest dimension.
• N2b Metastasis in multiple ipsilateral lymph nodes, none more than 6 cm in greatest
dimension
• N2c Metastasis in bilateral or contralateral lymph nodes, none more than 6 cm in greatest
dimension.
• N3 metastasis in a lymph >6cm in greatest dimension.
46. M : D I S TA N T M E TA S TA S I S
• Mx Distant metastasis cannot be assessed.
• M0 No distant metastasis.
• M1 Distant metastasis.
47.
48. I NVOLV EMENT OF V I RUSES I N T HE DEV ELOPMENT AND PROGRESSI ON OF
ORAL CANCER
• Various viruses such as Epstein-Barr virus (EBV), cytomegalovirus, herpes simplex virus type 1 and
human papilloma virus (HPV) are known to reside in the oral cavity.
• Patients with HPV-positive tongue cancer have more significant alveolar bone loss than HPV-
negative patients, and chronic periodontitis tends to be more common in HPV-positive patients
with primary SCC of the pharynx, larynx and mouth. As is the case for cervical cancer, HPV has long
been considered to be involved in OSCC. However, recent studies have revealed that HPV is much
more commonly associated with cancers of the pharynx, larynx and tonsil, than with oral cancer.
• Latent EBV infection is common in adults. In the oral regions, EBV is detectable in normal gingival
epithelium and significantly detected in periodontal disease . EBV-associated tumors are divided
into those of the epithelial and lymphatic systems. Among epithelial tumors, nasopharyngeal
carcinoma is the most common tumor associated with EBV .
• EBV has also been associated with cancers of stomach, salivary gland, and breast .
• We examined EBV latent infection genes and their expression in normal and dysplastic oral
epithelium as well as in squamous cell carcinoma, and showed an association of EBV with the
dysplasia-carcinoma sequence .
• Although EBV is also associated with Burkitt’s lymphoma and Hodgkin’s lymphoma , EBV latent
infection genes and their expression have been detected in immunodeficiency-related
lymphoproliferative disorders (LPDs) such as methotrexate (MTX) and age-related LPDs. LPDs of the
oral cavity occur as intractable ulcers and are associated with severe periodontal disease.
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