Oral cavity Lips Tongue Floor of Mouth Buccal mucosa Palate Retromolar trigone.

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Transcript of Oral cavity Lips Tongue Floor of Mouth Buccal mucosa Palate Retromolar trigone.

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Oral cavity

Lips Tongue Floor of Mouth Buccal mucosa Palate Retromolar

trigone

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Reactive lesions

Inflammatory lesions

Oral cancer

Precancerous lesions (Leukoplakia &

erythroplakia)

Benign Tumors of Oral Cavity

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1-Irritation fibroma : Most common 61 % of all the

reactive lesions Can occur

throughout the oral cavity

Most common along the "bite line."

Microscopically: fibrous tissue covered by squamous mucosa.

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2-Pyogenic granulomas 12 % Highly vascular lesions

similar to granulation tissue.

3-Peripheral giant cell granuloma (giant cell epulis)

5% Aggregation of

multinucleated foreign body-like giant cells

Separated by fibroangiomatous stroma.

Giant cell epulis

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Epulis is a clinical term applied to swellings at the gum margin.

Most of them are granulomas associated with chronic gingivitis

A few are true neoplasms

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Reactive lesions

Inflammatory lesions

Oral cancer

Precancerous lesions (Leukoplakia &

erythroplakia)

Benign Tumors of Oral Cavity

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1. Viral infection2. Fungal infection3. Bacterial infection

A - Vincent’s anginaB - SyphilisC - Oral tuberculosis

4. Aphthous ulcers (aphthous stomatitis)5. Dermatoses

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Inflammation of the mouth (Stomatitis)(Stomatitis) Inflammation of the Lips (Cheilitis)(Cheilitis) Inflammation of the soft tissues around teeth

typically resulting from inadequate oral hygiene (Gingivitis)(Gingivitis)

Inflammmation of the tongue (Glossitis).(Glossitis). GlossitisGlossitis more commonly applied to the "beefy-red" "beefy-red"

tonguestongues of certain deficiency states (e.g.; vitamin (e.g.; vitamin B12, and iron, deficiencies).B12, and iron, deficiencies).

Other causes of glossitis: Other causes of glossitis: hot and spicy foods, chronic irritation by excessive smoking, ragged tooth or syphilitic inflammation

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Herpes simplex virus (usually type 1) infection causes "cold sores"

The virus infects the mouth in children.

Most adults have had HSV1 infection, but it remains latent and produces this small sore: During periods of stress From local trauma Environmental changes

Cold sores consist of numerous vesicles and shallow ulcerations.

Cold sore of lower lip (herpes labialis)Sore = abraded or painful area of the body

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Treatment Antipyretics, analgesics, hydration Valacyclovir and famciclovir inhibit viral DNA polymerase – help to suppress and control help to suppress and control symptoms, symptoms, but does not cure but does not cure (given for 1 week)

If catch in the prodrome - 5% acyclovir cream for 1 week has shown to shorten course or completely abort reactivation altogether

KEY TO DIAGNOSIS – Clinical + Fluid analysis Clinical + Fluid analysis (PCR) and/or serology (Elisa, Western Blot)(PCR) and/or serology (Elisa, Western Blot)

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Coxackie A virus causes herpangia

Acute vesiculo-ulcertaive mucosal lesion

Occurs in epidemics Affects children Begins in tonsils, soft tonsils, soft

palate & uvulapalate & uvula Painful Heal spontaneously

within few days

Koplik’s spots are a feature of measles Koplik’s spots

Herpangia

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Herpangina

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Candida albicans is an oral commensal in oral commensal in 20-40% 20-40% of population.

Infection occurs in: Infants Patients on broad spectrum antibiotics, steriod or cytotoxic

therapy Diabetes Neutropenia Immunodeficiency (AIDS)

Presents as superficial gray-white inflammatory membranes comprising fungus in a fibrinosuppurative exudate.

White exudate can be removed by scraping

Exudate bleeds on removal ?

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Erythematous Candidiasis

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Treatment Mild, acute forms Mild, acute forms – topical Nystatin Mild, chronic Mild, chronic – topical Nystatin +

Clotrimazole troches (troche=lozenge)

Refractory or immunocomprimised Refractory or immunocomprimised WITHOUT systemic involvement WITHOUT systemic involvement – add oral Fluconazole

Severe forms (systemicsystemic) – IV Amphotericin B with or without Fluconazole

KEY TO DIAGNOSIS: Clinical + KOH Prep; culture and serum (1,3)β-D-glucan detection assay if unclear

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Caused by Borellia vincenti and fusiform bacilli

Both are normal inhabitants of oral cavity

Decreased resistance (inadequate nutrition, immunofeciency) is a predisposing factor to infection

Punched out erosions → ulceration → spreads → invovles all gingival margin, which become covered by a necrotic pseudomembrane

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A-Ulcerated chancre B-Ulcerated mucous patches (snail track ulcers)

C-Gummatous ulcer

C - Tuberculosis of The Tongue

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Apthous ulcers are extremely common lesions (up to 20% of population)

They are painful, multiple, small, shallow, recurrent ulcerations

Presented clinically as white lesions (1<,1> CM)

Etiology is unknown Aphtha = Whitish spot

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○ Most common cause of non-traumatic ulcerations of the oral cavity

○ Etiology unclear○ 10-20% of general population○ Diagnosis of exclusion○ Classifications

Minor aphthous ulcerMinor aphthous ulcer- < 1cm < 1cm in diameter- Located on freely mobile oral mucosa- Appears as a well-delineated white lesion with an erythematous

halo- Prodrome of burning or tingling in area prior to ulcer’s

appearance- Resolve in 7-10 days- Never scars

Major aphthous ulcerMajor aphthous ulcer- > 1cm > 1cm in diameter- Involves freely mobile mucosa, tongue, and palate- Last much longer – 6 weeks or more- Typically scar upon healing

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Herpetiform ulcers- Small, 1-3mm in diameter ulcerations appearing in crops

of 20-200 ulcers- Typically located on mobile oral mucosa, tongue, and

palate- Last 1-2 weeks- Called herpetiform because ulcerations resemble Called herpetiform because ulcerations resemble

those of HSV, but there is those of HSV, but there is no vesicular phaseno vesicular phase Treatment

Topical tetracycline solution for 5-7 days has shown good results

Topical steroids shown to shorten disease duration Sucralfate suspension shown to improve pain as well as

shorten disease duration Major aphthous ulcers or more severe forms of Major aphthous ulcers or more severe forms of

disease require 2 week course of systemic steroidsdisease require 2 week course of systemic steroids KEY TO DIAGNOSIS: Diagnosis of exclusion; clinical

appearance/course

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Lichen planus

White plaques

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whitish linear lesions in lacy patternwhitish linear lesions in lacy pattern

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Reactive lesions

Inflammatory lesions

Oral cancer

Precancerous lesions (Leukoplakia &

erythroplakia)

Benign Tumors of Oral Cavity

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Incidence: Geographic variation: Accounts for 2% of

cancers in UK Commoner in S. East

Asia

Ages & sex : Old Men (50-60 years)

• Site : 1.Lip (lower lip)

2.Tongue (anterior ⅔)

3.Mouth floor4.Tonsil and Fauces

Squamous Cell Carcinoma constitutes 95% of oral cancers

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Aetiology:1-Tobacco and alcohol are the most

common associations: Smokers can have 15-fold greater risk ( than

nonsmokers ) of malignancy. Chewing tobacco and betel nuts are important causes

in India and parts of Asia.2- Leukoplakia and Erythroplakia3- Human papilloma virus (HPV) (type16)4- Genetic factors may also play a role (deletions in chromosomes 18q, lap, 8p, and 3p are

implicated).

5- Exposure to ultra-violet light (cancer of the lip).

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Gross: Ulcerated nodule with

raised everted edges Often on lower lipHistologically: Well differentiated

squamous carcinomasSpread: Growth is relatively

slow Submandibular nodes Deeper cervical lymph

nodes

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More aggressive than tumors of the lips Grossly starts as a nodule → malignant

ulcer Spread:1-Local Local infiltration to floor of the mouth,

facuces and pharynx leads to fixation the tongue, interfering with speech and swallowing.

Local spreads into the medullary cavity of the mandible.

2-lymphatic spread (occurs early) → deep cervical lymph nodes.

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Perform incisional Bx in any oral lesion persist for more than 2wks

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Prognosis is best with lip lesions Poorest with mouth floor and tongue

base lesions (20%-30% 5-year survival rate ).

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Malignant melanoma

Lymphomas Leukemic

infiltration Adenocarcinoma

of minor salivary glands

Sarcomas

Acute Leukemia: gum involvement

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Reactive lesions

Inflammatory lesions

Oral cancer

Precancerous lesions (Leukoplakia &

erythroplakia)

Benign Tumors of Oral Cavity

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Premalignant lesions○ Leukoplakia

Whitish plaque that cannot be scrapped off 5-20% malignant potential5-20% malignant potential Microscopic examination reveals hyperkeratosis

and atypia Lesions on lateral tongue, lower lip, and floor of

mouth more likely to progress to malignancy○ Erythroplakia

Red patch or macule with soft, velvety texture Much higher chance of harboring malignancy – 60-– 60-

90% 90% of untreated cases Treatment is surgical excision or laser ablation

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Causes include:

1- Chronic tobacco use (pipe - smoking).

2- Chronic irritation (e.g.; dentures).

2- Alcohol abuse.

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An oral lesion seen in HIV infected, AIDS patients

Caused by Epstein-Barr virus (EBV) infection, often with superimposed candida

Lesions are white patches of fluffy ("hairy") hyperkeratosis on tongue lateral borders.

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Reactive lesions

Inflammatory lesions

Oral cancer

Precancerous lesions (Leukoplakia &

erythroplakia)

Benign Tumors of Oral Cavity

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1-Squamous cell papilloma.****

2-Capillary hemangioma

3-Cavernous hemangioma & lymphangioma → macrochelia & macroglossia

4-leiomyoma5-Schwannoma

Cavernous hemangioma

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Bastaninejad, Shahin, MD