9. Oral cavity cancer presentation Part 1.pptx

oral cavity cancer part 1

1. CARCINOMA ORAL CAVITY PART 1 PRESENTER- Dr. ABHISHEK MEWARA MODERATOR- Dr. UPEN K MATHUR DATE- 16.05.2024 1

2. OVERVIEW- INTRODUCTION INCIDENCE, EPIDEMIOLOGY AND ETIOLOGY ANATOMY MOLECULAR BIOLOGY NATURAL HISTORY- THE PREMALIGNANT LESIONS PATTERN OF SPREAD PATHOLOGICAL CLASSIFICATION STAGING 2

3. 1. INTRODUCTION 3

4. SCC of the lip and oral cavity is primarily a surgical disease. Two clinical pathways for the subsequent management: For early stage disease. For locally advanced disease. Surgery is the preferred treatment approach for early stage T1 or T2N0 lesions of the oral cavity or lip. For more advanced disease (T3/T4a, N0 or T1-T4a, N1-N3), a combined modality approach is adopted involving surgery followed by adjuvant RT or CTRT. 4

5. 5 CA LIP

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7. 7 CA TONGUE, FLOOR OF MOUTH, BUCCAL MUCOSA, HARD PALATE, ALVEOLAR RIDGE, AND RETROMOLAR TRIGONE

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9. 2. INCIDENCE, EPIDEMIOLOGY AND ETIOLOGY 9

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12. RISK FACTORS- TOBACCO- 5 to 25 times increased risk. ALCOHOL SMOKING BETEL NUT UV RADIATION- Particularly Ca lip. HPV- M/C HPV 16 SYNDROMES- Xeroderma pigmentosum, Li-Fraumeni, Ataxia telangiectasia, Bloom syndrome, and Fanconi anemia. 12

13. 3. ANATOMY 13

14. The oral cavity consists of the lips, oral tongue, floor of the mouth, retromolar trigone, alveolar ridge, buccal mucosa, and hard palate. The anterior boundary is the skin–vermilion junction. The superior portion extends posteriorly to the junction between the hard and soft palate, whereas the inferior portion extends to the circumvallate papillae. 14

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16. LIP- Begins at the junction of the vermilion border with the skin and form the anterior aspect of the oral vestibule. Vermilion surface is the portion of the lip that comes in contact with the opposing lip. The primary motor control is by the buccal and mandibular branches of the facial nerve. 16

17. ORAL TONGUE- The anterior two-third is mobile and is part of the oral cavity. Extends anteriorly from the circumvallate papillae to the undersurface of the tongue at the junction of the floor of the mouth. Demarcated into 4 areas: the tip, lateral borders, dorsal surface, and undersurface (ventral surface). 6 pair of muscles form the oral tongue. 3 are extrinsic, 3 are intrinsic. Extrinsic muscles include the genioglossus, hyoglossus, and styloglossus. Intrinsic muscles include the lingual, vertical, and transverse muscles. The former primarily move the body of the tongue, whereas the latter alter the shape and conformation of the tongue during speech and swallowing. 17

18. Arterial supply : Lingual artery, tonsillar branch of the facial artery, and the ascending pharyngeal artery. Venous drainage : Internal jugular vein. General sensation of the anterior two-thirds of the tongue: Lingual nerve. Excluding the circumvallate papillae, taste fibers from the anterior two-thirds of the tongue run in the Chorda tympani branch of the facial nerve; and the glossopharyngeal nerve provides sensation and taste to the posterior third of the tongue and circumvallate papillae. 18

19. FLOOR OF THE MOUTH- Semilunar space extending from the lower alveolar ridge to the undersurface of the tongue. Overlies the mylohyoid and hyoglossus muscles. The posterior boundary is the base of the anterior tonsillar pillar. Innervation of the floor of the mouth is provided by the lingual nerve . 19

20. HARD PALATE- Extends from the inner surface of the superior alveolar ridge to the posterior edge of the palatine bone. ALVEOLAR RIDGE- Includes the alveolar processes of the maxilla and mandible and the overlying mucosa. RETROMOLAR TRIGONE- A triangular area overlying the ascending ramus of the mandible. The base of the triangle is formed by the posterior most molar, and the apex lies at the maxillary tuberosity. BUCCAL MUCOSA- Includes the mucosal surfaces of the cheek and lips from the line of contact of the opposing lips to the pterygomandibular raphe posteriorly. Innervation is by the buccal nerve , a branch of the mandibular nerve . 20

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22. NODAL LEVELS- There are 5 primary nodal levels, plus the retropharyngeal nodes, that are relevant to the staging and management of oral cavity carcinoma. LEVEL I - submental ( Ia ) and submandibular ( Ib ) nodes. LEVEL II - upper jugular chain lymph nodes. The level II nodal region is further subdivided into IIa and IIb (anterior and posterior respectively). LEVEL III - caudal extension of level II. Includes the mid-jugular nodes. LEVEL IV - inferior jugular nodes. LEVEL V - nodes in the posterior triangle, which are located posterior to the sternocleidomastoid muscle. Retropharyngeal nodes. 22

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24. 4. MOLECULAR BIOLOGY 24

25. Several steps occur during tumor development, viz oncogenes become activated, and tumor suppressor genes become deactivated. In the oral mucosa, this genetic progression is reflected histologically by the transformation from normal mucosa to dysplastic epithelium, and ultimately to frankly invasive squamous cell carcinoma. Loss of heterozygosity at chromosomes 3p14 and 9p21 is documented as being involved in tumor development. Mutations in the region of chromosome 17p13, which encompasses the tumor suppressor gene TP53, are among early events that contribute to malignant transformation. 25

26. Known tumor suppressor genes and oncogenes were found to be mutated, including TP53, PIK3CA, PTEN, HRAS, and CDKN2A. Loss-of-function mutations in NOTCH1 can cause tumor development. Activating mutations in HRAS or PIK3CA are associated with improved clinical outcomes. Other clinically important IHC markers are p16, p40, p53 etc. Smoking was seen to have a minimal effect on genomic changes. 26

27. 5. NATURAL HISTORY- THE PREMALIGNANT LESIONS 27

28. LEUKOPLAKIA- A white patch or plaque that cannot be rubbed off, and cannot be characterized clinically or pathologically as any other disease. Most common precursor of cancer of the oral cavity. Hyperkeratosis and acanthosis- morphological hallmark. Begin as a thin gray or gray/ white plaque that may appear translucent, is sometimes fissured or wrinkled, and typically soft and flat. Frequently have sharply demarcated borders. 28

29. Pathology: High-risk oral leukoplakia shows abnormal orientation of cells, nuclear hyperchromatism, increased mitosis and nuclear cytoplasmic ratio. 1% to 18% of oral leukoplakia develops into oral cancer. May regress spontaneously without therapy. A baseline biopsy may be performed to establish diagnosis and rule out malignant transformation. Leukoplakia with clinically or histologically aggressive features, demonstrating dysplasia, should be excised. 29

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31. ERYTHROPLAKIA- A chronic, red, generally asymptomatic lesion or patch on the mucosal surface that cannot be attributed to a traumatic, vascular, or inflammatory cause. Erythroplakia , like leukoplakia, is a clinical diagnosis of exclusion that requires the clinician to rule out all other erythematous oral lesions. Associated with a higher risk of malignant transformation than leukoplakia. The treatment of choice is surgical excision. 31

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33. ORAL SUBMUCOUS FIBROSIS- A generalized fibrosis of the oral cavity tissues resulting in marked rigidity and trismus. At early stages, it is characterized by blanching of the mucosa with a marble-like appearance. At more advanced stages, palpable fibrous bands become evident around the buccal mucosa and the mouth opening is compromised. In India, it is estimated that nearly 5 million individuals are affected with oral submucous fibrosis, due to the abuse of betel nut and pan masala. 33

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35. ORAL CAVITY CANCER- Carcinoma of buccal mucosa is the most common carcinoma of the oral cavity in Southeast Asia because of the widespread abuse of betel nut and pan masala. The second most common site is tongue. The third most common site is the floor of the mouth. Carcinoma of the alveolar ridge, retromolar trigone and hard palate are other rare types. 35

36. 6. PATTERN OF SPREAD 36

37. LOCAL SPREAD- Majority of lip cancers are local growths that do not invade deeply into the tissues of the oral cavity or mandible. Floor of the mouth cancers can secondarily involve the ventral tongue, extend along the lingual nerve and submandibular duct, or invade the cortex of the mandible. Tumors in this location can invade deeply, involving the muscles of the floor of the mouth. Also, there is an anatomical gap between the mylohyoid and hyoglossus muscles through which a carcinoma can gain access to submandibular and sublingual areas. 37

38. Alveolar ridge and retromolar trigone cancers tend to invade bone early. Tumors of the inferior alveolar ridge may access the mandibular canal and the inferior alveolar nerve, whereas tumors of the superior alveolar ridge may pass into the maxillary antrum or floor of the nose. Buccal mucosa cancer can invade the buccinator muscle, extend to the buccal fat pad, and invade the subcutaneous tissue. 38

39. LYMPHATIC SPREAD- The retro-styloid space is potentially at risk for involvement by metastatic disease when upper level II nodes are involved. The principal lymphatic drainage of the upper lip is to preauricular, peri-parotid, submental, and submandibular lymph nodes. The medial portion of the lower lip drains primarily to the submental lymph nodes, whereas the lateral portion drains to the submandibular triangle. The anterior portion of the tongue drains to the submental nodes, and the lateral portion drains to the submandibular and deep jugular nodes. The posterior oral tongue drains into the upper jugulodigastric group of lymph nodes. 39

40. The lymphatics of the oral tongue have extensive communication across the midline, thus carcinomas of the oral tongue can metastasize bilaterally. Some carcinomas of the lateral oral tongue may metastasize to level IV lymph nodes without involving levels I, II, or III. This implies that there may be separate lymphatic channels draining from the oral tongue directly to level IV nodes, allowing for apparent “skip metastases.” The floor of the mouth has superficial and deep lymphatic drainage systems. The superficial system crosses randomly in the midline and drains into both the ipsilateral and contralateral submandibular lymph nodes. 40

41. DISTANT METASTASIS- The risk of distant metastases increases with the degree of lymph node involvement. Patients with recurrent disease are also at higher risk for distant metastases. In general terms, 66% of distant metastases are to the lungs, 22% to the bones, and 9.5% to the liver. 41

42. 7. PATHOLOGICAL CLASSIFICATION 42

43. The predominant histopathologic type of cancer in the oral cavity is squamous cell carcinoma. 2 main variants of squamous cell carcinoma, including basaloid and verrucous carcinoma, and other variant being sarcomatoid carcinoma. Basaloid squamous cell carcinoma has a worse prognosis due to higher incidence of advanced disease at presentation, distant metastases, and poorer overall survival rate. Verrucous carcinoma is a less common variant of squamous cell carcinoma. It is generally considered a low-grade malignancy with low metastatic potential and good overall prognosis Sarcomatoid carcinomas carry a poor prognosis, with a mean survival of approximately 2 years. 43

44. < 10% of neoplasms of the oral cavity have non-squamous histology. Most of these are minor salivary gland tumors, which tend to arise in the hard palate. Adenoid cystic carcinoma accounts for approximately 30% to 40% of minor salivary gland cancers of the oral cavity. Other types includes adenocarcinomas, melanoma, ameloblastoma, lymphoma, and Kaposi sarcoma. Most lymphomas in the head and neck arise in Waldeyer ring (tonsil, base of the tongue, and nasopharynx). Melanomas are also present, with mucosal melanomas generally having a worse prognosis than cutaneous melanomas. 44

45. 8. STAGING (AJCC 8 th Ed.) 45

46. There are several pertinent changes from prior editions of the AJCC Staging Manual: Clinical and pathologic depth of invasion are now used in indicating the T category. Extrinsic tongue muscle involvement is no longer denoted as T4. Separate N staging categories are now present for patients treated with and without neck dissection. The presence of extra-nodal extension (ENE) is introduced as a descriptor of HPV negative squamous cell carcinoma. 46

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51. REFERENCES- PEREZ & BRADY’S DHINGRA’S ENT ROBBINS PATHOLOGY NCCN v.2018 GLOBOCAN 2022 AJCC 8 TH Edition 51

52. CA ORAL CAVITY PART 2 CLINICAL PRESENTATION DIAGNOSTIC EVALUATION MANAGEMENT- GENERAL OVERVIEW SURGERY RADIATION THERAPY CHEMOTHERAPY 52

53. THANK YOU, AND HAVE A NICE DAY! 53