Clinical Anatomy of the Salivary Glands Minor salivary glands Use of saliva as diagnostic fluid Change in sal composition and flow rate Sialadenitis Na amp Cl secretion increases ID: 915240
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Slide1
The Salivary Glands diseases
Slide2Slide3Clinical Anatomy of the Salivary Glands
Slide4Minor salivary glands
Slide5Slide6Slide7Slide8Use 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.
Slide9Cont
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
.
Slide10Reactive lesions
Mucocele is a clinical term that includes mucus extrava
sation phenomenon and mucus retention cyst.
Slide11Slide12Mucocele
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.”
Slide13Clinical 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
Slide14Slide15Diagnosis
Presentation
Microscopic findings
Differential Diagnosis
Hemangioma
Pyogenic
granuloma
Salivary neoplasm
Connective tissue neoplasm
Slide16Treatment
Excision with associated local minor salivary glands
Prognosis
Occasional recurrence
Slide17Mucus Retention Cyst
Etiology
Represents dilatation of salivary excretory duct due to obstruction
Duct obstruction may be due to a mucous plug or sialolith formation
Slide18Clinical 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
Slide19Slide20Slide21Microscopic Findings
Thin, dilated, epithelial-lined salivary excretory duct
Lining is cuboidal to columnar with occasional mucus-producing 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
Slide22Treatment
Excision of cyst with adjacent gland(s)
Prognosis
Recurrence is rare.
Slide23Necrotizing Sialometaplasia
Etiology
Local ischemic injury of salivary gland lobules
May be preceded by trauma or local anesthetic injury, or it may appear spontaneously
Slide24Clinical 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
Slide25Slide26Microscopic 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
Slide27Diagnosis
Microscopic findings
Differential Diagnosis
Salivary gland neoplasm
Squamous cell carcinoma
Granulomatous disease
Slide28Treatment
Follow-up only
Prognosis
Excellent
Slide29Ranula
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
Slide30Clinical 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.
Slide31Clinical picture
Slide32Plunging
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.
Slide33Slide34Diagnosis
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
Slide35Differential Diagnosis
Dermoid
cyst
Salivary gland tumor
Soft tissue tumor
Cystic
hygroma
Thymic
cyst
Slide36Treatment
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
Slide37Sialolithiasis
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.
Slide38Salivary obstruction from stones, mucous plugs, and mucous extravasation phenomenon.
Slide39Clinical 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.
Slide40C/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.
Slide41ClinicaI
presentation
Slide42Slide43Diagnosis
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.
Slide44Differential Diagnosis
Calcified lymph nodes from previously resolved tuberculosis
Phleboliths
(particularly if an old cavernous
hemangioma
were present)
Tonsoliths
Calcifications of the carotid bifurcation.
Slide45Treatment
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.
Slide46Prognosis
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.
Slide47Sialorrhea (Sialosis)
Etiology
Varied; may include idiopathic paroxysmal sialorrhea, parkinsonism, stomatitis (acute), newly inserted oral appliances, expectorants, neostigmine, and others
Slide48Clinical Presentation
Clinical Presentation
Excess saliva resulting in drooling
Angular
cheilosis
Diffuse
parotid
/
submandibular
salivary
gland
enlargement
Slide49Clinical presentation
Slide50Diagnosis
Diagnosis
Direct observation and analysis of history
Flow-rate measurement
Slide51Treatment
Treatment
Scopolamine
If related to medication use, an alternate medication should be chosen, if possible.
Prognosis
Guarded/indeterminate
Slide52Adenomatoid 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.
Slide53Clinical 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.
Slide54Differential Diagnosis
Differential Diagnosis
Salivary
neoplasms
Lymphoma
Extension of nasopharyngeal or
sinonasal
disease into the oral cavity.
Slide55Treatment
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.
Slide56Sjögren’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
Slide57Clinical 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
Slide58Slide59Sialography
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
Slide62Differential 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
Slide63Treatment
Directed at associated connective tissue or autoimmune disease
Systemic corticosteroids if acute symptoms arise
Frequent dental/ophthalmic examinations
Slide64Treatment
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
Slide65Prognosis
Guarded
High risk of lymphoma compared with risk in those without autoimmune disease.
Slide66Salivary Gland Neoplasms
Benign Neoplasms
Malignant NeoplasmsControversial Issues
Slide67Salivary Gland Neoplasms
Diverse histopathology
Relatively uncommon2% of head and neck neoplasms
Distribution
Parotid: 80% overall; 80% benign
Submandibular: 15% overall; 50% benign
Sublingual/Minor: 5% overall; 40% benign
Slide68Tumors 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
.
Slide70Pleomorphic
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
.
Slide71Pleomorphic
Adenoma
Slide72Pleomorphic
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.
Slide73Pleomorphic
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 .
Slide74Cont-
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
4
th
-6
th
decades
F:M = 3-4:1
Slide75Pleomorphic Adenoma
Slow-growing, painless mass
Parotid: 90% in superficial lobe, most in tail of glandMinor salivary gland: lateral palate, submucosal mass
Solitary vs. synchronous/metachronous neoplasms
Slide76Pleomorphic Adenoma
Gross pathology
SmoothWell-demarcated
Solid
Cystic changes
Myxoid stroma
Slide77Pleomorphic 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
Slide78Pleomorphic Adenoma
Slide79Pleomorphic 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
Slide80Warthin’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
Slide81Warthin’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
Slide82Warthin’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
Slide83Warthin’s Tumor
Slide84Oncocytoma
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
Slide85Oncocytoma
Presentation
Enlarging, painless massTechnetium-99m pertechnetate scintigraphy
Mitochondrial hyperplasia
Slide86Oncocytoma
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
Slide87Oncocytoma
Electron microscopy:
Mitochondrial hyperplasia60% of cell volume
Slide88Monomorphic Adenomas
Basal cell, canalicular, sebaceous, glycogen-rich, clear cell
Basal cell is most common: 1.8% of benign epithelial salivary gland neoplasms
6
th
decade
M:F = approximately 1:1
Caucasian > African American
Most common in parotid
Slide89Basal Cell Adenoma
Solid
Most common
Solid nests of tumor cells
Uniform, hyperchromatic, round nuclei, indistinct cytoplasm
Peripheral nuclear palisading
Scant stroma
Slide90Basal Cell Adenoma
Trabecular
Cells in elongated trabecular patternVascular stroma
Slide91Basal Cell Adenoma
Tubular
Multiple duct-like structuresColumnar cell lining
Vascular stroma
Slide92Basal Cell Adenoma
Membranous
Thick eosinophilic hyaline membranes surrounding nests of tumor cells
“jigsaw-puzzle” appearance
Slide93Monomorphic Adenomas
Canalicular adenoma
7th decade
F:M – 1.8:1
Most common in minor salivary glands of the upper lip (74%)
Painless submucosal mass
Slide94Canalicular Adenoma
Histology
Well-circumscribedMultiple foci
Tubular structures line by columnar or cuboidal cells
Vascular stroma
Slide95Myoepithelioma
<1% of all salivary neoplasms
3rd-6
th
decades
F>M
Minor salivary glands > parotid > submandibular gland
Presentation: asymptomatic mass
Slide96Myoepithelioma
Histology
Spindle cellMore common
Parotid
Uniform, central nuclei
Eosinophilic granular or fibrillar cytoplasm
Plasmacytoid cell
Polygonal
Eccentric oval nuclei
Slide97Mucoepidermoid Carcinoma
Most common salivary gland malignancy
5-9% of salivary neoplasmsParotid 45-70% of cases
Palate 18%
3
rd
-8
th
decades, peak in 5
th
decade
F>M
Caucasian > African American
Slide98Mucoepidermoid 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
Slide99Mucoepidermoid Carcinoma
Gross pathology
Well-circumscribed to partially encapsulated to unencapsulated
Solid tumor with cystic spaces
Slide100Mucoepidermoid Carcinoma
Histology—Low-grade
Mucus cell > epidermoid cells
Prominent cysts
Mature cellular elements
Slide101Mucoepidermoid Carcinoma
Histology—Intermediate- grade
Mucus = epidermoid
Fewer and smaller cysts
Increasing pleomorphism and mitotic figures
Slide102Mucoepidermoid Carcinoma
Histology—High-grade
Epidermoid > mucus
Solid tumor cell proliferation
Mistaken for SCCA
Mucin staining
Slide103Mucoepidermoid Carcinoma
Treatment
Influenced by site, stage, gradeStage I & II
Wide local excision
Stage III & IV
Radical excision
+/- neck dissection
+/- postoperative radiation therapy
Slide104Adenoid Cystic Carcinoma
Overall 2
nd most common malignancy
Most common in submandibular, sublingual and minor salivary glands
M = F
5
th
decade
Presentation
Asymptomatic enlarging mass
Pain, paresthesias, facial weakness/paralysis
Slide105Adenoid Cystic Carcinoma
Gross pathology
Well-circumscribedSolid, rarely with cystic spaces
infiltrative
Slide106Adenoid Cystic Carcinoma
Histology—cribriform pattern
Most common“swiss cheese” appearance
Slide107Adenoid Cystic Carcinoma
Histology—tubular pattern
Layered cells forming duct-like structuresBasophilic mucinous substance
Histology—solid pattern
Solid nests of cells without cystic or tubular spaces
Slide108Adenoid 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%
Slide109Acinic Cell Carcinoma
2
nd most common parotid and pediatric malignancy5
th
decade
F>M
Bilateral parotid disease in 3%
Presentation
Solitary, slow-growing, often painless mass
Slide110Acinic Cell Carcinoma
Gross pathology
Well-demarcatedMost often homogeneous
Slide111Acinic Cell Carcinoma
Histology
Solid and microcystic patterns
Most common
Solid sheets
Numerous small cysts
Polyhedral cells
Small, dark, eccentric nuclei
Basophilic granular cytoplasm
Slide112Acinic Cell Carcinoma
Treatment
Complete local excision+/- postoperative XRT
Prognosis
5-year survival: 82%
10-year survival: 68%
25-year survival: 50%
Slide113Adenocarcinoma
Rare
5th
to 8
th
decades
F > M
Parotid and minor
salivary glands
Presentation:
Enlarging mass
25% with pain or facial weakness
Slide114Adenocarcinoma
Histology
Heterogeneity
Presence of glandular structures and absence of epidermoid component
Grade I
Grade II
Grade III
Slide115Adenocarcinoma
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%
Slide116Malignant 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
Slide117Carcinoma Ex-Pleomorphic Adenoma
2-4% of all salivary gland neoplasms
4-6% of mixed tumors
6
th
-8
th
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
Slide118Carcinoma Ex-Pleomorphic Adenoma
Gross pathology
Poorly circumscribed
Infiltrative
Hemorrhage and necrosis
Slide119Carcinoma Ex-Pleomorphic Adenoma
Histology
Malignant cellular change adjacent to typical pleomorphic adenoma
Carcinomatous component
Adenocarcinoma
Undifferentiated
Slide120Carcinoma Ex-Pleomorphic Adenoma
Treatment
Radical excisionNeck dissection (25% with lymph node involvement at presentation)
Postoperative XRT
Prognosis
Dependent upon stage and histology
Slide121Carcinosarcoma
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
Slide122Carcinosarcoma
Gross pathology
Poorly circumscribedInfiltrative
Cystic areas
Hemorrhage, necrosis
Calcification
Slide123Carcinosarcoma
Histology
Biphasic appearance
Sarcomatous component
Dominant
chondrosarcoma
Carinomatous component
Moderately to poorly differentiated ductal carcinoma
Undifferentiated
Slide124Carcinosarcoma
Treatment
Radical excision
Neck dissection
Postoperative XRT
Chemotherapy (distant metastasis to lung, liver, bone, brain)
Prognosis
Poor, average survival less than 2 ½ years
Slide125Squamous Cell Carcinoma
1.6% of salivary gland neoplasms
7th-8
th
decades
M:F = 2:1
MUST RULE OUT:
High-grade mucoepidermoid carcinoma
Metastatic SCCA to intraglandular nodes
Direct extension of SCCA
Slide126Squamous Cell Carcinoma
Gross pathology
UnencapsulatedUlcerated
fixed
Slide127Squamous Cell Carcinoma
Histology
InfiltratingNests of tumor cells
Well differentiated
Keratinization
Moderately-well differentiated
Poorly differentiated
No keratinization
Slide128Squamous Cell Carcinoma
Treatment
Radical excisionNeck dissection
Postoperative XRT
Prognosis
5-year survival: 24%
10-year survival: 18%
Slide129Polymorphous Low-Grade Adenocarcinoma
2
nd
most common malignancy in minor salivary glands
7
th
decade
F > M
Painless, submucosal mass
Morphologic diversity
Solid, glandular, cribriform, ductular, tubular, trabecular, cystic
Slide130Polymorphous Low-Grade Adenocarcinoma
Histology
Isomorphic cells, indistinct borders, uniform nuclei
Peripheral “Indian-file” pattern
Treatment
Complete yet conservative excision
Slide131Clear Cell Carcinoma
AKA glycogen-rich
Palate and parotid
6
th
-8
th
decade
M = F
Histology
Uniform, round or polygonal cells
Peripheral dark nuclei
Clear cytoplasm
Treatment
Complete local excision
Slide132Epithelial-Myoepithelial Carcinoma
< 1% of salivary neoplasms
6
th
-7
th
decades, F > M, parotid
? Increased risk for 2
nd
primary
Histology
Tumor cell nests
Two cell types
Thickened basement membrane
Treatment
Surgical excision
Slide133Undifferentiated Carcinoma
Lymphoepithelial
Eskimos: parotid, F > M, familial
Asian: submandibular, M > F
Large-cell
Bimodal peaks
M > F
Parotid
Small-cell
6
th
-7
th
decades
M:F = 1.6:1
parotid
Slide134Controversial 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
Slide135Management 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
Slide136Management 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
Slide137Management 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
Slide138Fine-Needle Aspiration Biopsy
Efficacy is well established
Accuracy = 84-97%Sensitivity = 54-95%
Specificity = 86=100%
Safe, well tolerated
Slide139Fine-Needle Aspiration Biopsy
Opponents argument:
Doesn’t change managementSurgery regardless of reported diagnosis
Obscuring final pathologic diagnosis
Frequency of “inadequate” sampling, requires multiple biopsies, prolongs course until definitive treatment, increases cost
Slide140Fine-Needle Aspiration Biopsy
Proponent’s argument:
Important to distinguish benign vs. malignant nature of neoplasmPreoperative patient counseling
Surgical planning
Differentiate between neoplastic and non-neoplastic processes
Avoid surgery in large number of patients
Slide141Bicellular Theory
Intercalated Ducts
Pleomorphic adenomaWarthin’s tumor
Oncocytoma
Acinic cell
Adenoid cystic
Excretory Ducts
Squamous cell
Mucoepidermoid
Slide142Multicellular Theory
Striated duct—oncocytic tumors
Acinar cells—acinic cell carcinoma
Excretory Duct—squamous cell and mucoepidermoid carcinoma
Intercalated duct and myoepithelial cells—pleomorphic tumors
Slide143Tumorigenesis
Contradictory evidence:
Luminal cells are readily capable of replicationAcinar cells participate in gland regeneration
Immunohistochemical staining of S-100 protein
Present in many salivary gland neoplasms
Not present in normal ductal cells
Slide144Conclusions
Hugely diverse histopathology
Accurate pathologic diagnosis does influence managementRelatively rare malignancies
Utilize preoperative studies when indicated
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