pathology of the gastrointestinal tract

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PATHOLOGY OF THE ORAL CAVITY & SALIVARY GLAND Professor Dr . Nafea Sami ,MRC-Path Department of Pathology - 4 th Stage Al Anbar medical college 2020-2021

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PATHOLOGY OF THE ORAL

CAVITY & SALIVARY GLAND

Professor Dr . Nafea Sami ,MRC-Path

Department of Pathology - 4th Stage

Al –Anbar medical college 2020-2021

OFTHE ORAL CAVITYANATOMY & HISTOLOGY Anatomy

Orifice to digestive & respiratory tracts

Lips, buccal mucosa, tongue, soft & hard palate

Teeth & periodontal tissue.

Histology

Lined by nonkeratinized stratified squamous epithelium

Minor salivary glands & sebaceous glands in lips & buccal mucosa

Lymphoid tissue .

DISEASE OF ORAL CAVITY :

Congenital anomalies, e.g. cleft lip & cleft palate, macroglossia, branchial cleft

cysts

Inflammations: Aphthous ulcers, Herpes stomatitis, Candidiasis ...

Pre-malignant lesions: leukoplakia, erythroplasia

Tumors: Squamous cell carcinoma

Salivary gland inflammations

Salivary gland tumors

ULCERATIVE & INFLAMMATORY LESIONS OF THE ORAL CAVITY‏‏

(CANKER SORES) APHTHOUS ULCERS

Extremely common, up to 40% of population.

Single or multiple shallow fibrin & exudates-coated painful ulcers with erythematous rim of oral mucosa, usually <1 cm, may coalesce together to be larger .

The etiology Unknown (?viruses, hypersensitivity).

Triggered by stress, fever, menstruation, pregnancy, certain foods; may be familial .

May be associated with inflammatory bowel disease & Behcet syndrome.

Self limiting in a few weeks, may recurrent in same or different location in oral cavity.

ULCERATIVE & INFLAMMATORY LESIONS OF THE ORAL CAVITY‏‏

HERPETIC STOMATITIS HSV I>>II; person to person transmission ( Kissing ).

After primary infection it is usually asymptomatic but virus will persist in perioral ganglia(triageminal ) in dormant state

Reactivation: fever, sun or cold exposure, URTI, ..

Herpes labialis: cold sores or fever blisters

Vesicular lesion, edema, degeneration of epidermis

Tzanck test: diagnostic test for HSV (intranuclear inclusions & giant cells) in smear of blister fluid .

In immunocompromised: virulent dissiminated infection: gingivostomatitis, encephalitis , keratoconjuctivitis...

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ULCERATIVE & INFLAMMATORY LESIONS OF THE ORAL CAVITY ‏

FUNGAL INFECTIONS Candida albicans is part of normal flora (30-40%)

Oral candidiasis (moniliasis, thrush): common in association with other medical disorders ( Comorbidity) .

Diabetes mellitus

Anemia

Antibiotic or glucocorticoid Rx

Immunodeficiencies & debilitating diseases

Soft white cheese-like plaques any where in oral cavity.

Pseudomembrane ( composed of myriad of fungi ) : may scrapped off to reveals underlying erythematous inflamed base .

Minimal- marked ulceration with inflammatory exudate and fungal microorganisms (pseudohyphae)

In vulnerable patients, disease may spread .

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ULCERATIVE & INFLAMMAT ORY LESIONS OF THE ORAL CAVITY‏‏

ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)

HIV infection is associated with different lesions in the oral cavity

Candidiasis

Herpetic vesicles

Other oppurtunistic infections

Kaposi’s sarcoma: multifocal vascular tumor, present in 25% of AIDS patients; related to HSV8.

Hairy leukoplakia: white patches with hairy surface:

Caused by EBV

Rare, but seen mainly in AIDS

The patches may look hairy

Histology shows acanthosis, hyperkeratosis

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PRE-MALIGNANT LESIONS OF THE ORAL CAVITY

LEUKOPLAKIA A clinical term used to describe a whitish well- defined

mucosal patch or plaque caused by epidermal thickening or

hyperkeratosis .

C/P :Older men; associated with tobacco, chronic friction

(dentures), alcohol & irritant foods; HPV link.

Microscopically, they vary from hyperkeratosis without

dysplasia to mild to severe dysplasia or CIS.

Only histologic examination distinguishes these changes (

impossible to distinguish on visual inspection ).

3-6% transform into squamous cell carcinoma

PRE-MALIGNANT LESIONS OF THE ORAL CAVITY

ERYTHROPLAKIA

Red velvety areas which may remain at level with or slightly depressed in relation to surrounding mucosa

Have greater tendency for epithelial cell atypia and marked dysplasia than leukoplakia.

M/E :Hyperkeratosis is less frequent; red color is due to intense inflammation and vascular congestion

Higher risk (50%) of malignant transformation (the risk corresponds to the degree of atypia)

Erythroleukoplakia: speckled leukoplakia; mixture of erythroplasia and leukoplakia

SQUAMOUS CELL CARCINOMA

Represent 90% of oral cavity malignancies (3% of all malignant

tumors); M>F

Site : Lip > ant. floor of mouth > tongue >palate .

Etiology: Smoking, smokeless tobacco, protracted irritation (e.g.

dentures), chronic dental & oral infections, sunlight, heat, alcohol,

atrophy, HPV.

Gross appearance :Plaque, mucosal thickening or ulcer.

M/E :Invasive &/or in situ carcinoma; well differentiated to

undifferentiated.

Spread to local drained LN (submandibular, high jugular…)

Prognosis: depends on location (e.g. lip), grade, stage.

Mortality :50% lead to death in 5 years ;overall 5 YS without L.N

mets is 40% after chemo & radio ;and 20% with L.N mets

DISEASES OF THESALIVARY GLANDS

Inflammation Viral sialadenitis

Bacterial sialadenitis

Autoimmune sialadenitis

Sialolithiasis

Tumors Benign

Pleomorhpic adnoma (mixed tumor)

Warthin’s tumor

Malignant Carcinoma ex-pleomorphic adenoma

Mucoepidermoid carcinoma

Adenoid cystic carcinoma

Mickulicz’s syndrome

VIRAL SIALADENITIS

Most common cause is mumps, which usually affects the parotid gland (epidemic parotitis) .

70% bilateral parotid; 20% unilateral; 10% others .

Mumps is an acute contagious childhood disease .

Pathogen :Paramyxovirus, acquired by respiratory droplets.

Usually self limited, but may lead to complications, which are commoner in adults:

Pancreatitis

Orchitis: usually unilateral; rarely leads to infertility

CNS inflammation: rare but serious

AUTOIMMUNE SIALADENITIS

Sjogren’s syndrome: Inflammation of salivary glands &

mucus-secreting salivary glands of oral mucosa (resulting in

dry mouth or xerostomia) and lacrimal glands (resulting in

dry eyes or keratoconjunctivitis sicca)

90% are females; Parotid enlargement in 50% (bilateral ).

May be primary or secondary (60%) to other autoimmune

disease (RA, SLE, polymyositis ..)

M/E : Lymphocytic infiltration & fibrosis.

DX:RF, ANAs +/-; anti-ribonucleoprotein SS-A & B Abs

High risk to develop lymphomas

SIALOLITHIASIS & NONSPECIFIC SIALADENITIS

Etiology :Bacterial & usually chronic course.

Secondary to ductal obstruction by stones (sialolithiasis) in major

excretory duct .

Usually unilateral .

Pathogenesis: impacted food debris & edema around orifice

following injury and secondary bacterial invasion .

M/E :Ductal dilatation, periductal inflammation, & suppuration

Predisposing factors: Hx of major surgery, dehydration, long-

term phenothiazines Rx.

SALIVERAY GLANDS TUMORS

Relatively uncommon; 2% of tumors in humans.

80% of tumors occur in parotid gland .

Equal M:F ratio; all ages [6th - 7th decade]

Most of these neoplasms are benign: 70-80% of parotid tumors and only 50% of submandibular tumors .

C/P: mass at angle of jaw

Wide histologic variations:

Benign: Pleomorphic adenoma, Warthin’s tumor

Malignant: Carcinoma ex-pleomorphic adenoma, Mucoepidermoid carcinoma .

Adenoid cystic carcinoma: The most aggressive & locally invasive salivary gland carcinoma.

PLEOMORPHIC ADENOMA aka: benign mixed tumor: Most common tumor (65-80%) of the

salivary glands.

C/P: Slowly growing painless well-demarcated, encapsulated swelling, mostly arising from superficial lobe of parotid gland.

Pathology: heterogeneous histology with epithelial elements, myxoid stroma, often containing chondroid foci or, rarely, bone.

Despite its capsulation microscopic examination reveals multiple site where tumor penetrate the capsule .

Adequate margins of surgical resection are necessary to prevent recurrence.

Prognosis: Recurrence after surgery: 10%.

Malignant transformation: 15% in parotid, 40% in submandibular gland.

S TUMOR’WARTHIN

aka: Papillary cystadenoma lymphomatosum

Benign slowly growing tumors

5-10% of all parotid tumors; extremely rare in other salivary glands

Pathology: Composed of cystic spaces lined by tall columnar cells overlying abundant lymphoid tissue

Histogenesis: vestigial embryonic remnants of branchial cleft origin?&also :thought to represent hetrotopic salivary tissue trapped within a regional lymph node during embryogenesis .

Prognosis : rare malignant transformation .

Rx: cured by surgical excision .