Salivary Gland Diseases

MUCOCELE
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Common lesion due to rupture of salivary gland duct

CT swells due to collection of Mucin
Has no epithelial lining ( Mucus retention cyst contains epithelial lining )
Can have bluish or translucent color
1 to 2 mm
Common in children and young adults
Fluctuant but sometimes firm
Usually found on the lower lip ( 81% )
Present for normally a few weeks
Superficial mucocele: Variant that develops along the posterior buccal
mucosa
HISTOPATHOLOGY: Area of spilled mucin surrounded by a granulation
tissue. Inflammation includes histocytes.
TREATMENT: Most are self-limiting / Chronic = local surgical excision

RANULA
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Mucoceles that are found in the floor of the mouth

Source of mucin is from Sublingual gland ( Can be submandibular or minor
salivary glands )
Often develop into large masses and elevate tongue
Located lateral to the midline
TREATMENT: Removal of feeding sublingual gland or marsupialization

SIALOLITHIASIS
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Calcified structures that develop within the salivary duct system

Develop w/in submandibular gland ( Whartons duct near tongue )
Can form within minor salivary gland
RADIOGRAPHICALLY: Radiopaque mass/ masses
HISTOPATHOLOGICALLY:
Hard, round, and yellowish mass
Submandibular glands stones are larger than other glands
Calcified mass: Concentric lamination surrounding nidus of amorphous
debris
Duct: Exhibits squamous, oncocytic, or mucous cell metaplasia
TREATMENT:
Sialagogues = Drugs that stimulate salivary flow
Passage of stone
Large sialolithiasis should be removed surgically

SIALADENITIS

Inflammation of a salivary gland

Can be due to infectious and noninfectious causes ( Sjogrens syndrome or
Sarcoidosis )
Subdivided into :
ACUTE
CHRONIC
ACUTE: ( subacute necrotizing )
Predisposing factors
o
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o
o
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o

Sialolithiasis
Viral infection ( Mumps systemic enters through URT )
Coxsackie A & B, ECHO virus, cytomegalovirus and adenovirus
decreased flow (dehydration, post-operative, drugs)
poor oral hygiene
Due to Kuttner tumor
Stapphylococcus aureus
exacerbation of low grade chronic sialoadenitis

Clinical features
o
o
o
o
o
o
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Painful swelling
Reddened skin
Common in parotid gland ( serous ) ( bilaterally ) [ B/c parotid gland is
adjacent to molar which can have calculus and debris, causing infection ]
Other glands have mucin which has large antimicrobial activity
Edema of the cheek, Periorbital region and neck
Lesions do not ulcerate or slough necrotic tissue ( seen in necrotizing
sialometaplasia )
low grade fever and trismus
malaise
raised ESR, CRP, leucocytosis
purulent exudate from duct when massaged
HISTOPATHOLOGY:
Heavy mixed inflammatory infiltrate in duct and acini
( neutrophils, lymphocytes, histocytes, and esonophils )
Loss of acinar cells and the ones that are left are necrotized
Ducts are atrophic ( No hyperplasia or squamous metaplasia )
TREATMENT: Antibiotic therapy or surgical drainage, can be self-limiting

CHRONIC: ( Chronic sclerosing )

Clinical Features

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o
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o
o

unilateral
mild pain / swelling
can occur in minor salivary glands
duct orifice is reddened and flow decreases
may or may not have visible/palpable stone.
Parotid gland
Recurrent painful swellings as well duct obstruction
Submandibular gland
Usually secondary to sialolithiasis or stricture
RADIOGRAPHICALLY:
Stensens duct ( From parotid gland to next to UMax 2 nd molar ) shows
sausaging pattern due to scar formation
HISTOPATHOLOGY:
Scattered infiltration of salivary parenchyma by lymphocytes and
plasma cells
Atrophy of acini
Ductal dilation
Fibrosis
TREATMENT:
Conservative therapy to surgical intervention
Antibiotics, Analgesics, Sialagogues, and glandular massage

SARCOIDOSIS
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Disease involving abnormal collections of inflammatory cells (granulomas)

that can form as nodules in multiple organs
Common in parotid gland
20 40 years
Slow enlargement of gland
Xerostomia
Associated with patients who have Heerfordts Syndrome ( uveoparotid
fever )
Parotid enlargement
Anterior uveitis of eye
Facial paralysis
Fever
Self-limiting

CAT SCRATCH DISEASE

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Subacute regional lymphadenitis

benign infectious disease caused by bacterium ( Rochalimaea henselae )
Parotid gland becomes enlarged
Self-limiting

SJOGREN SYNDROME
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Chronic, systemic autoimmune disorder that involves the salivary and

lacrimal gland (results in xerostomia and xerophthalmia = Sicca syndrome )
Two forms:
PRIMARY SS: Sicca syndrome WITHOUT other autoimmune disorders
SECONDARY SS: Sicca syndrome WITH other autoimmune disorder
Rheumatoid Arthritis ( 15% )
SLE ( 30% )
Genetic influence
HLA-B8 & HLA-DR3 are seen in Primary form
EBV & T-cell lymphotropic virus play a pathogenic role
Middle aged adults
Female > Male
Saliva can appear frothy and difficulty in swallowing
Tongue is dry and fissured w/ atrophy of papillae
Oral mucosa is red and tender due to secondary candidiasis
Denture sore mouth & Angular cheilitis
Predisposes patient to cervical caries
Bilateral swelling ( diffuse enlargement ) of major salivary glands
Increases risk of bacterial sialadenitis
Other symptoms are dry skin, fatigue, lymphadenopathy, nasal and vaginal
mucosae
RADIOGRAPHICALLY:
Punctate sialectasia (dilatation of a salivary duct )
Lack arborization of ductal system
Demonstrates fruit-laden, branchless tree pattern
LABORATORY VALUES:
High ESR
High Ig (IgG)
Positive rheumatoid factor ( 60% of cases )
Antinuclear Antibodies ( 80% of cases )

HISTOPATHOLOGY:
Lymphocytic infiltration of salivary gland
Destruction of acinar units
Enlarged major glands present progression to lymphoepithelial lesion
w/ epimyoepithelial islands in a background lymphoid stroma
Biopsy test of minor salivary glands of lower lip
Glands present focal chronic inflammatory aggregates ( 50 or
more lymphocytes and plasma cells )
TREATMENT: Supportive by sialagogue

SIALADENOSIS (SIALOSIS)

Non-inflammatory disorder which causes salivary gland enlargement ( mostly

Parotid gland )
Associated with Endocrine disorders, nutritional conditions, and neurogenic
medications
Diabetes Mellitius
Malnutrition
Alcoholism
Bulimia
Shows marked enlargement of acinar cells
Swelling w/ or w/o pain
Usually bilateral ( sometimes unilateral )
Decreased salivary secretion may occur
RADIOGRAPHICALLY:
leafless tree pattern ( caused by compression of finer ducts by
hypertrophic acinar cells )
HISTOPATHOLOGY:
Hypertrophy of acinar cells
Nuclei are displaced to cell base
Cytoplasm is engorged w/ zymogen granules

NECROTIZING SIALOMETAPLASIA
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Destructive inflammatory condition of salivary glands can be due to ischemia

of salivary tissue
Mimics a malignant process
Predisposing factors
Traumatic injury
Dental injection
Ill-fitting dentures
URT infections
Adjacent tumors
Previous surgery

Develops in palatal salivary glands ( 75% posterior hard palate )

Unilateral ( 75% of cases )
Submandibular & Sublingual glands rarely affected
40 50 years
Males > Females
CONDITION:
A) Non-ulcerated swelling w/ pain or paresthesia
B) W/in 2 to 3 weeks necrotic tissue sloughs out
C) Leaves a craterlike ulcer ( 1 to 5 cm in diameter )
HISTOPATHOLOGY:
Acinar necrosis in early lesion
Then, squamous metaplasia of salivary ducts ( confused w/ Squamous
Cell Carcinoma or Mucoepidermoid Carcinoma )

Lobular structure of gland is still preserved

TREATMENT: Self-limiting ( 5 to 6 weeks to heal )

HIV ASSOCIATED WITH SALIVARY GLAND DISEASE

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Parotid enlargement due to

Glandular lymphadenopathy
Multiple lymphoepithelial cysts

CLASSIFICATION OF SALIVARY GLAND TUMORS

Benign Tumors:
A)
B)
C)
D)

Pleomorphic Adenoma
Oncocytoma
Warthin Tumor
Monomorphic Adenoma
Canalicular Adenoma
Basal Cell Adenoma

Malignant Tumors: ( myoepitheliomas )

A)
B)
C)
D)
E)

Mucoepidermoid Carcinoma
Acinic Cell Adenocarcinoma
Malignant Mixed Tumors
Adenoid Cystic Carcinoma
Polymorphous Low-Grade Adenocarcinoma

PLEOMORPHIC ADENOMA
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Most common benign salivary gland neoplasm characterised by neoplastic

proliferation of parenchymatous glandular cells along with myoepithelial
components
Has a variable appearance through microscope
Makes up 65% of parotid tumors ( Submandibular 50% ) ( Minor salivary
glands 40% )
Mostly occurs in superficial lobe of parotid gland ( 10% of tumors occur in
deep lobe )
Palate is the most common site for minor gland mixed tumors ( 2 nd is upper
lip )
Can cause atrophy of the mandibular ramus
Painless, slow growing, firm mass
30 60 years
Female > Male
Dumbbell shaped tumor

Bilateral pleomorphic adenomas of parotid gland develop in either a

synchronous or metachronous fashion
HISTOPATHOLOGY:
Well-circumscribed, encapsulated tumor
Incomplete encapsulation in minor salivary glands
Tumor is made up of glandular epithelium and myoepithelial cells
within a mesenchyme-like background ( varying in thickness )
Epithelial cells: nests, sheets, ducts, trabeculae
Stroma: myxoid, chrondroid, fibroid, osteoid
No true capsule
Tumor pseudopods
TREATMENT: Complete surgical excision ( Avoid enucleation and tumor spill )

ONCOCYTOMA (OXYPHILIC ADENOMA)

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Benign salivary gland tumor composed of large epithelial known as oncocytes

The swelling in oncocytes is due to to excessive accumulation of
mitochondria
1% of all salivary tumors
70 -80 years
Female > Male
Primarily in parotid gland ( superficial lobe )
On occasion bilateral
Firm, slowly growing, painless mass ( 4 cm in diameter )
On electron microscopy: Shows mitochondrial hyperplasia ( 60% of cell
volume )

GROSS:
o
o
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Encapsulated
Homogeneous, smooth
Orange/rust color

HISTOLOGY:
o
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o
o
o
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Cords of uniform cells and thin fibrous stroma

Large polyhedral cells
Distinct cell membrane
Granular, eosinophilic cytoplasm
Central, round, vesicular nucleus
TREATMENT: Surgical excision

WARTHIN TUMOR (PAPILLARY CYSTADENOMA LYMPHOMATOSUM)

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Benign neoplasm of the parotid gland ( 10% of all parotid tumors )

Polyclonal ( type of antibody ) making it more of a tumor like process
Slowly growing, painless, nodular mass
Firm or fluctuant to palpitation

Occurs near the angle of the mandible

Can occur bilaterally
60 70 years
Male > Female
GROSS:
Encapsulated
Smooth/lobulated surface
Cystic spaces of variable size, with viscous fluid, shaggy epithelium
Solid areas with white nodules representing lymphoid follicles
HISTOLOGY:
Papillary projections into cystic spaces surrounded by lymphoid stroma
Epithelium: double cell layer
o Luminal cells
o Basal cells
Stroma: mature lymphoid follicles with germinal centers

MONOMORPHIC ADENOMA
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Benign salivary glands that form more uniform histopathologic pattern

( unlike pleomorphic )
The most prominent ones are BASAL CELL ADENOMA & CANALICULAR
ADENOMA

CANALICULAR ADENOMA
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Uncommon tumor found in minor salivary gland

75 % of cases in upper lip ( 2nd most common case is buccal mucosa )
60 70 years
Female > Male
Slowly growing, firm, painless mass ( Grows up to 2 cm in size )
Can have bluish color Like Mucocele ( But Mucocele in upper lip is rare )
DIFFERENTIAL
HISTOLOGY:
Well-circumscribed
Multiple foci
Tubular structures line by columnar or cuboidal cells
Vascular stroma

BASAL CELL ADINOMA

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Benign salivary tumor of basaloid appearance ( 1-2% of all salivary tumors )

Tumor of parotid gland superficial lobe ( 75% of cases )
60 70 years
Female > Male
Slowly growing, freely movable mass ( Usually less than 3 cm )
SUBTYPES:
SOLID
o Most common
o Solid nests of tumor cells
o Uniform, hyperchromatic, round nuclei, indistinct cytoplasm
o Peripheral nuclear palisading
o Scant stroma
TRABECULAR
o Cells in elongated trabecular pattern
o Vascular stroma
TUBULAR
o Multiple duct-like structures
o Columnar cell lining
o Vascular stroma
MEMBRANOUS
o Thick eosinophilic hyaline membranes surrounding nests of
tumor cells
o jigsaw-puzzle appearance ( hereditary )

MYOEPITHELIOMAS
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Salivary gland tumors made up of myoepithelial cells

May be spindled, plasmacytoid, eithelioid or clear
TREATMENT: Simple excision
Minor salivary glands > parotid > submandibular gland
SUBTYPES:
Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Acinic cell carcinoma
Carcinoma ex-pleomorphic adenoma

MUCOEPIDERMOID CARCINOMA
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Most common salivary gland malignancy

Found mostly in the parotid gland ( 70% ) but can be found in the palate
( 18% )
30 80 years ; Peak is 50
Females > Males
Whites
Histologically classified from low grade to high grade ( High grade having a
low outcome )

Low grade tumors usually have many mucinous cells ( High grade has high
epithelial cells )
High grade tumors have
neural invasion
necrosis
intracystic component <20%
cellular anaplasia
PRESENTATION:
Low-grade: slow growing, painless mass
High-grade: rapidly enlarging, w/ or w/o pain
GROSS:
Well-circumscribed to partially encapsulated to unencapsulated
Solid tumor with cystic spaces
HISTOLOGY:
Low grade:
o Mucus cell > epidermoid cells
o Prominent cysts
o Mature cellular elements
Intermediate grade:
o Mucus = epidermoid
o Fewer and smaller cysts
o Increasing pleomorphism and mitotic figures

High grade:
o Epidermoid > mucus
o Solid tumor cell proliferation
o Mistaken for SCCA ( Do Mucin staining )
TREATMENT:
Influenced by site, stage and grade
Stage I & II = Wide local excision
Stage III & IV =
o Radical excision
o +/- neck dissection
o +/- postoperative radiation therapy

ADENOID CYSTIC CARCINOMA

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2nd most common salivary gland malignancy

Found in submandibular, sublingual, and minor salivary gland ( 60% )
Most common area is the palate
50 70 years
PRESENTATION:
Asymptomatic enlarging mass
Pain, paresthesias, facial weakness/paralysis
Characterized by slow growth, neurotropism, local recurrence, and distant
metastasis
GROSS:

Well-circumscribed
Solid, rarely with cystic spaces
Infiltrative
HISTOLOGY:
TUBULAR PATTERN:
o Layered cells forming duct-like structures
o Basophilic mucinous substance
SOLID PATTERN:
o Solid nests of cells without cystic or tubular spaces
TREATMENT:
Complete local excision
Tendency for perineural invasion: facial nerve sacrifice
Postoperative XRT
RECURRANCE = 42% ( can metastasize in the lung )
5-year survival 75% ( 20-year survival 13% )

ACINIC CELL CARCINOMA

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2nd most common salivary gland maliganancy

Mostly found in the parotid gland ( 85% ) ( Bilateral )
20 70 years ; peak at 40
Female > Male
Slow growing mass that is asymptomatic
Low grade malignancy w/ high survival rate
GROSS:
Well circumscribed
Often homogenous
HISTOLOGY:
Solid & Microcystic patterns are the most common
Small cystic spaces
Polyhedral cells
Small, dark, eccentric nuclei
Basophilic granular cytoplasm
TREATMENT:
If in superficial lobe = Lobectomy
If in deep lobe = Total parotidectomy
Sometimes facial nerve must be sacrificed
1/3 of patients have recurrences

MALIGNANT MIXED TUMORS

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The malignant counterpart to pleomorphic adenomas ( 2 to 6% of all salivary

tumors )
Divided into :

CARCINOMA EX-PLEOMORPHIC ADENOMA- Most common and

characterized by malignant transformation of epithelial component
CARCINOSARCOMA- Rare mixed tumor made up of carcinomatous and
sarcomatous elements
METASTASIZING MIXED TUMOR- Histopathologically common to
pleomorphic adenomas but the lesions metastasize

CARCINOMA EX-PLEOMORPHIC ADENOMA

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2-4% of all salivary gland neoplasms

4-6% of mixed tumors
6th-8th decades
Parotid > submandibular > palate
RISK OF MALIGNANT DEGENERATION:
1.5% in first 5 years
9.5% after 15 years
Longstanding painless mass that undergoes sudden enlargement
GROSS:
Poorly circumscribed
Infiltrative
Hemorrhage and necrosis
HISTOLOGY:
Malignant cellular change adjacent to typical pleomorphic adenoma
Carcinomatous component
o Adenocarcinoma
o Undifferentiated
TREATMENT:
Wide excision

CARCINOSARCOMA
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Extremely rare tumor

Mostly found in the parotid gland, but can be found in submandibular and
minor salivary glands
Associated w/ recurring pleomorphic adenomas
GROSS:
Poorly circumscribed
Infiltrative

Cystic areas
Hemorrhage, necrosis
Calcification
HISTOLOGY:
Biphasic appearance
Sarcomatous component
Carcinamatous component
TREATMENT: ( Avg. survival rate = 2.5 years )
Radical excision
Neck dissection
Postoperative XRT
Chemotherapy (distant metastasis to lung, liver, bone, brain)

POLYMORPHOUS LOW-GRADE ADENOCARCINOMA

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2nd most common malignancy in minor salivary glands

70 YEARS
F>M
Painless, submucosal mass
Morphologic diversity:
Solid, glandular, cribriform, ductular, tubular, trabecular, cystic
HISTOLOGY:
Isomorphic cells, indistinct borders, uniform nuclei
Peripheral Indian-file pattern
TREATMENT:
Complete excision

CLEAR CELL CARCINOMA

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Also known as glycogen-rich clear cell

Palate and parotid
60 80 years
HISTOLOGY:
Uniform, round or polygonal cells
Peripheral dark nuclei
Clear cytoplasm
TREATMENT:
Complete local excision