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Ca. Oral Cavity.pptx
This document provides tips and instructions for using a PowerPoint presentation on oral squamous cell carcinoma (OSCC). It recommends showing blank slides with learning objectives and asking students what they know, then filling them in. This active learning technique should be repeated three times for revision. The presentation covers topics like etiology, pathology, clinical features, investigations and management of OSCC over 12 slides. It aims to be useful for both teaching and self-study.
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Ca. Oral Cavity.pptx
- 1. Tips on usingmy ppt. 1. You can freely download, edit, modify and put your name etc. 2. Don’t be concerned about number of slides. Half the slides are blanks except for the title. 3. First show the blank slides (eg. Aetiology ) > Ask students what they already know about ethology of today's topic. > Then show next slide which enumerates aetiologies. 4. At the end rerun the show – show blank> ask questions > show next slide. 5. This will be an ACTIVE LEARNING SESSION x three revisions. 6. Good for self study also. 7. See notes for bibliography.
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- 3. Learning Objectives 1. Introduction& History 2. Relevant Anatomy, Physiology 3. Aetiology 4. Pathophysiology 5. Pathology 6. Classification 7. Clinical Features 8. Investigations 9. Management 10. Prevention 11. Guidelines 12. Take home messages
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- 5. Introduction & History. •Aka. OSCC Oral Squamous Cell Carcinoma. • Mouth (oral) cancer is a major neoplasm worldwide and accounts for most head and neck cancers. • It theoretically should be largely preventable or detectable at an early stage but it is not. • Approximately 90% of oral cancers are SCC,
- 6. Introduction & History. •Seen typically on the lateral border of the tongue, oropharynx, and floor of the mouth, • as a red lesion (erythroplakia), white lesion (leukoplakia), or a mix of the two (erythroleukoplakia) with an ulcer.
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- 8. Aetiology • Idiopathic • Congenital/Genetic • Nutritional Deficiency/excess • Traumatic • Infections /Infestation • Autoimmune • Neoplastic (Benign/Malignant) • Degenerative / lifestyle • Iatrogenic • Psychosomatic • Poisoning/ Toxins/ Drug induced
- 9. Aetiology • Idiopathic • Congenital/Genetic •Traumatic • Infections /Infestation • Autoimmune • Neoplastic (Benign/Malignant) • Degenerative • Iatrogenic
- 10. Aetiology • Multifactorial andstrongly related to lifestyle, mostly habits and diet (particularly tobacco alone or in combination with betel, and alcohol use. • Ca. oropharynx, possible due to human papillomavirus (HPV). • Immune defects or immunosuppression, defects of carcinogen metabolism, or defects in DNA-repair enzymes underlie some cases of SCC. • Sunlight exposure predisposes to lip cancer.
- 11. Aetiology • Tobacco andalcohol use • Betel-quid chewing and oral snuff • diet low in fresh vegetables and fruits • human papillomaviruses (HPVs) • Cigarette smoking: • Oral health • Mouthwash use: The effect of the alcohol in mouthwash appears to be similar to that of alcohol used for drinking,
- 12. Aetiology • oral submucousfibrosis • oral lichen planus • lupus erythematosus • dyskeratosis congenita • Fanconi anemia).
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- 14. Pathophysiology • The geneticaberrations involving chromosomes 9, 3, 17, 13, and 11. • Inactivated TSGs (Tumor Supressor Genes) especially P16, and TP53 in western countries • Overexpressed oncogenes, especially PRAD1 and Harvey ras (H-ras). In Indians. • Defective Carcinogen-metabolizing enzymes
- 15. Pathophysiology • Defective Carcinogen-metabolizingenzymes – – alcohol dehydrogenase type 3 genotypes – Cytochrome P450 – GSTM1 has a decreased capacity to detoxify tobacco carcinogens. – N-acetyl transferase NAT1*10 genotypes. • Defective DNA repair genes has also been found to underlie some OSCCs. • An immune deficiency state may predispose one to a higher risk of developing OSCC, especially lip cancer.
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- 17. Pathology • nests andislands of squamous cells invading the underlying connective tissue. • aberrant keratinization, forming whorls of keratin within • Poorly differentiated OSCC consists of sheets of cells showing extreme pleomorphism, giant nuclei, and multiple and bizarre mitoses difficult to distinguish from other malignancies, particularly poorly differentiated lymphoma or melanoma. • mmunocytochemical markers such as keratins, common leukocyte antigen, and melanoma- specific antibodies
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- 19. Clinical Features • Demography •Symptoms • Signs • Prognosis • Complications
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- 21. Demography • The oralcavity is one of the 10 most frequent sites of cancer internationally. • OSCC is particularly common in the developing world, mostly in older males. • In parts of India, oral cancer can represent more than 50% of all cancers. • The prevalence of lip cancer appears to be decreasing, but the prevalence of intraoral cancer appears to be rising in many countries, especially in younger people and women.
- 22. Demography • Race -higher(by approximately 50%) in blacks compared with whites. • More in males but equalising. • occurs in middle-aged and older persons. However, in recent years, an increase in younger patients
- 23. 7Warning Signs ofCancer .
- 24. 7Warning Signs ofCancer 1. Change in bowel or bladder habits. 2. A sore that does not heal. 3. Unusual bleeding or discharge. 4. Thickening or lump in the breast or elsewhere. 5. Indigestion or difficulty in swallowing. 6. Obvious change in a wart or mole. 7. Nagging cough or hoarseness.
- 25. History • Some OSCCsarise in apparently normal mucosa, but many are preceded by premalignant disorders- – Erythroplakia (red patch) 90% – Leukoplakia (white patch) –rare chance. – Erythroleukoplakia (red and white patch) – Verrucous leukoplakia. – Speckeled leukoplakia.
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- 27. Symptoms • A redlesion (erythroplakia) • A granular ulcer with fissuring or raised exophytic margins • A white or mixed white and red lesion • An indurated lump/ulcer (ie, a firm infiltration beneath the mucosa) • A nonhealing extraction socket • A lesion fixed to deeper tissues or to overlying skin or mucosa • Cervical lymph node enlargement,
- 28. Symptoms • Early carcinomasmay not be painful • later, they may cause pain and difficulty with speech and swallowing.
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- 30. Signs • The mostcommon sites tongue, mainly the lateral and ventrolateral aspects, and the floor of the mouth. • Ulcers, red or white areas, lumps, or fissures. • Red oral lesions usually are more dangerous than white oral lesions. • Erythroplakia is a red and often velvety lesion, which, unlike leukoplakias, may not form a plaque but is level with or depressed below the surrounding mucosa
- 31. Signs • Lesions alwaysmust be palpated after inspection to detect induration and fixation to deeper tissues. • Some OSCC can also appear as a white patch. • Late OSCC may manifest as an exophytic lesion or an area of ulceration with induration • A typical malignant ulcer is hard with heaped-up and often everted or rolled edges and a granular floor,
- 32. Signs • RULE Anysingle lesion that persists more than 3 weeks, especially if red, ulcerated, or a lump, especially with induration (ie, the RULE mnemonic) should be regarded with suspicion and a histopathological diagnosis established.
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- 37. Signs • Second primarytumors are additional primary carcinomas (synchronous tumors) present in as many as 10-15% . • From 30-80% of patients with oral cancer have metastases in the cervical lymph nodes at presentation. • Later, dissemination to the lungs, liver, or bones may occur.
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- 39. Prognosis • Depends onstage. • 5-year survival rate for oral and pharyngeal cancers is approximately 66%. • Lip carcinomas generally has the best 5- year survival rate (88%) • floor of mouth has the worst (54%). • HPV-positive tumors tend to respond better to chemotherapy and/or radiation therapy compared with those with HPV-negative tumors
- 40. Prognosis • When OSCCis fatal, it almost always is either because of failure to control the primary tumor or because of nodal metastases. Death resulting from distant metastasis is unusual.
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- 42. Investigations • Laboratory Studies –Routine – Special • Imaging Studies • Tissue diagnosis – Cytology • FNAC – Histology – Germ line Testing and Molecular Analysis • Diagnostic Laparotomy.
- 43. Investigations • Laboratory Studies –Routine – Special • Imaging Studies • Tissue diagnosis – Cytology • FNAC – Histology
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- 45. Investigations in Malignancy •For diagnosis • For staging • For Screening • For Monitoring
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- 47. Diagnostic Studies Imaging Studies •X-Ray • USG • CT • Angiography • MRI • Endoscopy • Nuclear scan PET CT Scan.
- 48. Diagnostic Studies Imaging Studies •Photography for monitoring the clinical state and site of premalignant lesions. • Chest radiography and endoscopy synchronous second primary tumors • Jaw radiography (often rotating pantomography) may show invasion • USG Abd. • CT Chest • PET scan
- 49. Diagnostic Studies Histopathology • Punchbiopsy Avoid excisional biopsy • Always take a biopsy specimen of the red lesions if both red and white lesions are present • Guided biopsy by vital staining- – Staining with toluidine blue followed by a rinse with 1% acetic acid and then saline – Various light sources are becoming available to help delineate areas for biopsy
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- 51. Differential Diagnosis • ActinicKeratosis • Erythroplasia • Lichen Planus • Lichenoid lesions • Mucosal Candidiasis • Traumatic lesion
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- 53. TNM Classification Primary tumor •T0 - No primary tumor • Tis - Carcinoma in situ • T1 - Tumor 2 cm or smaller • T2 - Tumor 4 cm or smaller • T3 - Tumor larger than 4 cm • T4 - Tumor larger than 4 cm and deep invasion to muscle, bone, or deep structures .
- 54. TNM Classification Lymphatic nodeinvolvement • N0 - No nodes • N1 - Single homolateral node smaller than 3 cm • N2 - Nodes(s) homolateral smaller than 6 cm • N3 - Nodes(s) larger than 6 cm and/or bilateral
- 55. TNM Classification • M0- No metastasis • M1 - Metastasis noted
- 56. TNM Classification • StageI - T1, N0, M0. • Stage II -T2, N0, M0. • Stage III : – T3, N0, M0 – T1, T2, T3, N1, M0 • Stage IV : – T4, N0, M0 – Any T, N2 or N3, M0 – Any T, any N, any M
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- 58. Management • Surgery • Radiotherapy •Chemotherapy • Targeted therapy
- 59. Management • Oral squamouscell carcinoma (OSCC) currently is treated largely by surgery and/or irradiation. • Photodynamic therapy and chemotherapy have occasional applications • There is an increased use of chemotherapy including targeted therapy
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- 61. Operative Therapy • Thegoal of surgery for oral squamous cell carcinoma (OSCC) is to remove the primary tumor together with a margin of clinically normal tissue. • If at least one node has clinical signs of invasion, a reasonable presumption is that others may be involved and must be removed by traditional radical neck dissection. • Reconstruction.
- 62. Operative Therapy Advantages- • Surgeryprovides complete tumor and lymph node excision. • A full histologic examination can be performed for staging purposes and to help predict prognosis and the need for adjuvant radiotherapy. • Surgery also provides another option of treatment for radiotherapy-resistant tumors.
- 63. Operative Therapy Disadvantages- • Perioperativemortality and morbidity. • aesthetic and functional defects.
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- 65. Radiotherapy • Advantages ofradiotherapy 1. Normal anatomy and function are maintained 2. General anesthesia is not needed. • Disadvantages 1. adverse effects are common 2. Cure is uncommon, especially for large tumors 3. Subsequent surgery is more difficult and hazardous and survival is reduced further.
- 66. Radiotherapy:Adverse effects • Shortterm complication- Oral mucositis invariable • Longer-term complications 1. dry mouth (xerostomia) 2. loss of taste 3. osteoradionecrosis (ORN) .of mandible.
- 67. Radiotherapy 1. External beamradiation (teletherapy), which is commonly accompanied by adverse effects, 2. Interstitial therapy
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- 69. Interstitial therapy 1. Brachytherapy-intrralesional 2. Plesiotherapy – Surface therapy • causes fewer complications but is suitable only for tumors that are smaller than 2 cm and located in selected sites.
- 70. Targeted therapy • Cetuximaband panitumumab. • Cetuximab • Erlotinib and gefitinib • Lapatinib
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- 72. cancer-prevention tips. • Don'tuse tobacco • Avoid Alcohol • Eat a healthy diet. ... • Maintain a healthy weight and be physically active. ... • Protect yourself from the sun. ... • Get vaccinated. ... • Avoid risky behaviors. ... • Get regular medical care. • .
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- 74. Prevention • Screening • Riskreduction
- 75. Prevention • Diet richerin vegetables and fruits • Avoid Tobacco • Avoid Betel nut, Paan, Gutkha • Avoid alcohol consumption. • Self examination. • Good oral hygiene.
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- 77. Early Detection • Dentalpractitioners and dental care professionals should remain vigilant for signs of potentially malignant disorders and oral cancer while performing routine oral examinations. • The mnemonic RULE – Red – Ulcerated – Lump – Extending for 3 or more weeks. • Biopsy
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- 81. Get this pptin mobile 1. Download Microsoft PowerPoint from play store. 2. Open Google assistant 3. Open Google lens. 4. Scan qr code from next slide.
- 82. Get this pptin mobile
- 83. Get my pptcollection • https://www.slideshare.net/drpradeeppande/ edit_my_uploads • https://www.dropbox.com/sh/x600md3cvj8 5woy/AACVMHuQtvHvl_K8ehc3ltkEa?dl =0 • https://www.facebook.com/doctorpradeeppa nde/?ref=pages_you_manage