Destructive lesions of palate

Destructive lesions of palate ppt

1. Destructive lesions of palate Presented by N.Narmatha II YEAR PG

2. introduction The palate is an integral part of the oral cavity constituting various tissue types that give rise to different types of pathological conditions. Palatal perforation can be defined as a communication between the nasal cavities and the oral cavity. Can pose a difficult diagnostic dilemma for the clinician

3. It forms both the roof of the mouth and the floor of the nasal cavity Reflecting this, the superior and inferior palatal surfaces have different  mucosae: Superior aspect   of palate  (nasal cavity) – respiratory epithelium. Inferior aspect of palate  (oral cavity) – oral mucosa, populated by secretory salivary glands

4. histology Keratinizing stratified squamous epithelium - ortho - or parakeratinized - explain the decreased incidence of squamous cell carcinoma in the hard palate as compared to other areas of the oral cavity

5. Early presentation Pain and discomfort Ulceration , foul odour and bleeding Late presentation Extension superiorly into the maxillary antrum and nasal cavity N asal obstruction Posterior extension into the structures of the oropharynx, into pterygoid muscles

6. Clinical assessment History and thorough head and neck exam Lymph nodes in neck Middle ear effusion Extension into nasopharynx Absent trigeminal blink reflex or palatal hypaesthesia

7. diagnosis CT scan MRI Biopsy FNA

8. classification Developmental Cleft palate Drug related Narcotics (cocaine, heroin etc.,) Trauma Iatrogenic, Thermal Infection Tertiary Syphilis, Tuberculosis, Leprosy, Typhoid, Mucormycosis, Actinomycosis , Aspergillosis, Paracoccidioidomycosis, Histoplasmosis, Naso -Oral Blastomycosis, Leishmaniasis , Diphtheria, Rhinoscleroderma Patil SR (2016) Proposed Classification for the Palatal Perforation” (Dr. Santosh Patil Classification). J Interdiscipl Med Dent Sci 4: 192

9. Contd …… Neoplasia Lymphoma, Carcinoma, Melanoma, Acute Lymphoblastic Leukemia Collagen vascular disease Wegener's granulomatosis, Systemic lupus erythematous Idiopathic Midline lethal granuloma Granulomatous disease Sarcoidosis, Crohns’s disease Other Rhinoliths Patil SR (2016) Proposed Classification for the Palatal Perforation” (Dr. Santosh Patil Classification). J Interdiscipl Med Dent Sci 4: 192

10. Cocaine-Induced Palatal Perforation Coca leaves ( erythroxylon coca ), the source of cocaine Purified chemical, cocaine hydrochloride- isolated from the plant Local complications Chronic rhinitis Sinusitis Epistaxis O ssification or necrosis of the nasal septum palatal perforation Cocaine - potent vasoconstrictor- ischemia - necrosis- ulceration

11. Palatal perforations secondary to inhaled cocaine abuse. Presentation of five cases V asoconstrictive and caustic effect of the drug direct irritation ischemia of the nasal and palatine mucosa secondary to maxillary bone destruction creation of an oronasal perforation

12. Management Antibiotics, analgesics Prostheses (obturators) Surgical reconstructions of the defect Nasal septal button INSERTION OF NASAL SEPTAL BUTTON IN THE TREATMENT OF SEPTAL PERFORATION : A CASE REPORT - Semantic Scholar

13. syphilis Syphilis   - sexually transmitted infection-  bacterium  Treponema pallidum   Primary stage - single  chancre  - a firm, painless, non-itchy skin ulceration but there may be multiple sores Secondary syphilis - diffuse  rash  - palms of the hands and soles of the feet , sores in the mouth or vagina

14. In latent syphilis - few or no symptoms  In tertiary syphilis-   gummas  (soft, non-cancerous growths) neurological problems, or heart symptoms Gummata - ulcerated nodular granulomatous lesions - causing localised destruction and perforation of the palate and lobulated enlargement and surface irregularities of the tongue

15. CONTD…..

16. Management Recommended Regimen for Adults Benzathine  penicillin G 2.4 million units IM in a single dose Infants and Children - 50,000 units/kg IM - 2.4 MU Penicillin Allergy  D oxycycline 100 mg orally bid - 14 days Tetracycline (500 mg four times daily for 14 days)  Tertiary Syphilis Benzathine  penicillin G 7.2 million units total, 3 doses of 2.4 million units IM each at 1-week intervals June 4, 2015Content source: Division of STD Prevention , National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention,  Centers for Disease Control and Prevention

17. TUBERCULOSIS Tuberculosis (TB) - caused by  Mycobacterium tuberculosis   Pulmonary TB - most common form Both primary and secondary types of TB - cause lesion in the oral cavity . In secondary TB, lesions of the oral cavity may accompany lesions in the pharynx, lungs, lymph nodes and skin Primary tuberculosis of palate

18. Oral TB is rarely seen Few factors that attribute to relative resistance of oral cavity TB are protection by the oral saliva, presence of saprophytes, resistance of the striated muscles to bacterial invasion thickness of the protective epithelial covering

19. The most common site for oral TB - tongue Others - soft palate, hard palate, lip, cheek, tonsils, gingiva, floor of the mouth, uvula, and alveolar mucosa. Manifestation of oral TB is an ulcerative lesion of the mucosa.

20. opalescent vesicle or a nodule caseation necrosis ulcer A typical TB lesion - ragged undermined edges, minimal induration and often with a yellowish apple jelly like granular base - ulcerate leaving radiating scars. Primary tuberculosis of palate

21. Diagnosis C an mimic a malignant neoplasm Primary lesions of TB manifest in the oral cavity as non-healing chronic ulcers. C hest radiograph and tissue biopsy for histological studies

22. Management: Isoniazid – 300 mg twice weekly Rifampicin – 600 mg Rifabutin – 300 mg Pyrazinamide - 2g Ethambutol – 1.6 g

23. LEPROSY Leprosy is a chronic infectious disease - Mycobacterium leprae Two forms - lepromatous and tuberculoid forms Mainly it affects skin, peripheral nerves and nasal mucosa It can also affect the oral cavity

24. Oral lesions are more common in lepromatous type of leprosy. In the oral cavity, it can involve the palate, buccal mucosa, tongue M . leprae prefer to colonize the cooler parts of the body The commonest site of oral cavity - hard palate >soft palate, labial and buccal maxillary gingiva, tongue, lips, labial mandibular gingiva > buccal mucosa.

25. palate ulceration perforation oro -nasal fistula E rythema nodosum leprosum is an important but rare cause of the destruction of the hard and soft palate Palatal nodulo ulcerative lesions of leprosy may mimic squamous cell carcinoma

26. mucormycosis Cotran , Kumar, Robbins Robbins ' pathologic basis of disease, (4' °  sub ed.) WB Saunders and Co, Philadelphia, 356,1989 O pportunistic fungal infection - caused by normally saprobic organism of the class Zygomycetes Invasion of surrounding tissue - necrotizing ulceration of palate with a blackish slough and exposure of bone

27. The 5 major clinical forms are as follows: 1. Rhinocerebral   2. Pulmonary  3. Abdominal pelvic and gastrointestinal 4. cutaneous 5. Disseminated forms Rhinocerebral mucormycosis – typically commences in the nasal cavity or paranasal sinuses – invade the palate (black necrotic ulceration)

28. Early diagnosis of mucormycosis

29. Lab investigation: D irect morphologic identification of mycotic elements and recovery of Mucorales organisms in culture from specimens  Histologic examination - periodic acid-Schiff and Gomori methanamine silver stains

30. actinomycosis S lowly progressing infection caused by anaerobic bacteria Actinomyces Three distinct clinical forms Cervicofacial abdominopelvic Thoracopulmonary Destroy local tissue in a highly vascularised and therefore aerobic region and replaces it with granulation tissue.

31. Treatment : IV penicillin -2-4 weeks – 6-12 months

32. Wegener’s granulomatosis Rare chronic granulomatous disease Immunological C/F : Necrotizing granulomatous lesions of the respiratory tract ,generalized focal necrotizing vasculitis and necrotizing glomerulonephritis.

33. Oral manifestation : solitary or multiple irregular ulcers, surrounded by an inflammatory zone Tongue, palate ,buccal mucosa and gingiva. Lab investigation : c-ANCA –anti neutrophil cytoplasm test

34. 1.5 – 2 mg/kg 7– 15mg/kg 2 mg/kg ,1.5 mg,1 mg/kg

35. sarcoidosis Systemic granulomatous disease Non caesating granuloma – characteristic lesion. Oral manifestation: multiple, nodular, painless ulceration of the gingiva, buccal mucosa, tongue, lips and palate

36. Midline lethal granuloma Lethal midline granuloma  ( LMG ) is an historical term for a condition in which necrotic and highly destructive lesions develop progressively in the middle of the face, principally the nose and  palate

37. Manifestation of three or four different diseases: the well-characterized disease of granulomatosis with polyangiitis the ill-defined disorders of polymorphic reticulosis mid-line malignant reticulosis , and an incompletely defined form of non- Hodkgins disease malignant lymphoma

38. managemeNt

39. noma Noma  is a rapidly progressive, polymicrobial , often gangrenous infection of the mouth or genitals.

40. The mucous membranes of the mouth develop  ulcers - rapid , painless tissue degeneration - degrade tissues of the bones in the face Bacterial cause: Fusobacterium necrophorum and   Prevotella intermedia   ( such as  Borrelia vincentii ,  Porphyromonas gingivalis ,  Tannerella forsythia, Treponema denticola , Staphylococcus aureus , and certain species of nonhemolytic   Streptococcs ).

41. Necrotising sialometaplasia Uncommon locally destructive inflammatory condition of the salivary glands Cause: unknown Result of ischemia of the salivary tissue t hat leads to local infarction.

42. B enign , ulcerative lesion, usually located towards the back of the hard palate. It is thought to be caused by ischemic necrosis (death of tissue due to lack of blood supply) of minor salivary glands in response to trauma.

43. Clinical features Most frequently develops in palatal salivary glands Hard palate> soft palate 2/3 of palatal cases are unilateral ,with the rest being bilateral or midline in location Appears initially as non- ulcerated swelling often associated with pain or parasthesia with crater like ulcer <1cm >5cm in diameter appearing within 2-3 weeks.

44. Investigation: biopsy Management : I rrigation, self limiting disorder

45. Phossy jaw Phossy jaw , formally known as  phosphorus necrosis of the jaw an  occupational disease  affecting those who worked with  white phosphorus white phosphorus vapour- destroys the bones of the jaw

46. Treatment: T opical antimicrobials C onservative  debridement of  sequestra   Surgical removal of the afflicted jaw bones Diagnosis:  In radiographs, the  sequestra  present as a typical worm-eaten appearance. Sequestra appear osteoporotic and decalcified. Separation of the dead bone from the surrounding bone appears clearly demarcated in the radiographs

47. TUMORS OF THE PALATE P alate - most common site for minor gland neoplasms. Cancer of the soft palate - 2 % of head and neck mucosal malignancies. H ard palate cancers are squamous cell carcinomas (SCCs )

48. Non squamous cell cancers - minor salivary gland cancers, sarcomas, and melanomas. Benign tumors - pleomorphic adenomas Malignant tumors - mucoepidermoid carcinoma, adenoid cystic carcinoma, and polymorphous low-grade adenocarcinoma.

49. BENIGN PLEOMORPHIC ADENOMA M ost common benign mixed tumor composed of epithelial and myoepithelial cells arranged with various morphological patterns, demarcated from surrounding tissues by fibrous capsule .

50. Malignant squamous Epithelial neoplasms MUCOEPIDERMOID CARCINOMA (MEC) Arise from pluripotent reserve cells of excretory ducts that are capable of differentiating into squamous, columnar, and mucous cells

51. Adenoid cystic carcinoma A ccounts for <1% of all head and neck malignancies 4-10 % of all salivary gland tumors commonest malignant tumor of the minor salivary glands Intraorally 50% - occur on the palate

52. POLYMORPHOUS LOW-GRADE ADENOCARCINOMA Malignant epithelial tumor Characterized by cytological uniformity, morphological diversity, an infiltrative growth pattern and low metastatic potential Most common location - palate More frequent in women

53. Conclusion: It is well understood that the palatal perforation can pose a difficult diagnostic dilemma for the clinician . The perforation may present with the common characteristics and may be indistinguishable clinically. Emphasis is placed on the importance of obtaining a thorough and comprehensive history and collecting relevant laboratory information.

54. references 1.Textbook of oral medicine , burkett -11 th edition 2.Oral pathology – shafer’s 3.Cotran, kumar , robbins pathologic basis of disease, (4' °  sub ed.) WB saunders and co, philadelphia , 356,1989 4.June 4, 2015content source: division of STD prevention, national center for HIV/AIDS, viral hepatitis, STD, and TB prevention,  centers for disease control and prevention

55. Thank you