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

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Presentation on theme: " Oral cavity  Lips  Tongue  Floor of Mouth  Buccal mucosa  Palate  Retromolar trigone."— Presentation transcript:

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2  Oral cavity  Lips  Tongue  Floor of Mouth  Buccal mucosa  Palate  Retromolar trigone

3  Reactive lesions  Inflammatory lesions  Oral cancer  Precancerous lesions (Leukoplakia & erythroplakia)  Benign Tumors of Oral Cavity

4 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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6 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

7  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

8  Reactive lesions  Inflammatory lesions  Oral cancer  Precancerous lesions (Leukoplakia & erythroplakia)  Benign Tumors of Oral Cavity

9 1. Viral infection 2. Fungal infection 3. Bacterial infection A - Vincent’s angina B - Syphilis C - Oral tuberculosis 4. Aphthous ulcers (aphthous stomatitis) 5. Dermatoses

10 (Stomatitis)  Inflammation of the mouth (Stomatitis) (Cheilitis)  Inflammation of the Lips (Cheilitis) (Gingivitis)  Inflammation of the soft tissues around teeth typically resulting from inadequate oral hygiene (Gingivitis) (Glossitis).  Inflammmation of the tongue (Glossitis).  Glossitis"beefy-red" tongues (e.g.; vitamin B12, and iron, deficiencies).  Glossitis more commonly applied to the "beefy-red" tongues of certain deficiency states (e.g.; vitamin 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

11  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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13  Treatment  Antipyretics, analgesics, hydration help to suppress and control symptoms, but does not cure  Valacyclovir and famciclovir inhibit viral DNA polymerase – help to suppress and control symptoms, 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 Clinical + Fluid analysis (PCR) and/or serology (Elisa, Western Blot)  KEY TO DIAGNOSIS – Clinical + Fluid analysis (PCR) and/or serology (Elisa, Western Blot)

14  Coxackie A virus causes herpangia  Acute vesiculo-ulcertaive mucosal lesion  Occurs in epidemics  Affects children tonsils, soft palate & uvula  Begins in tonsils, soft palate & uvula  Painful  Heal spontaneously within few days  Koplik’s spots are a feature of measles Koplik’s spots Herpangia

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16 Herpangina

17 oral commensal in 20-40%  Candida albicans is an oral commensal in 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 ?

18 Erythematous Candidiasis

19  Treatment  Mild, acute forms  Mild, acute forms – topical Nystatin  Mild, chronic  Mild, chronic – topical Nystatin + Clotrimazole troches (troche=lozenge)  Refractory or immunocomprimised WITHOUT systemic involvement  Refractory or immunocomprimised WITHOUT systemic involvement – add oral Fluconazole systemic  Severe forms (systemic) – 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

20  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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22 A-Ulcerated chancre B-Ulcerated mucous patches (snail track ulcers) C-Gummatous ulcer C - Tuberculosis of The Tongue

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25  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 CM)  E tiology is unknown Aphtha = Whitish spot

26 ○ Most common cause of non-traumatic ulcerations of the oral cavity ○ Etiology unclear ○ 10-20% of general population ○ Diagnosis of exclusion ○ Classifications Minor aphthous ulcer Minor 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 ulcer Major aphthous ulcer - > 1cm - > 1cm in diameter - Involves freely mobile mucosa, tongue, and palate - Last much longer – 6 weeks or more - Typically scar upon healing

27 Herpetiform ulcers - Small, 1-3mm in diameter ulcerations appearing in crops of ulcers - Typically located on mobile oral mucosa, tongue, and palate - Last 1-2 weeks - Called herpetiform because ulcerations resemble those of HSV, but there is no 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 disease require 2 week course of systemic steroids  KEY TO DIAGNOSIS: Diagnosis of exclusion; clinical appearance/course

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29  Lichen planus White plaques

30 whitish linear lesions in lacy pattern

31  Reactive lesions  Inflammatory lesions  Oral cancer  Precancerous lesions (Leukoplakia & erythroplakia)  Benign Tumors of Oral Cavity

32  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 floor 4.Tonsil and Fauces Squamous Cell Carcinoma constitutes 95% of oral cancers

33 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 Erythroplakia 3- 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).

34 Gross:  Ulcerated nodule with raised everted edges  Often on lower lip Histologically:  Well differentiated squamous carcinomas Spread:  Growth is relatively slow  Submandibular nodes  Deeper cervical lymph nodes

35  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.

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

37  Prognosis is best with lip lesions  Poorest with mouth floor and tongue base lesions (20%-30% 5-year survival rate ).

38  Malignant melanoma  Lymphomas  Leukemic infiltration  Adenocarcinoma of minor salivary glands  Sarcomas Acute Leukemia: gum involvement

39  Reactive lesions  Inflammatory lesions  Oral cancer  Precancerous lesions (Leukoplakia & erythroplakia)  Benign Tumors of Oral Cavity

40 Premalignant lesions ○ Leukoplakia  Whitish plaque that cannot be scrapped off  5-20% 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 – 60-90%  Much higher chance of harboring malignancy – 60-90% of untreated cases  Treatment is surgical excision or laser ablation

41  Causes include: 1- Chronic tobacco use (pipe - smoking). 2- Chronic irritation (e.g.; dentures). 2- Alcohol abuse.

42  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.

43  Reactive lesions  Inflammatory lesions  Oral cancer  Precancerous lesions (Leukoplakia & erythroplakia)  Benign Tumors of Oral Cavity

44 1-Squamous cell papilloma.**** 2-Capillary hemangioma 3-Cavernous hemangioma & lymphangioma → macrochelia & macroglossia 4-leiomyoma 5-Schwannoma Cavernous hemangioma

45 Bastaninejad, Shahin, MD


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