Lect.1.mouth cavity

ULCERATIVE LESIONS OF THE ORAL CAVITY

Pathophysiology of Gastrointestinal System

SMS 2044

ORAL CAVITYLIPSTEETHGINGIVAORAL MUCOUS MEMBRANESPALATETONGUEORAL LYMPHOID TISSUES

Acute: small, recent onset, short duration, recurrent

TraumaRecurrent Aphthous StomatitisHerpesvirus InfectionHerpangina

Trauma:Cheek Biting

Trauma: Ill-Fitting dentures

Trauma:Chemical Burns

Trauma:Abrasions from Teeth

Recurrent Aphthous Stomatitis(RAS)

Most common ulcerative lesion of oral cavity

Recurrent, painful ulcersConfined to soft mucosaSubdivided into three types:

Minor aphthae Major aphthae Herpetiform aphthae

INFLAMMATORY and ULCERATIVE LESIONS

Aphthous Ulcers (Canker Sores): These lesions are extremely common, small (usually less than 5 mm in diameter), painful, shallow ulcers. Characteristically, they take the form of rounded, superficial erosions, often covered with a gray-white exudate and having an erythematous rim.

• They appear singly or in groups on the no keratinized oral mucosa, particularly the soft palate, buccolabial mucosa, floor of the mouth, and lateral borders of the tongue.

• The sores are self-limited and usually resolve within a few weeks, but they may recur in the same or a different location in the oral cavity.

• Frequent episodes-four times or more per year-earn the moniker of recurrent

• aphthous stomatitis.

Causes The life often apparently triggered by stress, fever, ingestion of certain foods, and activation of inflammatory bowel disease.

In patients who are not immunosuppressed or do not have known viral infection such as with herpesvirus, an autoimmune basis is suspected.

Recurrent Aphthous Stomatitis(RAS)

Minor aphthae: Less than 1 cm Heal completely in 7-10 days without scarring Painful Prodromal stage Shallow and round to oval Gray to yellow membrane Clusters of up to 5 ulcers Steroids

Recurrent Aphthous Stomatitis (RAS)

Minor apthae


Major Aphthae Uncommon Irregular, deep ulcers 1-3 cm in size Raised borders Heal in 4-6 weeks Extensive scarring and distortion BIOPSY!! Steroids


Major apthae


Herpetiform Aphthae Uncommon Crops of up to 150 very small (<3mm)

ulcers Heal completely in 7-10 days COMPLETELY UNRELATED TO

HERPESVIRUS


Herpetiform aphthae

RAS Treat…. A number of different treatments exist for

apthous ulcers including: analgesics, anesthetics agents, antiseptics.

anti-inflammatory agents, steroids, sucralfate, tetracycline suspension, and silver nitrate.

Amlexanox paste has been found to speed healing and alleviate pain.

Vitamin B12 has been found to be effective in treating recurrent aphthous ulcers, regardless of whether there is a vitamin deficiency present

Herpesvirus InfectionHSV-1 and/or HSV-2

Primary Infection Secondary Infection

Varicella zoster virus (HHV-3)

Herpesvirus InfectionPrimary Infection

Herpetic gingivostomatitis Younger patients Often asymptomatic May be associated with fever, chills,

malaise Vesicles-ulcers-crusting Anywhere in the oral cavity

Herpesvirus InfectionPrimary Infection

Herpesvirus InfectionSecondary Infection

Reactivation of latent virus Not associated with systemic symptoms Small vesicles Occur only on the hard palate and gingiva Prodromal signs (prodrome is an early

symptom)

Herpesvirus InfectionSecondary infection

Herpesvirus InfectionVaricella zoster virus (HHV-3)

Latent infection Oral ulcers Dermatomal distribution

Herpesvirus InfectionVaricella zoster virus

Herpes virus Infection Herpetic stomatitis is an extremely common infection caused

by herpes simplex virus (HSV) type 1.

The pathogen is transmitted from person to person, most often by kissing; by middle life over three fourths of the population have been infected.

In most adults, the primary infection is asymptomatic, but the virus persists in a dormant state within ganglia about the mouth (e.g., trigeminal).

With reactivation (fever, sun or cold exposure, respiratory tract infection, trauma), solitary or multiple small (less than 5 mm in diameter) vesicles containing clear fluid appear.

Herpes V……. Inf…. They occur most often on the lips or about the

nasal orifices and are well known as "cold sores" or "fever blisters."

They soon rupture, leaving shallow, painful ulcers that heal within a few weeks, but recurrences are common.

Histologically, the vesicles begin as an intraepithelial focus of intercellular and intracellular edema.

The infected cells become ballooned and develop intranuclear acidophilic viral inclusions.

Sometimes adjacent cells fuse to form giant cells or polykaryons.

Necrosis of the infected cells and the focal collections of edema fluid account for the intraepithelial vesicles seen clinically.

Cont……….

Identification of the inclusion-bearing cells or polykaryons in smears of blister fluid constitutes the diagnostic Tzanck test for HSV infection; antiviral agents may accelerate healing.

In the worst case, viremia may seed the brain (encephalitis) or produce disseminated visceral lesions.

Herpesvirus pharyngitis. A, Herpesvirus blister in mucosa. B, High-power view of cells from blister, showing glassy intranuclear herpes simplex inclusion body

HSV type 1 may localize in many other sites, including the conjunctivae (keratoconjunctivitis) and the esophagus when a nasogastric tube is introduced through an infected oral cavity.

HSV type 2 (the agent of herpes genitalis), on the other hand, is transmitted sexually and produces vesicles on the genital mucous membranes and external genitalia that have the same histologic characteristics as those that occur about the mouth.

This is a photomicrograph of infected cells, with inclusion bodies in both the nucleus and the cytoplasm.

Herpangina NOT caused by Herpesvirus Coxsackie A virus Children < 10 years of age Common in summer and fall Often subclinical presentation Headache/Abdominal pain 48hrs prior to

papulovesicular lesions on tonsils and uvula. Sore throat

Herpangina

Chronic: longer duration, well circumscribed, raised borders, indurated

base with craterTrauma InfectionNeoplasmNecrotizing sialometaplasia

Trauma: Ill-Fitting dentures

InfectionRareHIV/AIDS patientsBacterialDeep mycotic infectionCandida

InfectionBacterial

Usually secondary infection Primary infection: syphilis, tuberculous, or

actinomycosis

InfectionBacterial-Syphilis

InfectionMycotic

Blastomycosis Histoplasmosis

InfectionHistoplasmosis; Histoplasmosis is common among

AIDS patients because of their depressed immune system

InfectionCandida

Candida albicans Most common Normal flora Predisposing factors White creamy patches KOH prep Nystatin oral suspension

Fungal Infection Candida albicans is a normal inhabitant of the oral

cavity found in 30% to 40% of the population; it causes disease only when there is some impairment of the usual protective mechanisms.

Oral candidiasis (thrush, moniliasis) is a common fungal infection among persons rendered vulnerable by diabetes mellitus, anemia, antibiotic or glucocorticoid therapy, immunodeficiency, or debilitating illnesses such as disseminated cancer.

Patients with the acquired immunodeficiency syndrome (AIDS) are at particular risk.

Typically, oral candidiasis takes the form of an adherent white, curd like, circumscribed plaque anywhere within the oral cavity.

The pseudomembrane can be scraped off to reveal an underlying granular erythematous inflammatory base.

InfectionCandida

Oral candidiasis ("thrush"). A white plaque like membrane coats the gingival mucosa of the left lower jaw in an edentulous young patient.

This pseudomembrane is composed of a layer of candidal

• In the particularly vulnerable host, candidiasis may spread into the esophagus, especially when a nasogastric tube has been introduced, or it may produce widespread visceral lesions when the fungus gains entry into the bloodstream.

• Disseminated candidiasis is a life-threatening infection that must be treated aggressively.

• For poorly understood reasons, local candidal lesions may appear in the vagina, not only in predisposed persons but also in apparently healthy young women, particularly ones who are pregnant or using oral contraceptives or using broad-spectrum antibiotics.

Histologically, the pseudomembrane is composed of a myriad of fungal organisms superficially attached to the underlying mucosa.

In milder infections there is minimal ulceration, but in severe cases the entire mucosa may be denuded.

The fungi can be identified within these pseudomembranes as chains of tubular cells producing pseudohyphae from which bud ovoid yeast forms, typically 2 to 4 μm in greatest diameter.

Acquired Immunodeficiency Syndrome (AIDS)

• AIDS and less advanced forms of human immunodeficiency virus (HIV) infection are often associated with lesions in the oral cavity.

• They may take the form of candidiasis, herpetic vesicles, or some other microbial infection (producing gingivitis or glossitis).

• particular interest are the intraoral lesions of Kaposi sarcoma and hairy leukoplakia.

• Kaposi sarcoma, is a multifocal, systemic disease that eventually evolves into highly vascular tumor nodules.

Although Kaposi sarcoma may occur in the absence of HIV infection, it affects about 25% of AIDS patients, particularly homosexual or bisexual males.

More than 50% of those afflicted develop intraoral purpuric discolorations, raised,

nodular masses.

The peri-venular infiltrate of Kaposi sarcoma shows a mixture of spindle cells, inflammatory cells

KS lesions contain tumor cells with a characteristic abnormal elongated shape

The tumor is highly vascular, containing abnormally dense and irregular blood vessels, which leak red blood cells into the surrounding tissue and give the tumor its dark color.

Hairy leukoplakia is an uncommon lesion seen

virtually only in persons infected with HIV.

It constitutes white confluent patches, anywhere on the oral mucosa, that have a "hairy" or corrugated surface resulting from marked epithelial thickening.

It is caused by Epstein-Barr virus infection of epithelial cells. Occasionally, the development of hairy leukoplakia calls.

LEUKOPLAKIA As generally used, the term leukoplakia refers to a

whitish, well-defined mucosal patch or plaque caused by epidermal thickening or

hyperkeratosis.

The term is not applied to other white lesions, such as those caused by candidiasis, lichen planus, or many other disorders.

The plaques are more frequent among older men and are most often on the vermilion border of the lower lip, buccal mucosa, and the hard and soft palates and less frequently on the floor of the mouth and other intraoral sites.

They appear as localized, sometimes multifocal or even diffuse, smooth or roughened, leathery, white, discrete areas of mucosal thickening.

On microscopic evaluation they vary from banal hyperkeratosis without underlying epithelial dysplasia to mild to severe dysplasia bordering on carcinoma in situ.

Histologic evaluation, lesions are of unknown cause except that there is a strong association with the use of tobacco, particularly pipe smoking and smokeless tobacco (pouches, snuff, chewing).

Less strongly implicated are chronic friction, as from ill-fitting dentures or jagged teeth; alcohol abuse; and irritant foods.

More recently, human papillomavirus antigen has been identified in some tobacco-related lesions, raising the possibility that the virus and tobacco act in concert in the induction of these lesions.

Oral leukoplakia is an important finding because 3% to 6% (depending somewhat on location) undergo transformation to squamous cell carcinoma.

The transformation rate is greatest with lip and tongue lesions and lowest with those on the floor of the mouth.

Those lesions that display significant dysplasia on microscopic examination have a greater probability of cancerous transformation.

A, Leukoplakia of the tongue in a smoker. Microscopically, this lesion showed severe dysplasia with transformation to squamous cell carcinoma in the posterior elevated portion (arrow)..

Cont………

The treatment of leukoplakia mainly involves avoidance of predisposing factors — tobacco cessation, smoking, quitting betel chewing, abstinence from alcohol — and avoidance of chronic irritants, e.g., the sharp edges of teeth.

NeoplasmSquamous cell carcinoma (SCC)

Most common Irregular ulcers with raised margins May be exophytic, infiltrative or verrucoid Mimic benign lesions grossly

CANCERS OF THE ORAL CAVITY AND TONGUE The overwhelming preponderance of oral cavity

cancers are squamous cell carcinomas

Although they represent only about 3% of all cancers in the United States, they are disproportionately important. Almost all are readily accessible to biopsy and early identification.

These cancers tend to occur later in life and are rare before age 40.

The various influences thought to be important in development of these cancers are summarized in Table.

RISK FACTORS FOR ORAL CANCER

Factor Comments

Leukoplakia, erythroplasia

May including tobacco, long-term alcohol use and other chronic irritants

Tobacco use Best-established influence, particularly pipe smoking and smokeless tobacco

Human papillomavirus types 16, 18, and 33

Identified by molecular probes in one half to one third of cases; early involvement in carcinogenesis is hypothesized

Alcohol abuse Less strong influence than tobacco

Protracted irritation Weakly associated

MORPHOLOGY• The three predominant sites of origin of oral cavity

carcinomas are • (1) vermilion border of the lateral margins of the lower lip,

• (2) floor of the mouth,

• and (3) lateral borders of the mobile tongue.

• Early lesions appear as pearly white to gray, circumscribed thickenings of the mucosa closely resembling leukoplakic patches.

• They then may grow in an exophytic fashion to produce readily visible and palpable nodular and eventually fungating lesions,

• or they may assume an endophytic, invasive pattern with central necrosis to create a cancerous ulcer.

The squamous cell carcinomas are usually moderately to well-differentiated keratinizing tumors.

Before the lesions become advanced it may be possible to identify epithelial atypia, dysplasia, or carcinoma in situ in the margins, suggesting origin from leukoplakia or erythroplasia.

In about 50% of cases of tongue cancer, and in more than 60% of those with cancer of the floor of the mouth.

Clinical Features These lesions may cause local

pain or difficulty in chewing, but many are relatively asymptomatic and so the lesion (very familiar to the exploring tongue) is ignored.

The overall 5-year survival rates after surgery and adjuvant radiation and chemotherapy are about 40% for cancers of the base of the tongue, pharynx, and floor of the mouth without lymph node metastasis, compared with under 20% for those with lymph node metastasis.

When these cancers are discovered at an early stage, 5-year survival can exceed 90%.

Oral squamous cell carcinoma. Invasive tumor islands show formation of keratin pearls.

Squamous cell carcinoma

carcinoma

S=normal s c.

Squamous cell carcinoma (arrow) invasion to the skeletal muscle (arrowhead). The carcinoma cells have enlarged, hyperchromatic and pleomorphic


Squamous cell carcinoma (arrow) invasion to the skeletal muscle (M).

Necrotizing Sialometaplasia Inflammatory condition Ischemia to minor salivary glandsDeep ulcers of the hard palateResolves in 6 weeks

Sialometaplasia

Generalized: broad classification encompassing a wide variety of causative

agents or conditions

Contact stomatitisRadiation mucositisCancer chemotherapy

Dermatologic Disorders: cutaneous and oral manifestations

Erythema multiformeLichen planusBenign mucous membrane pemphigoidBullous pemphigoidPemphigus vulgaris

Dermatologic DisordersErythema multiforme

Rapidly progressive Antigen-antibody complex deposition in

vessels of the dermis Target lesions of the skin Diffuse ulceration, crusting of lips, tongue,

buccal mucosa Self-limited, heal without scarring

Dermatologic DisordersErythema multiforme

Dermatologic DisordersLichen planus

Chronic disease of skin and mucous membranes

Destruction of basal cell layer by activated lymphocytes

Reticular: fine, lacy appearance on buccal mucosa (Wickman’s striae)

Hypertrophic: resembles leukoplakia Atrophic or erosive: painful

Dermatologic DisordersLichen planus

Dermatologic Disorders Benign mucous membrane pemphigoid

Tense subepithelial bullae of skin and mucous membranes

Rupture, large erosions, heal without scarring Sloughing (Nikolsky sign)

Bullous pemphigoid Cutaneous lesions more common

Both show subepithelial clefting with dissolution of the basement membrane IgG in basement membrane

Dermatologic DisordersBenign mucous membrane pemphigoid

Dermatologic DisordersPemphigus vulgaris

Severe, potentially fatal Cause; Autoimmune response by secretion

antibodies create a reaction that cause skin cells to separate.

Intraepithelial bullae, Intraepithelial clefting and acantholysis bcz Loss of intracellular

bridges betwn cells. Nikolsky’s sign (top layers of the skin slip away

from the lower layers when slightly rubbed) Oozing or Draining skin,


suprabasal separation of the epithelial cells

intraepithelial vesicle

Lect.1.mouth cavity

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