SQUAMOUS CELL CARCINOMA - ORAL CANCER PPT

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).

1. Squamous cell carcinoma DR AMITHA G, BDS, MDS ORAL AND MAXILLOFACIAL PATHOLOGY

2. contents Introduction Epidemology Etiology Manifestations TNM staging

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.

8. ETIOLOGY

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.

12. Consumption Chewed : gutkha , pan, mawa , mainpuri tobacco, khaini , zarda Applied on gums and teeth : mishri , gudhaku , bajjar , tooth paste Inhaled : snuff

13. TYPES of smoke less tobacco Gutkha Khaini Mainpuri tobacco Mawa Mishri Paan Snuff Zarda

14. GUTKHA 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. ZARDA Tobacco leaves + lime+spices – boiled in water. Residual tobacco –dried & coloured.

15. MAINPURI TOBACCO Tobacco+ slaked lime + finely cut arecanut + camphor + cloves. Mainly-Uttar Pradesh. High incidence of oral cancer & leukoplakia . MAWA Gujarathi preparation made from shavings of arecanut , tobacco and slaked lime. Mixed & chewed excessively and kept in mandibular groove- causes oral cancer.

16. MISHRI Prepared by roasting tobacco on a hot metal plate-black-powdered-used with catechu. Used to clean teeth. PAN (BETEL QUID) WITH TOBACCO 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. SNUFF 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 TOBACCO Nitrosamines Polycyclic aromatic hydrocarbons Nitrasoproline Polonium TOBACCO SMOKE CONTAINS Carbon monoxide Thiocyanate Hydrogen cyanide Nicotine

19. ROLE OF CONSTITUENTS OF TOBACCO 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. Phenolic agents Recent studies have shown that wood products industry workers are exposed to chemicals such as phenoxyacetic acid . Causing nasal and nasopharyngeal carcinoma

22. radiation Uv radiation exposure can cause mutations in p53 gene Mutation in telomerase gene resulting in delayed apoptosis.

23. Iron deficiency 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. Vitamin a Reduced blood levels of retoinic acids,betacarotene Produces excessive keratinization May lead to dysplasia

25. Syphillis Arsenical agents ,heavy metals contain carcinogenic properties

26. Candidal infection 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. Oncogenic viruses 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. Immunosuprresion Decrease in immunosurveillence the produced malignant cells cannot be detected and destroyed at early stage Causing carcinoma

29. PATHOGENESIS Molecular basis of Cancer 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. 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

31. Hallmarks of cancer 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

32. Host defense

33. manifestations 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 .

34. 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.

35. TNM STAGING OF ORAL CANCER 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 6 th version was published in 2002.

36. objectives To aid the clinician in treatment planning To provide prognostic value To evaluate the results of treatment To facilitate exchange of information between surgical teams To contribute to the continuing investigation of human cancer.

37. T TUMOUR SIZE 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

38. 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 - T umor involves masticator space, pterygoid plates, or skull base and/or encases internal carotid artery  AJCC Cancer Staging Manual, Sixth Edition (2002 )

39. N: nodal metastasis 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

40. 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.

41. M: DISTANT METASTASIS Mx Distant metastasis cannot be assessed. M0 No distant metastasis. M1 Distant metastasis.

42. INVOLVEMENT OF VIRUSES IN THE DEVELOPMENT AND PROGRESSION 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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