The Salivary Glands diseases
Clinical Anatomy of the Salivary
Glands
Minor salivary glands
Use of saliva as diagnostic fluid
• Change in sal composition and flow rate
• Sialadenitis –Na &Cl secretion increases .
• Sjol gren syndrome –increased Na Cl cons
,decreased phosphate and IgA is increased.
• rate of flow is reduced .
• Cirrhosis liver Ca, K, of protein ,and amylase
concentration are increased rate of saliva is
also increased.
Cont
• Xerostomia –flow rare decreased
• Sialorrhoea Flow rate increased.
• Salivary IgA is higher in subject with more
dental caries.
• Cystic fibrosis causes decreased secretion
with marked increased in salivary Ca from sub
lingual ,sub mental and minor salivary glands .
• Ca and Phosphrous conc in saliva is raised in
hyperparathyrodism.
Reactive lesions
• Mucocele is a clinical term that
includes
mucus
extravasation
phenomenon and mucus retention
cyst.
Mucocele
Etiology
Extravasation type
• Physical-traumatic injury to minor gland
excretory duct
• Mucus extravasation into periductal soft
tissue produces a local inflammatory
response and granulation tissue
“encapsulation.”
Clinical Presentation
Lower lip most common site; also buccal mucosa,
anterior ventral tongue
Painless bluish hue when mucin is near surface
Often waxes and wanes in size
Microscopic Findings
Mucus pool surrounded by granulation tissue
Macrophage and neutrophil response to free
mucin
Focal chronic sialadenitis
Diagnosis
• Presentation
• Microscopic findings
Differential Diagnosis
•
•
•
•
Hemangioma
Pyogenic granuloma
Salivary neoplasm
Connective tissue neoplasm
Treatment
• Excision with associated local minor salivary
glands
Prognosis
• Occasional recurrence
Mucus Retention Cyst
Etiology
• Represents dilatation of salivary excretory
duct due to obstruction
• Duct obstruction may be due to a mucous
plug or sialolith formation
Clinical Presentation
• Major or minor salivary glands affected in
adulthood
• Asymptomatic, soft mucosal swelling
• Can occur at any intraoral minor salivary
gland site, especially upper lip
Microscopic Findings
 Thin, dilated, epithelial-lined salivary excretory duct
 Lining is cuboidal to columnar with occasional mucusproducing cells present
 Adjacent salivary gland lobules minimally altered but may
show obstructive inflammatory changes
Diagnosis
 Microscopic findings
Differential Diagnosis
 Extravasational mucocele
 Salivary gland neoplasm, especially mucoepidermoid
carcinoma
Treatment
• Excision of cyst with adjacent gland(s)
Prognosis
• Recurrence is rare.
Necrotizing Sialometaplasia
Etiology
• Local ischemic injury of salivary gland lobules
• May be preceded by trauma or local
anesthetic injury, or it may appear
spontaneously
Clinical Presentation
• Both major and minor salivary glands can be
affected.
• Hard palate most common site, usually
unilateral
• Initially a painful to dysesthetic submucosal
swelling
• Ultimately, a central necrotic crater develops.
• May extend to and involve deep soft tissue and
palatal bone
Microscopic Findings
• Salivary gland inflammation and lobular
necrosis (necrosis is not always demonstrable
on biopsy)
• Ductal squamous metaplasia (bland cytology)
• Lobular architecture of salivary glands
persists
Diagnosis
• Microscopic findings
Differential Diagnosis
• Salivary gland neoplasm
• Squamous cell carcinoma
• Granulomatous disease
Treatment
• Follow-up only
Prognosis
• Excellent
Ranula
Etiology
• Obstruction of the sublingual (usually) or
submandibular salivary gland by a sialolith or
by trauma
• Secondary to obstruction, extravasation of
saliva into the soft tissue of the floor of the
mouth
Clinical Presentation
 Unilateral, fluctuant, soft tissue mass on the
floor of the mouth
 Usually has a bluish, slightly translucent quality
 When
above
the
mylohyoid
muscle,
presentation is intraoral.
 If extravasation extends below the mylohyoid
muscle, a plunging ranula forms.
 Occlusal radiographs may demonstrate a
suspected sialolith.
Clinical picture
Plunging ranula
• An unusual clinical variant, the plunging
or cervical ranula, occurs when the
spilled mucin dissects through the
mylohyoid muscle and produces swelling
within the neck.
Diagnosis
Diagnosis
• Demonstration of sialolith
• Soft tissue imaging (T2-weighted magnetic
resonance image)
• Aspiration of mucinous salivary fluid
• Excised tissue with granulation tissue lining
around mucin pool
Differential Diagnosis
•
•
•
•
•
Dermoid cyst
Salivary gland tumor
Soft tissue tumor
Cystic hygroma
Thymic cyst
Treatment
Treatment
• Marsupialization as an initial procedure
• Excision of the involved gland (extravasation
type)
• Sialolithectomy (in obstructive type)
Prognosis
• No recurrence with sialadenectomy
• Recurrence risk with sialolithectomy secondary
to duct scarring or reformation of stone
Sialolithiasis
Etiology
Sialoliths are calcified structures that develop within
the salivary ductal system. They are believed to arise
from deposition of calcium salts around a nidus of
debris within the duct lumen. This debris may include
inspissated mucus, bacteria, ductal epithelial cells, or
foreign bodies.
The cause of sialoliths is unclear, but their formation
can be promoted by chronic sialadenitis and partial
obstruction. Their development is not related to any
systemic derangement in calcium and phosphorus
metabolism.
•
Salivary obstruction from stones, mucous plugs,
and mucous extravasation phenomenon.
Clinical Presentation
Clinical Presentation
• Sialolithiasis can form in all of the salivary glands,
including minor salivary glands, but the gland that
most commonly produces such stones is the
submandibular gland.
• The so‐called stones that form in the parotid duct
system are rarely calcified and are actually mucous
plugs that do not appear on radiographs.
• Stones that form in the submandibular duct system
are almost always radiopaque because they are
composed of calcium carbonate and calcium
phosphate.
C/F
 They can occur along any part of the duct and are most
frequent at anatomic bends.
 In the submandibular duct, stones are often found at the
duct's bend around the posterior edge of the mylohyoid
muscle.
 When sialoliths form, they will obstruct the duct either
partially or completely. Therefore, individuals present with
a painful swelling of the gland and usually with signs of
secondary infection, including a suppurative exudate from
the duct, fever, and mild to moderate leukocytosis .
 Individuals will report an increase in pain and swelling
upon eating. The gland will be palpably firm and anywhere
from mildly tender to very painful.
ClinicaI presentation
Diagnosis
Diagnosis
• CT scan with 2‐ to 3‐mm cuts to identify the
location of the stone.
• Most obstructed submandibular glands will
have both inflammation and fibrosis in a
homogeneous pattern throughout the gland.
Differential Diagnosis
• Calcified lymph nodes from previously
resolved tuberculosis
• Phleboliths (particularly if an old cavernous
hemangioma were present)
• Tonsoliths
• Calcifications of the carotid bifurcation.
Treatment
Treatment
• Stones that are accessible in the floor of the
mouth are removed via a direct approach, and
the damaged duct is sutured to the mucosa of
the floor of the mouth (sialodochoplasty).
• Parotid stones usually do not produce a
long‐term clinical problem. Most are passed with
parotid flow, and a few require removal from the
duct with either a repair or duct transposition.
Prognosis
Prognosis
• If the sialolith has been present for a short
time, the gland may recover after sialolith
removal.
• If the sialolith is of long standing, the gland
may harbor irreversible inflammation and
fibrosis, so that it cannot recover even if the
sialolith is removed.
Sialorrhea (Sialosis)
Etiology
• Varied; may include idiopathic paroxysmal
sialorrhea, parkinsonism, stomatitis (acute),
newly inserted oral appliances, expectorants,
neostigmine, and others
Clinical Presentation
Clinical Presentation
• Excess saliva resulting in drooling
• Angular cheilosis
• Diffuse parotid/submandibular salivary gland
enlargement
Clinical presentation
Diagnosis
Diagnosis
• Direct observation and analysis of history
• Flow-rate measurement
Treatment
Treatment
• Scopolamine
• If related to medication use, an alternate
medication should be chosen, if possible.
Prognosis
• Guarded/indeterminate
Adenomatoid hyperplasia
Etiology
• It is a nonneoplastic enlargement of the
minor salivary glands of the hard palate.
• The cause is unknown, although there is some
evidence to suggest that trauma plays a role.
Clinical Presentation
Clinical Presentation
The palate is the chief site of involvement of this
salivary gland hyperplasia.
There is a male predominance, and age ranges
from 24 to 63 years.
The clinical presentation is a unilateral swelling
of the hard and/or soft palate.
This lesion is asymptomatic, broad based, and
covered with intact mucosa of normal color and
quality.
Differential Diagnosis
Differential Diagnosis
• Salivary neoplasms
• Lymphoma
• Extension of nasopharyngeal or sinonasal
disease into the oral cavity.
Treatment
Treatment
• Subsequent to identification by means of an
incisional biopsy, no treatment is necessary,
given the purely benign nature of this
process.
Prognosis
• There is no neoplastic potential.
Sjögren’s Syndrome
Etiology
 An autoimmune disease resulting in exocrine gland
dysfunction secondary to mononuclear cell infiltration
 Increased prevalence of human leukocyte antigen DR/DQ
alleles
 Autoantibody production against nuclear antigens SS-A
and SS-B
 No specific agent identified; postulations include the
following:
 Potential role for viruses/retroviruses as cofactors
 Possible role of cytokine and hormonal influence on signal
transduction and secretion
Clinical Presentation
Clinical Presentation
 Decrease in exocrine gland function
 Xerostomia
 Xerophthalmia/keratoconjunctivitis sicca
 Salivary and lacrimal gland enlargement (one-third of cases)
 Secondary effects of exocrine dysfunction are as follows:
 Dental caries
 Oral candidiasis
 Ocular/corneal discomfort
 Primary form: exocrine dysfunction dominates
 Secondary form: exocrine dysfunction; other associated autoimmune
conditions—usually rheumatoid arthritis, less often lupus
erythematosus
Sialography
Diagnosis
Diagnosis
• Demonstration of objective xerostomia and
xerophthalmia
• Serologic demonstration of associated SS-A
or SS-B antibodies
• Correlation of clinical and serologic findings
with
labial
salivary
gland
biopsy;
demonstration of presence of periductal
lymphocytic sialadenitis
Differential Diagnosis
Differential Diagnosis (Xerostomia/Parotid Gland
Swelling)
• • Sarcoidosis
• Depression
• • HIV- associated
• Autonomic neuropathy
exocrinopathy
• Graft-versus-host disease
• • Drug side effects
• Alcoholism
• • Lymphoma
• Diabetes mellitus
• • Bulimia
Treatment
Directed at associated connective
tissue or autoimmune disease
 Systemic corticosteroids if
acute symptoms arise
 Frequent dental/ophthalmic
examinations
Treatment
 Usually symptomatic and preventative therapies are used,
including the following:
 Reduction of oral dryness
 Pilocarpine
 Cemiveline
 Oral moisturizing agents (saliva substitutes)
 Gustatory stimulation
 Ocular moisture replacement
 Saline
 Synthetic glycoprotein solutions
 Carboxymethylcellulose sodium
 Ocular punctual occlusion
Prognosis
Guarded
• High risk of lymphoma compared with risk in
those without autoimmune disease.
Salivary Gland Neoplasms
• Benign Neoplasms
• Malignant Neoplasms
• Controversial Issues
Salivary Gland Neoplasms
• Diverse histopathology
• Relatively uncommon
– 2% of head and neck neoplasms
• Distribution
– Parotid: 80% overall; 80% benign
– Submandibular: 15% overall; 50% benign
– Sublingual/Minor: 5% overall; 40% benign
Tumors of the salivary glands
•
•
•
•
•
•
•
Benign tumors.
Pleomorphic adenoma
Warthins tumors .
Basal cell adenoma
Canalicular adenoma
Oxyphilic adenoam
Myepithelial ductul adenoma
Tumors of the salivary glands
• Malignant tumors ( major and minor salivary
glands .}
• Mucoepidermoid carcinoma .
• Adenoid cystic carcinoma
• Malignant mixed tumour
• Acinic cell carcinaoma.
Pleomorphic adenoma (mixed tumor)
• More than 50% of all tumors and 90%of benign
tumors.
• Major and minor salivary glands but commonly
parotid gland
• Both epithelial and connective tissue elements so
it is mixed tumor.
• Clinical features
• Parotid and minor salivary gland tumor of
palate,lip.
Pleomorphic Adenoma
Pleomorphic adenoma (mixed tumor)
• Less frequently affects submandibular glands.
• Between 4 th to 6 th decade of life .
• More common in female.
• Small painless nodule either at the angle on
mandible of beneath the ear lobe.
• Slowly growing ,intermittent growth ,firm in
consistency ,well circumscribed encapsulated
,may show area of degenerations.
Pleomorphic adenoma
• Intra oral pleomorphic adenoma are noticed
early because of location on the palate .
• May show fixity to underlying bone but does
not invade the bone.
• D/D
• Hyperplastic lymph nodes
• Neurilemmoma of facial nerve .
Cont• Most common of all salivary gland neoplasms
•
•
•
•
70% of parotid tumors
50% of submandibular tumors
45% of minor salivary gland tumors
6% of sublingual tumors
• 4th-6th decades
• F:M = 3-4:1
Pleomorphic Adenoma
• Slow-growing, painless mass
• Parotid: 90% in superficial lobe, most in tail of
gland
• Minor salivary gland: lateral palate,
submucosal mass
• Solitary vs. synchronous/metachronous
neoplasms
Pleomorphic Adenoma
• Gross pathology
–
–
–
–
–
Smooth
Well-demarcated
Solid
Cystic changes
Myxoid stroma
Pleomorphic Adenoma
• Histology
– Mixture of epithelial,
myopeithelial and
stromal components
– Epithelial cells: nests,
sheets, ducts,
trabeculae
– Stroma: myxoid,
chrondroid, fibroid,
osteoid
– No true capsule
– Tumor pseudopods
Pleomorphic Adenoma
Pleomorphic Adenoma
• Treatment: complete surgical excision
– Parotidectomy with facial nerve preservation
– Submandibular gland excision
– Wide local excision of minor salivary gland
• Avoid enucleation and tumor spill.
• Irradiation is contra indicated. (radio resistant
Warthin’s Tumor
•
•
•
•
•
•
AKA: papillary cystadenoma lymphomatosum
6-10% of parotid neoplasms
Older, Caucasian, males
10% bilateral or multicentric
3% with associated neoplasms
Presentation: slow-growing, painless mass
Warthin’s Tumor
• Gross pathology
– Encapsulated
– Smooth/lobulated
surface
– Cystic spaces of
variable size, with
viscous fluid, shaggy
epithelium
– Solid areas with white
nodules representing
lymphoid follicles
Warthin’s Tumor
• Histology
– Papillary projections
into cystic spaces
surrounded by
lymphoid stroma
– Epithelium: double
cell layer
• Luminal cells
• Basal cells
– Stroma: mature
lymphoid follicles with
germinal centers
Warthin’s Tumor
Oncocytoma
•
•
•
•
•
•
Rare: 2.3% of benign salivary tumors
6th decade
M:F = 1:1
Parotid: 78%
Submandibular gland: 9%
Minor salivary glands: palate, buccal mucosa,
tongue
Oncocytoma
• Presentation
– Enlarging, painless mass
• Technetium-99m pertechnetate scintigraphy
– Mitochondrial hyperplasia
Oncocytoma
• Gross
– Encapsulated
– Homogeneous, smooth
– Orange/rust color
• Histology
– Cords of uniform cells and
thin fibrous stroma
– Large polyhedral cells
– Distinct cell membrane
– Granular, eosinophilic
cytoplasm
– Central, round, vesicular
nucleus
Oncocytoma
• Electron microscopy:
– Mitochondrial
hyperplasia
– 60% of cell volume
Monomorphic Adenomas
• Basal cell, canalicular, sebaceous, glycogenrich, clear cell
• Basal cell is most common: 1.8% of benign
epithelial salivary gland neoplasms
• 6th decade
• M:F = approximately 1:1
• Caucasian > African American
• Most common in parotid
Basal Cell Adenoma
• Solid
– Most common
– Solid nests of tumor
cells
– Uniform,
hyperchromatic, round
nuclei, indistinct
cytoplasm
– Peripheral nuclear
palisading
– Scant stroma
Basal Cell Adenoma
• Trabecular
– Cells in elongated
trabecular pattern
– Vascular stroma
Basal Cell Adenoma
• Tubular
– Multiple duct-like
structures
– Columnar cell lining
– Vascular stroma
Basal Cell Adenoma
• Membranous
– Thick eosinophilic
hyaline membranes
surrounding nests of
tumor cells
– “jigsaw-puzzle”
appearance
Monomorphic Adenomas
• Canalicular adenoma
– 7th decade
– F:M – 1.8:1
– Most common in minor salivary glands of the
upper lip (74%)
– Painless submucosal mass
Canalicular Adenoma
• Histology
– Well-circumscribed
– Multiple foci
– Tubular structures line
by columnar or
cuboidal cells
– Vascular stroma
Myoepithelioma
•
•
•
•
<1% of all salivary neoplasms
3rd-6th decades
F>M
Minor salivary glands > parotid >
submandibular gland
• Presentation: asymptomatic mass
Myoepithelioma
• Histology
– Spindle cell
•
•
•
•
More common
Parotid
Uniform, central nuclei
Eosinophilic granular or
fibrillar cytoplasm
– Plasmacytoid cell
• Polygonal
• Eccentric oval nuclei
Mucoepidermoid Carcinoma
•
•
•
•
•
•
•
Most common salivary gland malignancy
5-9% of salivary neoplasms
Parotid 45-70% of cases
Palate 18%
3rd-8th decades, peak in 5th decade
F>M
Caucasian > African American
Mucoepidermoid Carcinoma
• Presentation
– Low-grade: slow growing, painless mass
– High-grade: rapidly enlarging, +/- pain
– **Minor salivary glands: may be mistaken for
benign or inflammatory process
• Hemangioma
• Papilloma
• Tori
Mucoepidermoid Carcinoma
• Gross pathology
– Well-circumscribed to
partially encapsulated
to unencapsulated
– Solid tumor with cystic
spaces
Mucoepidermoid Carcinoma
• Histology—Low-grade
– Mucus cell > epidermoid
cells
– Prominent cysts
– Mature cellular elements
Mucoepidermoid Carcinoma
• Histology—Intermediategrade
– Mucus = epidermoid
– Fewer and smaller cysts
– Increasing pleomorphism
and mitotic figures
Mucoepidermoid Carcinoma
• Histology—High-grade
– Epidermoid > mucus
– Solid tumor cell
proliferation
– Mistaken for SCCA
• Mucin staining
Mucoepidermoid Carcinoma
• Treatment
– Influenced by site, stage, grade
– Stage I & II
• Wide local excision
– Stage III & IV
• Radical excision
• +/- neck dissection
• +/- postoperative radiation therapy
Adenoid Cystic Carcinoma
• Overall 2nd most common malignancy
• Most common in submandibular, sublingual
and minor salivary glands
• M=F
• 5th decade
• Presentation
– Asymptomatic enlarging mass
– Pain, paresthesias, facial weakness/paralysis
Adenoid Cystic Carcinoma
• Gross pathology
– Well-circumscribed
– Solid, rarely with cystic
spaces
– infiltrative
Adenoid Cystic Carcinoma
• Histology—cribriform
pattern
– Most common
– “swiss cheese”
appearance
Adenoid Cystic Carcinoma
• Histology—tubular
pattern
– Layered cells forming
duct-like structures
– Basophilic mucinous
substance
• Histology—solid pattern
– Solid nests of cells
without cystic or tubular
spaces
Adenoid Cystic Carcinoma
• Treatment
– Complete local excision
– Tendency for perineural invasion: facial nerve
sacrifice
– Postoperative XRT
• Prognosis
– Local recurrence: 42%
– Distant metastasis: lung
– Indolent course: 5-year survival 75%, 20-year
survival 13%
Acinic Cell Carcinoma
• 2nd most common parotid and pediatric
malignancy
• 5th decade
• F>M
• Bilateral parotid disease in 3%
• Presentation
– Solitary, slow-growing, often painless mass
Acinic Cell Carcinoma
• Gross pathology
– Well-demarcated
– Most often
homogeneous
Acinic Cell Carcinoma
• Histology
– Solid and microcystic
patterns
• Most common
• Solid sheets
• Numerous small cysts
– Polyhedral cells
– Small, dark, eccentric
nuclei
– Basophilic granular
cytoplasm
Acinic Cell Carcinoma
• Treatment
– Complete local excision
– +/- postoperative XRT
• Prognosis
– 5-year survival: 82%
– 10-year survival: 68%
– 25-year survival: 50%
Adenocarcinoma
•
•
•
•
Rare
5th to 8th decades
F>M
Parotid and minor
salivary glands
• Presentation:
– Enlarging mass
– 25% with pain or facial weakness
Adenocarcinoma
• Histology
– Heterogeneity
– Presence of glandular
structures and absence
of epidermoid
component
– Grade I
– Grade II
– Grade III
Adenocarcinoma
• Treatment
– Complete local excision
– Neck dissection
– Postoperative XRT
• Prognosis
–
–
–
–
Local recurrence: 51%
Regional metastasis: 27%
Distant metastasis: 26%
15-year cure rate:
– Stage I = 67%
– Stage II = 35%
– Stage III = 8%
Malignant Mixed Tumors
• Carcinoma ex-pleomorphic adenoma
• Carcinoma developing in the epithelial component
of preexisting pleomorphic adenoma
• Carcinosarcoma
• True malignant mixed tumor—carcinomatous and
sarcomatous components
• Metastatic mixed tumor
• Metastatic deposits of otherwise typical
pleomorphic adenoma
Carcinoma Ex-Pleomorphic Adenoma
•
•
•
•
•
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
• Presentation
• Longstanding painless mass that undergoes sudden
enlargement
Carcinoma Ex-Pleomorphic
Adenoma
• Gross pathology
– Poorly circumscribed
– Infiltrative
– Hemorrhage and
necrosis
Carcinoma Ex-Pleomorphic
Adenoma
• Histology
– Malignant cellular change
adjacent to typical
pleomorphic adenoma
– Carcinomatous component
• Adenocarcinoma
• Undifferentiated
Carcinoma Ex-Pleomorphic Adenoma
• Treatment
– Radical excision
– Neck dissection (25% with lymph node
involvement at presentation)
– Postoperative XRT
• Prognosis
– Dependent upon stage and histology
Carcinosarcoma
•
•
•
•
•
Rare: <.05% of salivary gland neoplasms
6th decade
M=F
Parotid
History of previously excised pleomorphic
adenoma, recurrent pleomorphic adenoma
or recurring pleomorphic treated with XRT
• Presentation
Carcinosarcoma
• Gross pathology
–
–
–
–
–
Poorly circumscribed
Infiltrative
Cystic areas
Hemorrhage, necrosis
Calcification
Carcinosarcoma
• Histology
– Biphasic appearance
– Sarcomatous component
• Dominant
• chondrosarcoma
– Carinomatous
component
• Moderately to poorly
differentiated ductal
carcinoma
• Undifferentiated
Carcinosarcoma
• Treatment
– Radical excision
– Neck dissection
– Postoperative XRT
– Chemotherapy (distant metastasis to lung,
liver, bone, brain)
• Prognosis
– Poor, average survival less than 2 ½ years
Squamous Cell Carcinoma
•
•
•
•
1.6% of salivary gland neoplasms
7th-8th decades
M:F = 2:1
MUST RULE OUT:
• High-grade mucoepidermoid carcinoma
• Metastatic SCCA to intraglandular nodes
• Direct extension of SCCA
Squamous Cell Carcinoma
• Gross pathology
– Unencapsulated
– Ulcerated
– fixed
Squamous Cell Carcinoma
• Histology
– Infiltrating
– Nests of tumor cells
– Well differentiated
• Keratinization
– Moderately-well
differentiated
– Poorly differentiated
• No keratinization
Squamous Cell Carcinoma
• Treatment
– Radical excision
– Neck dissection
– Postoperative XRT
• Prognosis
– 5-year survival: 24%
– 10-year survival: 18%
Polymorphous Low-Grade
Adenocarcinoma
• 2nd most common
malignancy in minor
salivary glands
• 7th decade
• F>M
• Painless, submucosal
mass
• Morphologic diversity
• Solid, glandular, cribriform,
ductular, tubular, trabecular,
cystic
Polymorphous Low-Grade
Adenocarcinoma
• Histology
– Isomorphic cells,
indistinct borders,
uniform nuclei
– Peripheral “Indian-file”
pattern
• Treatment
– Complete yet
conservative excision
Clear Cell Carcinoma
•
•
•
•
•
AKA glycogen-rich
Palate and parotid
6th-8th decade
M=F
Histology
• Uniform, round or
polygonal cells
• Peripheral dark nuclei
• Clear cytoplasm
• Treatment
• Complete local excision
Epithelial-Myoepithelial Carcinoma
• < 1% of salivary neoplasms
• 6th-7th decades, F > M,
parotid
• ? Increased risk for 2nd
primary
• Histology
• Tumor cell nests
• Two cell types
• Thickened basement
membrane
• Treatment
• Surgical excision
Undifferentiated Carcinoma
• Lymphoepithelial
• Eskimos: parotid, F > M,
familial
• Asian: submandibular,
M>F
• Large-cell
• Bimodal peaks
• M>F
• Parotid
• Small-cell
• 6th-7th decades
• M:F = 1.6:1
• parotid
Controversial Issues
• Management of the N0 Neck
– Recurrence in the neck = low likelihood of
salvage
– Parotid: clinical neck disease, 16%
• N- disease = 74% 5-year survival
• N+ disease = 9% 5-year survival
– Submandibular: clinical neck disease, 8%
• N- disease = 41% 5-year survival
• N+ disease = 9% 5-year survival
Management of the N0 Neck
• Increase risk of occult neck metastasis
– **High-grade malignancies
– **Advanced primary tumor stage (T3-T4)
– High risk histology
– Undifferentiated, SCCA, adenocarcinoma, high-grade
mucoepidermoid, salivary duct carcinoma
– Tumor size > 3cm
– Patient > 54 years of age
– Facial paralysis
– Extracapsular, perilymphatic spread
Management of the N0 Neck
• Neck Dissection
– Advantages
– Pathologic staging
– Improved counseling and prediction of prognosis
– Disadvantages
– Longer OR time, increase complications, increased cost
– Functional deficits, cosmetic effects
– Type
• Parotid: levels II-IV
• Submandibular: levels I-III
Management of the N0 Neck
• Radiation Therapy
– Advantage
– Avoids surgical sequlae
– Disadvantages
– Radiation effect on normal tissue
– Radiation induced malignancies
– Proponents argument: the same factors that
increase the risk of occult neck disease also increase
the risk for local recurrence and necessitate
postoperative XRT to the primary so it is reasonable
to treat the neck with XRT as well
Fine-Needle Aspiration Biopsy
• Efficacy is well established
• Accuracy = 84-97%
• Sensitivity = 54-95%
• Specificity = 86=100%
• Safe, well tolerated
Fine-Needle Aspiration Biopsy
• Opponents argument:
– Doesn’t change management
• Surgery regardless of reported diagnosis
– Obscuring final pathologic diagnosis
– Frequency of “inadequate” sampling, requires
multiple biopsies, prolongs course until definitive
treatment, increases cost
Fine-Needle Aspiration Biopsy
• Proponent’s argument:
– Important to distinguish benign vs. malignant
nature of neoplasm
– Preoperative patient counseling
– Surgical planning
– Differentiate between neoplastic and nonneoplastic processes
• Avoid surgery in large number of patients
Bicellular Theory
• Intercalated Ducts
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–
–
–
–
Pleomorphic adenoma
Warthin’s tumor
Oncocytoma
Acinic cell
Adenoid cystic
• Excretory Ducts
– Squamous cell
– Mucoepidermoid
Multicellular Theory
• Striated duct—oncocytic tumors
• Acinar cells—acinic cell carcinoma
• Excretory Duct—squamous cell and
mucoepidermoid carcinoma
• Intercalated duct and myoepithelial cells—
pleomorphic tumors
Tumorigenesis
• Contradictory evidence:
– Luminal cells are readily capable of replication
– Acinar cells participate in gland regeneration
– Immunohistochemical staining of S-100 protein
• Present in many salivary gland neoplasms
• Not present in normal ductal cells
Conclusions
• Hugely diverse histopathology
• Accurate pathologic diagnosis does influence
management
• Relatively rare malignancies
• Utilize preoperative studies when indicated
• Don’t believe everything you read!