Download pathology of the mouth and salivary glands

PATHOLOGY OF THE MOUTH AND SALIVARY GLANDS
Lecture Objectives
At the end of the lecture, the student should be able to:
1. Outline the causes of the main inflammatory lesions of the mouth and pharynx – stomatitis,
pharyngitis and tonsillitis.
2. Discuss the pathologic features of benign and malignant epithelial tumours of the mouth.
3. Describe the premalignant epithelial lesions of the oral cavity.
4. List other/non-epithelial tumours that can involve the mouth.
5. Outline the causes of inflammation of the salivary glands (sialadenitis)
6. Name the main benign & malignant tumours of the salivary glands and discuss the pathology of each.
I.
PATHOLOGY OF THE MOUTH AND PHARYNX
1) Inflammation

Stomatitis
 This refers to generalized inflammation of the oral mucosa
 A variety of lesion types may be seen including vesicobullous lesions (VB) and ulcers (U). Some
agents e.g. Candida sp. produce characteristic lesions.
CAUSES OF STOMATITIS
Class of agent
Virus
Fungus
Bacteria
Autoimmune
Other/unknown

Example
Herpes simplex
Varicella
Coxsackie, type A
Candida albicans
Vincent’s disease
Pemphigus
Bullous pemphigoid
SLE
Erythema multiforme
Lichen planus
Aphthous stomatitis
Type of
lesion
VB/U
VB/U
VB/U
Thrush/U
U
VB
VB
U
VB
U
U
Candidiasis
 Usually attributable to infection with C. albicans but other species can be causative
 Risk factors include immunosuppression, altered oral microflora (e.g. broad-spectrum
antibiotics), denture use and endocrine disorders e.g. poorly controlled diabetes mellitus
 There are numerous manifestations of oral candidiasis and some of the main ones are outlined:
Thrush: “pseudomembranous candidiasis”—loosely adherent white pseudomembrane (fungi,
inflammatory cells, debris, fibrin and bacteria) overlies inflamed mucosa
Angular stomatitis: infection in deep grooves of the lips
Candidal leukoplakia: tightly adherent membrane—?associated with heavy cigarette smoking
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Chronic mucocutaneous candidiasis: skin, nails and other mucous membranes involved; many variants
including familial, sporadic and those assoc. with various endocrine and chronic disorders

Vincent’s disease (Acute necrotizing ulcerative gingivitis)
 Incompletely understood but factors such as emotional stress and smoking may suppress immune
system and predispose to infection by commensal organisms such as Bacteroides sp.
 Characterized by gingival necrosis, ulceration and pseudomembrane formation

Aphthous stomatitis ( Recurrent aphthous ulcers)
 Condition characterized by recurrent shallow ulcers (aphthae); may be single or multiple
 10 to 20% of individuals affected—the most common disease of the oral mucosa; women>men;
10 to 30 yr.
 Seen in healthy people; occasionally assoc. with certain diseases e.g. Crohn’s
 Cause still unknown—? Trauma/stress/food products/nutritional deficiency/hormones
 Aphthae last 1 to 3 weeks, subsequent episodes vary in frequency and the condition eventually
spontaneously disappears in most people
 Acquired immunodeficiency syndrome



Oral lesions are prominent, often early features in HIV-related diseases
Refractory candidiasis e.g. thrush is often the first manifestation
Specific oral lesion of HIV is hairy leukoplakia—bilateral, soft, white, hairy excrescences on the
lateral margins of the tongue: squamous hyperplasia that appears to be induced by EBV ? in
assoc. with Candida or HPV.
Oral Manifestations of AIDS
Secondary infections
Fungal
Bacterial
Viral
Tumours
Miscellaneous
Candidiasis
Histoplasmosis
Cryptococcosis
Increased risk of dental caries and periodontitis
Acute necrotizing ulcerative gingivitis
Mycobacterial infection
(such as M. tuberculosis, M. avium-intracellulare)
Gram-negative bacteria (such as Klebsiella pneumoniae)
Herpetic stomatitis
Cytomegalovirus
Hairy leukoplakia
Herpes zoster
HPV (condyloma acuminatum)
Kaposi’s sarcoma
Squamous cell carcinoma
Non-Hodgkin’s lymphoma
Recurrent aphthous ulcers
Delayed wound healing
Xerostomia
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 Pharyngitis
 Very common condition; seen especially in children and caused mainly by viruses
 Approx. 15 to 20% of all pharyngeal infections are caused by beta-hemolytic streptococci—
children between 5 and 15 years of age are most susceptible
 Important complications of beta-hemolytic strep pharyngitis are rheumatic fever and
poststreptococcal glomerulonephritis
 Other forms of bacterial pharyngitis include diphtheria (pharynx and tonsils covered by adherent
membrane) and gonorrhea (lesions often ulcerative)
 Noninfectious causes of pharyngitis include allergies, pollutants and smoking
 Tonsillitis
 Seen also predominantly in children and causative agents similar to pharyngitis
 The inflamed tonsils are usually covered by a yellow-white exudate
 The adenoids may also be affected and associated hyperplasia of these organs may cause
blockage of the eustachian tube and otitis media
 Inadequately treated tonsillitis may result in tonsillar ulceration and peritonsillar abscess
2) Tumours
a) Benign epithelial proliferations
 Squamous papilloma
 Most common oral neoplasm—believed to be caused by HPV
 Painless exophytic mass with warty surface, usually < 1 cm and may be single
or multiple; preferred sites are the palate, tongue, gingivae and lips
b) Premalignant lesions
 Leukoplakia
 Clinical term for a white patch occurring on the surface of a mucous membrane
 In the mouth, the term is used to include only those white patches or plaques that will not rub off,
and that are not caused by another oral disease
 Has been associated with tobacco smoking and alcohol abuse
 Most common in fifth to seventh decade; M>F
 Lesions may be localized or diffuse; vary from faintly translucent areas to thick fissured,
indurated lesions
 6% lesions will have carcinoma; additional 4% will undergo malignant transformation
 Erythroplakia (erythroplasia of Queyrat)
 Initially described as syphilitic lesion of the glans penis—then recognized to also occur on vulva
and oral mucosa in patients who are not syphilitic
 Sixth to seventh decades; M=F
 Defined as bright red velvety plaques not due to any other condition (e.g.gingivitis, candidiasis,
hemangioma); unlike leukoplakia, almost all lesions will prove to be squamous dysplasia or
carcinoma on biopsy
c) Malignant epithelial proliferations
 Squamous cell carcinoma
 Account for majority of intraoral cancers; tobacco use and alcohol abuse implicated as causative
factors; role of viruses (e.g. HPV,EBV) being investigated
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 Predominantly affects males > 50 yr.
 Can present as mucosal ulcer, exophytic growth, endophytic growth, leukoplakia, erythroplakia
or painless lymphadenopathy
 Commonest sites of involvement are the tongue, lip and floor of mouth
 Spread primarily by local extension and lymphatic dissemination; distant sites of involvement
include lungs, bone and liver
 5year survival rates are 75% for localized disease, 41% for regional cases and18% for cases with
distant metastases
d) Nonepithelial tumours and tumour-like lesions
 Cysts of the gingiva, mucosa and jaw
 Benign soft tissue lesions (e.g. pyogenic granuloma, fibroma, schwannoma)
 Malignant soft tissue lesions (e.g. rhabdomyosarcoma)
 Lymphomas
 Odontogenic tumors (e.g. ameloblastoma)
 Tumours of the jaw (e.g. fibrous dysplasia, giant cell tumours, bone and cartilaginous
tumours)
II. PATHOLOGY OF THE SALIVARY GLANDS
1) Obstructive Disorders
 Mucocele
 Most common of the obstructive disorders; results from trauma to minor salivary glands with
extravasation and pooling of mucus in surrounding tissues
 Seen mainly in young persons; the lips are the favoured site
 Usually appear as small, fluctuant masses—large mucoceles of the floor of the
mouth are known as ranulas; these may extend into the neck
 Sialolithiasis
 This is the formation of stones (calculi) in the ducts of salivary glands
 The stones result from the calcification of an intraluminal nidus e.g. dried
secretions or cellular debris—they are composed mainly of calcium phosphate
 Inflammation of the salivary duct and stasis of saliva have been suggested as
predisposing factors—the submandibular duct is the most common site
 Peak incidence in the fourth and fifth decades
 The stones vary in size, surface texture and colour
 Recurrent infection of affected glands (secondary to obstruction) is common
2) Inflammation (Sialadenitis)
 Can be caused mechanical, physical, infectious and immunologic factors:
 Mechanical
 Mechanical obstruction of salivary ducts can be intraluminal (e.g. stones) or
extraluminal (e.g. tumours)
 It leads to chronic and recurrent sialadenitis that can result in partial or
complete destruction of the affected gland
 Physical
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 Physical causes of sialadenitis include radiation e.g. administered during
treatment of head and neck cancers
 Initial acute inflammation is followed by chronic sialadenitis and fibrosis

Infectious
 Acute suppurative sialadenitis
 Usually caused by Staphylococcus aureus and group A streptococci that enter salivary ducts
from the oral cavity: reduced or absent salivation thought to predispose
 Ductal epithelium and acini are destroyed by invading inflammatory cells and microabscesses
may form
Viral sialadenitis
 Several viruses can cause sialadenitis including paramyxovirus (the mumps virus),
coxsackieviruses A and B, influenza viruses and cytomegalovirus—of these mumps is the
most common to involve the glands

 HIV-associated cysts of the parotid
 HIV infection can cause lymphadenopathy of intraparotid lymph nodes
 There is marked lymphoid hyperplasia which can be accompanied by the formation of keratinfilled cysts (salivary duct epithelium undergoes metaplastic change)
 Unilateral or bilateral enlargement of the parotids can result
 Tuberculosis
 Tuberculosis may involve intraparotid and paraparotid lymph nodes; infection of these nodes
may originate from a tuberculous focus in the mouth or pharynx, or result from dissemination of
pulmonary TB
 Can present as painless mass/masses mimicking a tumour
 Histologic examination will reveal the typical caseating granulomas and the findings can be
confirmed with cultures and special stains

Immunologic
 Sjogren’s syndrome
 Autoimmune disease characterized by the progressive lymphocytic infiltration and destruction of
exocrine glands, particularly the salivary and lacrimal glands
 Clinical hallmarks are keratoconjunctivitis sicca, xerostomia, and rheumatoid arthritis; may also
be assoc. with other autoimmune disesases e.g. SLE
 90% patients are female; average age at diagnosis is 50 yr.
 Firm, diffuse, painless enlargement of the salivary glands, which is usually but not always
bilateral, is the typical presentation
 Histologic hallmark is a lymphocytic sialadenitis—lymphoid follicles may be presentThese
patients are at increased risk for non-Hodgkins lymphoma
3) Benign Tumours
 Pleomorphic Adenoma (Benign mixed tumour)
 Most common salivary gland tumour overall
 Accounts for 60 – 70% of parotid tumours, 40 – 60% of submandibular tumours, and 40 – 70% of
minor salivary gland tumours
 Peak incidence between 30 and 50 years; female to male ratio 3:1
 Slowly-growing painless, firm masses—in the parotid, most occur in the superficial lobe
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 A variety of growth patterns may be seen histologically—the basic components are epithelium,
myoepithelium and stroma .
 Recurrence may occur if the tumour is inadequately excised.
 Warthin’s tumour (Papillary cystadenoma lymphomatosum)
 Slow-growing benign tumour that arises almost exclusively in the parotid
 5 – 6% of parotid tumours; peak incidence 40 – 70 years; male to female ratio is 5:1.
 It is proposed that the tumour develops from parotid ductal epithelium present in lymph nodes
within the gland.
 Most tumours measure 2-3 cm at diagnosis; tumours are bilateral in 7% of patients
 The histology is distinctive and pathognomonic—epithelial-lined cystic spaces showing papillary
projections are present in a lymphoid stroma.
 As with pleomorphic adenomas, recurrence may occur if the tumour is incompletely removed.
4) Malignant Tumours
 Malignant salivary gland tumours are less common than benign ones; ratio of benign to malignant
approximately 4:1
 The most common tumours are mucoepidermoid carcinoma, adenoid cystic carcinoma, acinic cell
carcinoma and malignant mixed tumours.
 Mucoepidermoid carcinoma
 Most common malignant salivary gland tumour; accounts for 2-10% of major salivary gland
tumours and 10-40% of minor salivary gland tumours
 Most common in 35-65 year age group; however, it can affect children and adolescents
 They are slowly growing firm masses that are often clinically indistinguishable from the more
common pleomorphic adenoma, and range in size from 1-4 cm.
 Histologically these tumours are composed of epidermoid cells, mucus-secreting cells and
intermediate cells; classified as low, intermediate and high-grade
 The histologic grade is directly related to prognosis—survival rate in patients with low-grade
tumours is 90-100%; intermediate and high-grade tumours tend to show local invasion,
recurrence, and metastases, with survival rates of 40-60%.
 Adenoid Cystic Carcinoma
 Account for 3-10% of salivary gland tumours— more common in minor salivary glands
 Twenty-five percent arise in major salivary glands, most commonly the submandibular
 May arise at any age, but occur most frequently in the 4th to 6th decades
 Patients with tumours in the major glands commonly present with a painful mass. Those in the
minor glands can also produce respiratory obstruction
 Usually form well-defined masses, but histologically are seen to infiltrate surrounding tissues
 Perineural invasion is characteristic of this neoplasm, and this feature seems to account for the
poor long-term outcome in patients with this tumour.
 Metastasis can occur to cervical lymph nodes or distant sites e.g. lung, bone, liver, brain
 5-year survival rates as high as 70% have been reported, but rate declines to 5-15% at 20 years.
 Acinic Cell Carcinoma
 Relatively uncommon tumour; accounts for 2-3% of salivary gland tumours.
 Most often involves the parotid; most common malignant tumour involving >one salivary gland
 Most common in the 5th decade
 Range in size from 2-4 cm; most are solid, though cystic change can occur.
 These carcinomas are regarded as low-grade tumours—regional metastasis occurs in 5-10% of
patients, but distant metastasis is rare. Five and 10-year survival rates have been reported as 82%
and 68% respectively
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NB. The following link can provide you with additional information and images for this topic:
http://www.usc.edu/hsc/dental/opfs/index.html
SESHIRLEY/Oct 2005