Oral diseases - Benign and premalignant lesions

Oral Benign and premalignant lesions - presentation for MBBS students

1. Benign disorders of oral cavity Dr Dileep Ramesh Hoysal

2. Ranula Extravasation cyst arising from sublingual gland or mucous glands of Nuhn or glands of Blandin in the floor of the mouth . Blockage of the duct causing retention cyst, which causes rupture of the acini due to increased pressure leading into extravasation cyst

3. Clinical features Presents as a bluish smooth, soft, fluctuant, brilliantly transilluminant swelling Extends into the submandibular region through the deeper part of the posterior margin of mylohyoid muscle and is called as plunging ranula Nontender and cross fluctuant across mylohyoid .

4. Treatment Marsupialisation If ranula is small it can be excised In plunging ranula submandibular salivary gland needs to be excised.

5. Sublingual dermoid sequestration dermoids lined by squamous epithelium containing keratin . smooth, soft, fluctuant , nontransilluminant bidigitally palpable swelling . Types Median sublingual dermoid Lateral sublingual dermoid

6. Treatment: Small one is removed per orally. Larger one, through submandibular incision.

7. Stomatitis It is inflammation of oral mucosa by trauma, radiotherapy, chemicals , nutritional deficiency or infection. Types Traumatic stomatitis Aphthous stomatitis Candida stomatitis Vincent’s ulcerative stomatitis Angular stomatitis

8. Vincent’s ulcerative stomatitis ( Vincent’s angina/trench mouth) Infection by Gram – ve anaerobic bacteria Borrelia vincentii and Fusiformis fusiformis . Adolescents and young adults below the age of 35 Fever, excessive salivation, red swollen gums with painful ulcers covered with yellow slough ( pseudomembrane ) which can be removed like membrane–ulcerative gingivitis Musty foetor oris is typical Infection in tonsillar crypts is called Vincent’s angina . Treated by antibiotics

9. Cancrum oris Infective gangrene , a severe form of Vincent‘s acute ulcerative gingivitis and stomatitis .

10. Seen in poorly nourished, ill-child due to Borrelia vincentii and Fusiformis bacteria . It starts in lips later extends to gums, spreads into cheek Treatment 1. Systemic antibiotics, high dose penicillins , metro nidazole , 2. High protein and vitamin rich diet, through naso gastric tube. 3. Wound irrigation and liberal excision of the dead tissue. 4. Blood transfusion, TPN.

11. Tongue tie It is short, thick, fibrous frenum linguae . It causes speech defect, difficulty in cleaning the inner part of lower teeth . Treatment: Tongue tie release

12. Fissure tongue

13. Congenital fi ssures are transverse which run laterally from midline with normal papillae in between. Candida infection can occur on this . Syphilitic fissures are deep bald and longitudinal.

14. Glossitis Migrans (Geographic Tongue ) It begins as benign small red patches with white furred margin which spread and recede in an irregular way to appear as fresh patches . White margin contains keratinized epithelium and inflammatory cells over filiform papillae . Etiology is unknown Treatment is supportive

15. Hairy tongue Hairy tongue is overgrowth of filiform papillae with black/ brown stain on it due to bacteria, fungi, tobacco or drugs. There are no hairs. It is a misnomer. Cessation of causative agent, mechanical scraping, cleaning are the treatment methods.

16. PREMALIGNANT CONDITIONS High risks—lesions with definite risk of malignant change Leukoplakia . Erythroplakia . Chronic hyperplastic candidiasis

17. Medium risks—premalignant but not associated with higher incidence of carcinoma Oral submucosal fi brosis . Syphilitic glossitis . Sideropenic dysphagia Equivocal risk lesions Oral lichen planus . Dyskeratosis congenital—reticular atrophy, nail dystrophy, Discoid lupus erythematosus .

18. LEUKOPLAKIA It is a white patch in the mucosa of the oral cavity that cannot be characterised clinically or patho lo gi cally to any other disease. It is a premalignant condition . Treatment Pan chewing and smoking has to be stopped. Excision, if required skin grafting to be done. Regular follow-up is necessary. Isoretinoin is helpful . Beta-carotene, tocoferol are also used. CO2 laser excision

19. Types 1. Homogenous. 2. Nodular—more malignant . 3. Speckled—most malignant–highest .

20. ERYTHROPLAKIA It is red velvety appearance of the mucosa which cannot characterise any recognised condition . It is 17-20 times more potentially malignant than leukoplakia . Red color is due to decreased keratin causing shining and prominence of submucosal red vascularised connective tissue. Histologically parakeratosis with severe epithelial dysplasia is the typical feature . Treatment: Biopsy and surgical excision.

21. ORAL SUBMUCOSAL FIBROSIS It is a progressive fibrosis deep to the mucosa of the oral cavity which causes trismus and ankyloglossia . The mucosa of cheek, gingivae , palate and tongue shows a mottled/marbled pallor.

22. Aetiology : Hypersensitivity to chilli , betelnut , tobacco and vitamin deficiencies Soreness and burning in mouth which is more during meals; vesicular eruptions; trismus ; difficulty in protruding the tongue . Treatment — Local injection of dexamethasone (4 mg) with hyalase (1500 units) biweekly for 10 weeks ; Avoidance of irritants ; Vitamin supplements ; correction of anaemia ; Surgical wide excision and skin grafting

23. Lip

24. Cleft lip and palate Central—rare. In upper lip. Between two median nasal processes. ( Hare lip) Lateral—maxillary and median nasal process, commonest; can be unilateral or bilateral Incomplete cleft lip does not extend into nose Complete cleft lip extends into nasal fl oor Simple cleft lip is only cleft in the lip Compound cleft lip is cleft lip with cleft of alveolus

25. Classification I. Cleft lip alone: Unilateral . Bilateral. Median. II. Cleft of primary palate (in front of incisive foramen) only: a. Complete—means absence of pre-maxilla. b. Incomplete—means rudimentary pre-maxilla. i . Unilateral. ii. Bilateral. iii. Median. III. Cleft of secondary palate (behind the incisive foramen)only : a. Complete—nasal septum and vomer are separated from palatine process. b. Incomplete. c. Submucous . It can be - Cleft with soft palate involvement. - Cleft without soft palate involvement. IV. Cleft of both primary and secondary palates. V. Cleft lip and cleft palate together.

26. Aetiology Familial—more common in cleft lip or combined cleft lip and palate (Risk is 1:25 live births). Protein and vitamin deficiency . Rubella infection. Radiation. Chromosomal abnormalities. Maternal epilepsy and drug intake during pregnancy ( steroids/ eptoin /diazepam ).

27. Problems in Cleft Disorders Diffi culty in sucking and swallowing. This is commonly observed in cleft palate than in cleft lip . Speech is defective especially in cleft palate, mainly to phonate B, D, K, P, T and G. Altered dentition or supernumerary teeth. Recurrent upper respiratory tract infection. Respiratory obstruction (in Pierre Robin syndrome) Chronic otitis media, middle ear problems. Cosmetic problems. Hypoplasia of the maxilla.

28. Treatment cleft lip Millard criteria is used to undertake surgery for cleft lip. Millard criteria (Rule of ‘10’) 10 pound in weight 10 weeks old 10 gm % haemoglobin

29. Rx cleft palate Cleft palate is usually repaired in 12-18 months . Palatoplasty - Palatal defect is closed using 3 layers—nasal, muscle and oral layers Postoperative speech therapy.

30. Thank you