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.
Oral cavity
Lips Tongue Floor of Mouth Buccal mucosa Palate Retromolar
trigone
Reactive lesions
Inflammatory lesions
Oral cancer
Precancerous lesions (Leukoplakia &
erythroplakia)
Benign Tumors of Oral Cavity
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.
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
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
Reactive lesions
Inflammatory lesions
Oral cancer
Precancerous lesions (Leukoplakia &
erythroplakia)
Benign Tumors of Oral Cavity
1. Viral infection2. Fungal infection3. Bacterial infection
A - Vincent’s anginaB - SyphilisC - Oral tuberculosis
4. Aphthous ulcers (aphthous stomatitis)5. Dermatoses
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
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
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)
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
Herpangina
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 ?
Erythematous Candidiasis
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
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
A-Ulcerated chancre B-Ulcerated mucous patches (snail track ulcers)
C-Gummatous ulcer
C - Tuberculosis of The Tongue
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
○ 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
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
Lichen planus
White plaques
whitish linear lesions in lacy patternwhitish linear lesions in lacy pattern
Reactive lesions
Inflammatory lesions
Oral cancer
Precancerous lesions (Leukoplakia &
erythroplakia)
Benign Tumors of Oral Cavity
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
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).
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
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.
Perform incisional Bx in any oral lesion persist for more than 2wks
Prognosis is best with lip lesions Poorest with mouth floor and tongue
base lesions (20%-30% 5-year survival rate ).
Malignant melanoma
Lymphomas Leukemic
infiltration Adenocarcinoma
of minor salivary glands
Sarcomas
Acute Leukemia: gum involvement
Reactive lesions
Inflammatory lesions
Oral cancer
Precancerous lesions (Leukoplakia &
erythroplakia)
Benign Tumors of Oral Cavity
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
Causes include:
1- Chronic tobacco use (pipe - smoking).
2- Chronic irritation (e.g.; dentures).
2- Alcohol abuse.
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.
Reactive lesions
Inflammatory lesions
Oral cancer
Precancerous lesions (Leukoplakia &
erythroplakia)
Benign Tumors of Oral Cavity
1-Squamous cell papilloma.****
2-Capillary hemangioma
3-Cavernous hemangioma & lymphangioma → macrochelia & macroglossia
4-leiomyoma5-Schwannoma
Cavernous hemangioma
Bastaninejad, Shahin, MD