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The Salivary Glands diseases The Salivary Glands diseases

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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

gland salivary cell carcinoma salivary gland carcinoma cell adenoma parotid presentation treatment glands pleomorphic clinical diagnosis minor tumor cells

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Slide1

The Salivary Glands diseases

Slide2

Slide3

Clinical Anatomy of the Salivary Glands

Slide4

Minor salivary glands

Slide5

Slide6

Slide7

Slide8

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.

Slide9

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

.

Slide10

Reactive lesions

Mucocele is a clinical term that includes mucus extrava

sation phenomenon and mucus retention cyst.

Slide11

Slide12

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.”

Slide13

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

Slide14

Slide15

Diagnosis

Presentation

Microscopic findings

Differential Diagnosis

Hemangioma

Pyogenic

granuloma

Salivary neoplasm

Connective tissue neoplasm

Slide16

Treatment

Excision with associated local minor salivary glands

Prognosis

Occasional recurrence

Slide17

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

Slide18

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

Slide19

Slide20

Slide21

Microscopic 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

Slide22

Treatment

Excision of cyst with adjacent gland(s)

Prognosis

Recurrence is rare.

Slide23

Necrotizing Sialometaplasia

Etiology

Local ischemic injury of salivary gland lobules

May be preceded by trauma or local anesthetic injury, or it may appear spontaneously

Slide24

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

Slide25

Slide26

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

Slide27

Diagnosis

Microscopic findings

Differential Diagnosis

Salivary gland neoplasm

Squamous cell carcinoma

Granulomatous disease

Slide28

Treatment

Follow-up only

Prognosis

Excellent

Slide29

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

Slide30

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.

Slide31

Clinical picture

Slide32

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.

Slide33

Slide34

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

Slide35

Differential Diagnosis

Dermoid

cyst

Salivary gland tumor

Soft tissue tumor

Cystic

hygroma

Thymic

cyst

Slide36

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

Slide37

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.

Slide38

Salivary obstruction from stones, mucous plugs, and mucous extravasation phenomenon.

Slide39

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.

Slide40

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.

Slide41

ClinicaI

presentation

Slide42

Slide43

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.

Slide44

Differential Diagnosis

Calcified lymph nodes from previously resolved tuberculosis

Phleboliths

(particularly if an old cavernous

hemangioma

were present)

Tonsoliths

Calcifications of the carotid bifurcation.

Slide45

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.

Slide46

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.

Slide47

Sialorrhea (Sialosis)

Etiology

Varied; may include idiopathic paroxysmal sialorrhea, parkinsonism, stomatitis (acute), newly inserted oral appliances, expectorants, neostigmine, and others

Slide48

Clinical Presentation

Clinical Presentation

Excess saliva resulting in drooling

Angular

cheilosis

Diffuse

parotid

/

submandibular

salivary

gland

enlargement

Slide49

Clinical presentation

Slide50

Diagnosis

Diagnosis

Direct observation and analysis of history

Flow-rate measurement

Slide51

Treatment

Treatment

Scopolamine

If related to medication use, an alternate medication should be chosen, if possible.

Prognosis

Guarded/indeterminate

Slide52

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.

Slide53

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.

Slide54

Differential Diagnosis

Differential Diagnosis

Salivary

neoplasms

Lymphoma

Extension of nasopharyngeal or

sinonasal

disease into the oral cavity.

Slide55

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.

Slide56

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

Slide57

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

Slide58

Slide59

Sialography

Slide60

Slide61

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

Slide62

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

Slide63

Treatment

Directed at associated connective tissue or autoimmune disease

Systemic corticosteroids if acute symptoms arise

Frequent dental/ophthalmic examinations

Slide64

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

Slide65

Prognosis

Guarded

High risk of lymphoma compared with risk in those without autoimmune disease.

Slide66

Salivary Gland Neoplasms

Benign Neoplasms

Malignant NeoplasmsControversial Issues

Slide67

Salivary 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

Slide68

Tumors of the salivary glands

Benign tumors

.

Pleomorphic

adenoma

Warthins

tumors .

Basal cell adenoma

Canalicular

adenoma

Oxyphilic

adenoam

Myepithelial

ductul

adenoma

Slide69

Tumors of the salivary glands

Malignant tumors (

major and minor salivary glands .}Mucoepidermoid

carcinoma .

Adenoid cystic carcinoma

Malignant mixed

tumour

Acinic

cell

carcinaoma

.

Slide70

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

.

Slide71

Pleomorphic

Adenoma

Slide72

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.

Slide73

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 .

Slide74

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

4

th

-6

th

decades

F:M = 3-4:1

Slide75

Pleomorphic 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

Slide76

Pleomorphic Adenoma

Gross pathology

SmoothWell-demarcated

Solid

Cystic changes

Myxoid stroma

Slide77

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

Slide78

Pleomorphic Adenoma

Slide79

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

Slide80

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

Slide81

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

Slide82

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

Slide83

Warthin’s Tumor

Slide84

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

Slide85

Oncocytoma

Presentation

Enlarging, painless massTechnetium-99m pertechnetate scintigraphy

Mitochondrial hyperplasia

Slide86

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

Slide87

Oncocytoma

Electron microscopy:

Mitochondrial hyperplasia60% of cell volume

Slide88

Monomorphic 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

Slide89

Basal Cell Adenoma

Solid

Most common

Solid nests of tumor cells

Uniform, hyperchromatic, round nuclei, indistinct cytoplasm

Peripheral nuclear palisading

Scant stroma

Slide90

Basal Cell Adenoma

Trabecular

Cells in elongated trabecular patternVascular stroma

Slide91

Basal Cell Adenoma

Tubular

Multiple duct-like structuresColumnar cell lining

Vascular stroma

Slide92

Basal Cell Adenoma

Membranous

Thick eosinophilic hyaline membranes surrounding nests of tumor cells

“jigsaw-puzzle” appearance

Slide93

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

Slide94

Canalicular Adenoma

Histology

Well-circumscribedMultiple foci

Tubular structures line by columnar or cuboidal cells

Vascular stroma

Slide95

Myoepithelioma

<1% of all salivary neoplasms

3rd-6

th

decades

F>M

Minor salivary glands > parotid > submandibular gland

Presentation: asymptomatic mass

Slide96

Myoepithelioma

Histology

Spindle cellMore common

Parotid

Uniform, central nuclei

Eosinophilic granular or fibrillar cytoplasm

Plasmacytoid cell

Polygonal

Eccentric oval nuclei

Slide97

Mucoepidermoid 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

Slide98

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

Slide99

Mucoepidermoid Carcinoma

Gross pathology

Well-circumscribed to partially encapsulated to unencapsulated

Solid tumor with cystic spaces

Slide100

Mucoepidermoid Carcinoma

Histology—Low-grade

Mucus cell > epidermoid cells

Prominent cysts

Mature cellular elements

Slide101

Mucoepidermoid Carcinoma

Histology—Intermediate- grade

Mucus = epidermoid

Fewer and smaller cysts

Increasing pleomorphism and mitotic figures

Slide102

Mucoepidermoid Carcinoma

Histology—High-grade

Epidermoid > mucus

Solid tumor cell proliferation

Mistaken for SCCA

Mucin staining

Slide103

Mucoepidermoid Carcinoma

Treatment

Influenced by site, stage, gradeStage I & II

Wide local excision

Stage III & IV

Radical excision

+/- neck dissection

+/- postoperative radiation therapy

Slide104

Adenoid 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

Slide105

Adenoid Cystic Carcinoma

Gross pathology

Well-circumscribedSolid, rarely with cystic spaces

infiltrative

Slide106

Adenoid Cystic Carcinoma

Histology—cribriform pattern

Most common“swiss cheese” appearance

Slide107

Adenoid 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

Slide108

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%

Slide109

Acinic 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

Slide110

Acinic Cell Carcinoma

Gross pathology

Well-demarcatedMost often homogeneous

Slide111

Acinic Cell Carcinoma

Histology

Solid and microcystic patterns

Most common

Solid sheets

Numerous small cysts

Polyhedral cells

Small, dark, eccentric nuclei

Basophilic granular cytoplasm

Slide112

Acinic Cell Carcinoma

Treatment

Complete local excision+/- postoperative XRT

Prognosis

5-year survival: 82%

10-year survival: 68%

25-year survival: 50%

Slide113

Adenocarcinoma

Rare

5th

to 8

th

decades

F > M

Parotid and minor

salivary glands

Presentation:

Enlarging mass

25% with pain or facial weakness

Slide114

Adenocarcinoma

Histology

Heterogeneity

Presence of glandular structures and absence of epidermoid component

Grade I

Grade II

Grade III

Slide115

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%

Slide116

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

Slide117

Carcinoma 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

Slide118

Carcinoma Ex-Pleomorphic Adenoma

Gross pathology

Poorly circumscribed

Infiltrative

Hemorrhage and necrosis

Slide119

Carcinoma Ex-Pleomorphic Adenoma

Histology

Malignant cellular change adjacent to typical pleomorphic adenoma

Carcinomatous component

Adenocarcinoma

Undifferentiated

Slide120

Carcinoma Ex-Pleomorphic Adenoma

Treatment

Radical excisionNeck dissection (25% with lymph node involvement at presentation)

Postoperative XRT

Prognosis

Dependent upon stage and histology

Slide121

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

Slide122

Carcinosarcoma

Gross pathology

Poorly circumscribedInfiltrative

Cystic areas

Hemorrhage, necrosis

Calcification

Slide123

Carcinosarcoma

Histology

Biphasic appearance

Sarcomatous component

Dominant

chondrosarcoma

Carinomatous component

Moderately to poorly differentiated ductal carcinoma

Undifferentiated

Slide124

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

Slide125

Squamous 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

Slide126

Squamous Cell Carcinoma

Gross pathology

UnencapsulatedUlcerated

fixed

Slide127

Squamous Cell Carcinoma

Histology

InfiltratingNests of tumor cells

Well differentiated

Keratinization

Moderately-well differentiated

Poorly differentiated

No keratinization

Slide128

Squamous Cell Carcinoma

Treatment

Radical excisionNeck dissection

Postoperative XRT

Prognosis

5-year survival: 24%

10-year survival: 18%

Slide129

Polymorphous 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

Slide130

Polymorphous Low-Grade Adenocarcinoma

Histology

Isomorphic cells, indistinct borders, uniform nuclei

Peripheral “Indian-file” pattern

Treatment

Complete yet conservative excision

Slide131

Clear 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

Slide132

Epithelial-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

Slide133

Undifferentiated 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

Slide134

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

Slide135

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

Slide136

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

Slide137

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

Slide138

Fine-Needle Aspiration Biopsy

Efficacy is well established

Accuracy = 84-97%Sensitivity = 54-95%

Specificity = 86=100%

Safe, well tolerated

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Fine-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

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Fine-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

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Bicellular Theory

Intercalated Ducts

Pleomorphic adenomaWarthin’s tumor

Oncocytoma

Acinic cell

Adenoid cystic

Excretory Ducts

Squamous cell

Mucoepidermoid

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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

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Tumorigenesis

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

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Conclusions

Hugely diverse histopathology

Accurate pathologic diagnosis does influence managementRelatively rare malignancies

Utilize preoperative studies when indicated

Don’t believe everything you read!