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Benign disorders of oral cavityDr Dileep Ramesh Hoysal

RanulaExtravasation 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

Clinical featuresPresents as a bluish smooth, soft, fluctuant, brilliantly transilluminant swellingExtends into the submandibular region through the deeper part of the posterior margin of mylohyoid muscle and is called as plunging ranulaNontender and cross fluctuant across mylohyoid.

Treatment MarsupialisationIf ranula is small it can be excisedIn plunging ranula submandibular salivary gland needs to be excised.

Sublingual dermoidsequestration dermoids lined by squamous epithelium containing keratin.smooth, soft, fluctuant, nontransilluminant bidigitally palpable swelling.TypesMedian sublingual dermoidLateral sublingual dermoid

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

Stomatitis It is inflammation of oral mucosa by trauma, radiotherapy, chemicals, nutritional deficiency or infection.TypesTraumatic stomatitisAphthous stomatitisCandida stomatitisVincents ulcerative stomatitisAngular stomatitis

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

Cancrum orisInfective gangrene, a severe form of Vincents acute ulcerative gingivitis and stomatitis.

Seen in poorly nourished, ill-child due to Borrelia vincentii and Fusiformis bacteria.It starts in lips later extends to gums, spreads into cheekTreatment1. 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.

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

Fissure tongue

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.

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 unknownTreatment is supportive

Hairy tongueHairy 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.

PREMALIGNANT CONDITIONSHigh riskslesions with definite risk of malignant change Leukoplakia. Erythroplakia. Chronic hyperplastic candidiasis

Medium riskspremalignant but not associated with higher incidence of carcinoma Oral submucosal fi brosis. Syphilitic glossitis. Sideropenic dysphagiaEquivocal risk lesions Oral lichen planus. Dyskeratosis congenitalreticular atrophy, nail dystrophy, Discoid lupus erythematosus.

LEUKOPLAKIAIt 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

Types1. Homogenous.2. Nodularmore malignant.3. Speckledmost malignanthighest.

ERYTHROPLAKIAIt 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.

ORAL SUBMUCOSAL FIBROSISIt 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.

Aetiology: Hypersensitivity to chilli, betelnut, tobacco and vitamin deficienciesSoreness and burning in mouth which is more during meals; vesicular eruptions; trismus; difficulty in protruding the tongue.TreatmentLocal 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

Lip

Cleft lip and palateCentralrare. In upper lip. Between two median nasalprocesses. (Hare lip) Lateralmaxillary and median nasal process, commonest; canbe 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

ClassificationI. Cleft lip alone: Unilateral.Bilateral.Median.II. Cleft of primary palate (in front of incisive foramen) only:a. Completemeans absence of pre-maxilla.b. Incompletemeans rudimentary pre-maxilla.i. Unilateral.ii. Bilateral.iii. Median.III. Cleft of secondary palate (behind the incisive foramen)only:a. Completenasal 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.

Aetiology Familialmore common in cleft lip or combined cleft lipand 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).

Problems in Cleft DisordersDiffi 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.

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

Rx cleft palateCleft palate is usually repaired in 12-18 months.Palatoplasty- Palatal defect is closed using 3 layersnasal, muscle and oral layersPostoperative speech therapy.

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