Oral Benign and premalignant lesions - presentation for MBBS students

1. 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

4. 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.

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

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

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

9. 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

10.  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

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

12.  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.

13. 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

14. Fissure tongue

15.  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.

16. 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

17. 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.

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

19. 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.

20. 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

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

22. 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.

24. 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.

25.  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

26. Lip

27. 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

28.  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.

33. 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).

34. 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.

35. 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

36. 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.

37. Thank you