Salivary gland

tumours
TUMOR

OR

NEOPLASM
TUMOR:
 It constitute a group of heterogenous lesions that range
from hamartomatous or non neoplastic tissue
proliferation to malignant neoplasms with metastatic
capacity
NEOPLASM:
• It is an abnormal mass of tissue, the growth of
which exceeds and uncordinated with that of
normal tissue and persists in same excessive
manner after cessation of the stimuli that evoked
the change.
TERMINOLOGY
 CHORISTOMA: it is non neoplastic tumour like mass of
developmental origin in which there are found tissues foreign
to the part of the body
 HAMARTOMA: It is a tumour like malformation in which
the tissues of a particular part of the body are arranged
haphazardly usually with an excess of one or more of its
components
 TERATOMA: It is a tumour consisting of multiple tissues
foreign to the part from which it arises. Tissue representative
of the three primitive germinal layers may be found
CHORISTOMA
 ANATOMY OF SALIVARY GLANDS

 Two submandibular glands

 Two parotid glands
 Two sublingual glands
 Approximately 450 minor
salivary glands
 DIFFERENTIAL DIAGNOSIS OF A
SALIVARY GLAND MASS

 INFLAMMATION (PAROTIDITIS)
 MUMPS
 CALCULI
 NEOPLASM
 HISTOGENESIS
BASAL RESERVE CELL THEORY :
 Salivary neoplasms- reserved (stem
cells) of the salivary duct system
 e.g. adenoid cystic carcinoma and
acinic cell carcinoma -intercalated duct
reserve cell.
 The mucoepidermoid carcinoma,
squamous cell carcinoma, and salivary
duct carcinoma -excretory reserve
cell.
PLURIPOTENT RESERVE CELL
THEORY:
 Excretory duct
Salivary gland unit
 HISTOGENESIS
 SEMIPLURIPOTENT BICELLULAR RESERVE CELL
THEORY :
outer (basal) and inner (luminal)
 MULTICELLULAR THEORY :
Salivary neoplasm arise from already differentiated cells along the
salivary gland unit. For example, squamous cell carcinoma arises
from the excretory duct epithelium and acinic cell carcinoma
arise from the acinar cells.
 GENERAL FEATURES
 Annual incidence of salivary glands around the world- 1 to 6.5 cases
per 100,000 people
PAROTID TUMOURS:
-64-80% with 15-32% malignant changes
 Pleomorphic adenoma- 53-77%
 Warthin tumours-6-14%
SUBMANDIBULAR TUMOURS:
- 8-11% with 37-45 % malignant changes
 ACC- 12-27%
SUBLINGUAL TUMOURS:<1
-Most of them are malignant- 70-90%
 Minor salivary gland tumours: 9-23%
 Palate most common-42-54%
CLASSIFICATION
 CLASSIFICATION
SALIVARY GLAND NEOPLASMS

PRIMARY SECONDARY/METASTATIC

EPITHELIAL NON-EPITHELIAL
Benign mesenchymal
BENIGN Malignant mesenchymal
lymphomas

MALIGNANT
BENIGN TUMOR : MALIGNANT TUMOR :
growth resembling tissue of origin, Soft tissue mass ,
Characterised by • aggressive ,
• insidous onset , • grow by invasion,
• slow growth , • May be ill defined
• well defined mass , and
• smooth outline , • destruction of adjacent
• a fibrous capsule and tissue and
• displacement of adjacent • metastasizing to
normal tissue. distant parts.
 BENIGN EPITHELIAL TUMOURS
 Pleomorphic adenoma (mixed tumor)
 Myoepithelioma
 Basal cell adenoma
 Warthin tumour (papillary cystadenoma lymphomatosum)
 Oncocytoma
 Canalicular adenoma
 Sebaceous adenoma
 Ductal papillomas:
 Inverted ductal papilloma
 Intraductal papilloma
 Sialadenoma papilliferum
 Cystadenoma
 Papillary cystadenoma
 Mucinous cystadenoma
 MALIGNANT EPITHELIAL TUMOURS
 Acinic cell carcinoma  Salivary duct carcinoma
 Mucoepidermoid carcinoma  Adeno carcinoma
 Adenoid cystic carcinoma  Mailgnant myoepithelioma
 Polymorphous low-grade (myoepithelial carcinoma)
adenocarcinoma
 Carcinoma ex-pleomorphic adenoma
 Epithelial-myoepithelial carcinoma
 Squamous cell carcinoma
 Basal cell adenocarcinoma
 Small cell carcinoma
 Sebaceous carcinoma
 Large cell carcinoma
 Papillary cystadenocarcinoma
 Mucinous adenocarcinoma
 Lymphoepithelial carcinoma
 Oncocytic carcinoma  Other carcinomas
 FEATURES SUGGESTIVE OF
BENIGNANCY
1. Movable(except palate)
2. Unattached to skin or mucosa
3. No ulceration of skin/mucosa
4. Slow growing
5. Soft/rubbery in consistency
6. Long duration
7. No pain
8. No facial nerve palsy
PLEOMORPHIC ADENOMA
 Pleomorphic(focal minor atypia)
 Most common of all salivary gland neoplasms
 53-77% of parotid tumors
 44-68 % of submandibular tumors
 38-43% of minor salivary gland tumors
 6% of sublingual tumors
 Mixture of ductal and myoepithelial elements
 HISTIOGENESIS
 It is not a mixed tumour, as it is not teratomatous or derived
from more than one primary tissue.
 The morphogenic complexity is because of differentiation of
the tumour cells into fibrous, hyalinised, myxoid, chondroid
and even osseous tissue.
 Myoepithelial and reserve cell in intercalated duct.
 Morphogenic complexity- myoepithelial cells
 Regezi and Batsakis:
Intercalated reserve duct cell

Ductal cell Myoepithelial cell

 HISTIOGENESIS

 Dardick: Neoplastic altered epithelial cell

 Cytogenetic abnormalities 12q13-15
 Putative pleomorphic adenoma (PLAG1)-8q12
 CLINICAL FEATURES
 Age: 4th-6th decades(30-50 yrs)
 M:F = 4:6
 Presentation: Slow-growing, firm
painless mass
 Site:
 Parotid: 90% in superficial lobe
(mostly lower pole) presenting as swelling overlying mandibular ramus
infront of the ear.
 Minor salivary gland: Palate presenting as smooth-surface dome shaped
mass, secondary ulceration which may cause difficulty in mastication,
talking and breathing
 Solitary vs. synchronous/metachronous neoplasms
 DUMBELL TUMOUR
 Dumbell shaped tumour-b/w ascending ramus and
stylomandibular ligament.
 CURTAIN SIGN
 Curtain sign – swelling
cannot be moved above
zygomatic bone
 GROSS PATHOLOGY
 – Well-demarcated,
encapsulated
 Capsule – incomplete/
absent for minor salivary
gland tumours
 – Smooth
 – cut surface: fleshy, mucoid,
glistening with homogenous
tan
 HISTO PATHOLOGY
 – Mixture of epithelial,
myoepithelial and stromal
components
 Foote and Frazell:
 Principally myxoid
 Myxoid and cellular-equal
proportions
 Predominantly cellular
 Extremely cellular
 HISTO PATHOLOGY
 – Epithelial cells: nests, sheets, ducts, trabeculae
 - Keratinising squamous cells and mucous producing cells can also
be seen
 Myoepithelial cells: angular/spindled plasmacytoid
appearance(minor glands).
 HISTO PATHOLOGY
 – Stroma: myxoid, chrondroid, fibroid, osteoid
 – No true capsule
 – Tumor pseudopods
 CELLULAR ADENOMAS
 MYOEPITHELIOMAS

MYXOID CHONDROID
 TREATMENT
 Complete surgical excision
 – Parotidectomy with facial nerve
preservation
 – Submandibular gland excision
 – Wide local excision of minor salivary
gland
 Avoid enucleation and tumor spill
 Complication: Malignant
transformation- carcinoma ex
pleomorphic adenoma-5%
 WARTHIN TUMOUR
 Papillary cystadenoma lymphomatosum
 Albrecht –first recognised, Warthin-described
 6-10% of parotid neoplasms
 Second most common benign tumour
PREDISPOSING FACTORS
 Smoking
 EBV
 HISTOGENESIS
 BRANCHIOGENIC THEORY (Hildebrad):
-Variant of lateral cervical cyst and remnants of
branchial pouches

 HETEROTROPHIC SALIVARY GLAND THEORY

(Albrecht and Arzt):
-Heterotopic salivary rests in parotid lymph nodes

 Warthin:
-Ectopic pharyngeal endoderm

 EUSTACHIAN TUBE THEORY (Hevenor and Clark )

supported warthin’s ectopic eustachian tube endoderm as
tissue of origin
 HISTOGENESIS
 Thompson and Bryant:
-Embryology study on PCL- parotid ductal epithelium in
lymph nodes in immediate vicinity of parotid gland.
Second theory: neoplastic proliferation of parotid ductal
epithelium and secondary formation of lymphoid tissue
 Bernier and Bhaskar:
-Lymphoid tissue appeared to be true lymph nodes with
subcapsular spaces and medullary sinusoids
 Azzopardi and Smith:
-Salivary ducts in lymphoid stroma
 HISTOGENESIS
 HETEROTROPHIC SALIVARY GLAND DUCT THEORY
(Azzopardi and Hou):
-Enclaved parotid epithelium in lymph node.
 Other theories: orbital inclusions, heterotopic oncocytes,
sebaceous glands, heterotopic lymph node, endothelium
and thymic anlage
 Other concepts: secondary neoplastic proliferation and
inflammatory process
 Bilateral occurrence and absence of lymphnode architecture
suggests reactive pathogenesis
 Development from heterotopic tissue in lymph node-most
accepted
 DELAYED HYPER SENSITIVITY THEORY(Allergo):
-Hypersensitivity:

Oxyphilic metaplasia of striated ducts

Papillary formation with secretions

Cyst formation

Infiltration of basement membrane by basophils and histiocytes

Delayed hypersensitivity and formation of lymphoid stroma

 CLINICAL FEATURES
 Age: 60-70 YRS
 Race: Caucasian, Blacks<whites
 M:F=10:1 Few studies equal predilection.
 Site: tail of parotid near the angle of the mandible
 Presentation: slow-growing, painless mass
 5-14% bilateral or multicentric
 3% with associated neoplasms
 GROSS PATHOLOGY
 – Encapsulated
 – Smooth/lobulated surface
 – Cystic spaces of variable size,
with viscous fluid, shaggy
epithelium
 – Solid areas with white nodules
representing lymphoid follicles
 HISTOPATHOLOGY
 Ductal epithelium and lymphoid stroma
 – Papillary projections into cystic spaces
surrounded by lymphoid stroma
 – Epithelium: Oncocytic in nature double
cell layer
 Inner Luminal cells-tall columnar
palisaded slightly hyperchromatic nuclei
 HISTOPATHOLOGY

 Basal cells-cuboidal/polygonal
cells with more vesicular
nuclei
 Focal areas of squamous
metaplasia/mucous
prosoplasia
 – Stroma: mature lymphoid
follicles with germinal centers
 TREATMENT

 Surgical removal
 Complications:
 6-12% recurrence rate
 Malignant transformation-carcinoma ex papillary
cystadenoma lymphomatosum
 ONCOCYTOMA
 Oncocytic adenoma, oxyphilic adenoma, acidophilic
adenoma
 Ionising radiation-predisposing factor
 Composed of large epithelial cells Rare: 2.3% of benign
salivary tumors
 CLINICAL FEATURES
 Age: 50-80yrs
 M:F = 1:1/ slight female predilection
 Site: Parotid: 78%
 Submandibular gland: 9%
 Minor salivary glands: palate, buccal mucosa, tongue
 Presentation
 – firm, slow growing painless mass
 Occasionally-bilateral-multinodular oncocytic
hyperplasia(oncocytosis)
 GROSS FEATURES

 – well circumscribed, Encapsulated

 – Homogeneous, smooth
 – Orange/rust colour
 HISTOPATHOLOGY
 – Cords of uniform cells and thin
fibrous stroma
 – Large polyhedral cells
 – Distinct cell membrane
 – with centrally located nuclei
which may vary from small,
hyperchromatic- large, vesicular
 Granular, eosinophilic cytoplasm
(Mitochondrial hyperplasia).
 sometimes clear cytoplasm
 Oncocytic cystadenoma
 Clear cell oncocytoma
 ELECTRON MICROSCOPY
 – Mitochondrial hyperplasia
 – 60% of cell volume
 TREATMENT

 Surgical excision
 Minor salivary glands- excision of tumour along with small
margin of normal tissue
 Malignant transformation- malignant oncocytoma/ oncocytic
carcinoma
Monomorphic adenoma

Basal cell, canalicular, sebaceous,

glycogen-rich, clear cell
 BASAL CELL ADENOMA
 Kleinsasser and Klein (1967)-first reported
 Basal cell accounts for 1-2% of all salivary gland neoplasms
 Combination of salivary duct epithelium and myoepithelial
cells
 Membranous basal cell adenoma-hereditary often occurs
with skin appendage tumours (dermal cylindomas and
trichoepitheliomas)
 Arise denovo
 CLINICAL FEATURES
 Age: 6th decade
 M:F = approximately 1:2
 Caucasian > African American
 Site: Most common in parotid (superficial lobe), 2nd minor
glands
 Presentation: Firm, slowly growing freely movable mass
 May be bilateral
 HISTOPATHOLOGY
 Encapsulated/ well circumscribed
 Cut surface: homogenous with gray to brown in colour and
may have cystic areas
 Two cells:
1. small cell with scanty cytoplasm and round deeply
basophilic nucleus
2. large cell with eosinophilic cytoplasm and ovoid pale
staining nucleus
 Based on morphologic appearance:
o Solid
o Tubular
o Trabecular
o Membranous
 SOLID
 – Most common
 – Solid nests of tumor cells
 Sharply demarcated from
connective tissue by basement
membrane
 –Cuboidal to columnar peripheral
cells hyperchromatic, round nuclei, indistinct
cytoplasm and nuclear palisading
 Central cells have pale staining
nuclei and occasionally form eddies/keratin pearls.
 – Scant fibrous stroma
 TRABECULAR

 –narrow cordlike epithelial

strands and are interconnected
with one other
 – Vascular stroma
 TUBULAR
 -formation of multiple small round
duct like structures
 Lined by inner cuboidal ductal
cells and outer basaloid cells
 – Vascular stroma
 MEMBRANOUS
 – Thick eosinophilic hyaline
membranes (reduplicated basement
membrane) surrounding nests of
tumor cells
 – “jigsaw-puzzle” appearance
 TREATMENT
 Complete surgical removal
 Membranous- 25-37% recurrence
 Malignant transformation: BASAL CELL
ADENOCARCINOMA
CANALICULAR ADENOMA
 Uncommon neoplasm
 Clinical features:
 Age: 4-7th decade
 Sex: F:M – 1.8:1
 Site: Most common in minor salivary glands of the
upper lip (74%), buccal mucosa
 Presentation: slow growing painless submucosal mass
 Normal / blue colour mucosa- DD mucoceles
 HISTOPATHOLOGY
 – Well-circumscribed
 – Multiple foci
 – Tubular structures line by
columnar or cuboidal cells with
basophilic nuclei.
Party wall appearance
cystic spaces are usually filled with
an eosinophilic coagulum.
 – Vascular stroma
 MYOEPITHELIOMA

 <1% of all salivary neoplasms

 Age:3rd-6th decades
 Sex: M=F
 Site: Parotid gland , Palate
 Presentation: Asymptomatic mass
 HISTOPATHOLOGY

 – Spindle cell
 – Plasmacytoid cell
 Uniform, central nuclei
 Eosinophilic granular or fibrillar cytoplasm
DUCTAL PAPILLOMAS
 Group of three rare benign papillary salivary gland tumours
 Arise from salivary gland ductal system
 Sialadenoma papilliferum
 Arise from minor salivary glands – palate
 Age: older
 M:F= 1.5:1
 Presentation:
 Exophytic papillary surface growth
and endophytic
 Histopathology:
 Multiple exophytic papillary
Projections-stratified squamous epithelium
 Multiple ductal lumina- lined by
 Luminal layer-tall columnar cells
 Basilar layer- smaller cuboidal cells
 Stroma: Inflammatory infiltrate of plasma cells, lymphocytes and neutrophils
 Inverted ductal papilloma
 Age: adults
 Site: minor salivary glands
(lower lip, mandibular vestibule)
 No gender predilection
 Presentation:
 submucosal swelling
 Histopathology:
 Proliferation of squamoid
epithelium with multiple
thick bulbous papillary projections that fill the ductal lumen
 Mucus producing cells
 Intraductal papilloma

 Age: adults
 Site: minor salivary glands
lower lip>upperlip>palate and
buccal mucosa
 No gender predilection
 Presentation:
 submucosal swelling
 Histopathology:
 Dilated, unicystic structure that is located below the mucosal surface
 Lined by single or double row of cuboidal or columnar epithelium
 PAPILLARY CYSTADENOMA
WHO: a tumour that resembles Warthin’s tumour but without
lymphoid elements, constituting multiple papillary
projections and a greater variety of epithelial lining cells.
 Mucous cells- mucinous cystadenoma
Clinical features:
 Age: Older, 8th decade
 Sex: Female
 Site: Major and minor glands
 Presentation: Slow growing painless swelling slightly
compressible
 HISTOPATHOLOGY
 Cystic lining 1-3 cell layer thickness: tall columnar
cells/ cuboidal cells sometimes mucous / oncocytic
cells
 Limited papillary growth
Stroma:
 Dense connective tissue with scattered inflammatory
cells
 Eosinophilic secretions-stroma
 PAPILLARY CYSTADENOMA

MUCINOUS CYSTADENOMA
MALIGNANT TUMOURS
FEATURES OF MALIGNANCY
 Induration
 Fixed to overlying skin/mucosa
 Ulceration of skin/mucosa
 Rapid growth
 Short duration
 Pain, often severe
 Facial N.palsy
ADENOID CYSTIC CARCINOMA
 Cylindroma, adenoid cystic carcinoma, adenocystic basal
cell carcinoma, pseudoadenomatous basal cell carcinoma,
basaloid mixed tumour
 Slow growing but aggressive neoplasm with remarkable
capacity of recurrence
 5th most common malignant salivary tumour
CLINICAL FEATURES
 Age: 5-6th decade
 Sex: Female predilection
 Site: Parotid, submaxillary and accessory glands in palate
and tongue
 Presentation: swelling
 Early local pain
 Fixation to deeper tissues
 Local invasion
 PERINEURAL INVASION
 HISTOPATHOLOGY
 Composed of myoepithelial cells and ductal cells
Cribriform: Basaloid epithelial nests that form multiple
cystlike patterns-swiss cheese/honey comb appearance
 Tumour cells surrounded by hyaline material
Tubular pattern:
 Small ducts/tubular structures that are lined by
stratified cuboidal epithelium
Solid pattern:
 Solid groups of cuboidal cells with little tendency
towards duct/cyst formation. High recurrence rate
Dedifferentiation of adenoid cystic
carcinoma:

 Dedifferentiated adenoid cystic carcinomas are a recently

defined, rare variant of adenoid cystic carcinomas
characterized histologically by two components: conventional
low-grade adenoid cystic carcinoma and high-grade
"dedifferentiated" carcinoma.
 TREATMENT

 Surgical excision
 Radiotherapy
 ACINIC CELL CARCINOMA
 Serous cell adenoma, adenocarcinoma
 6% of all salivary gland neoplasms
 Malignant tumour- cells show serous acinar differentiation.
 CLINICAL FEATURES
 Age : 2nd-7th decades
 Gender: Female predilection
 Site: Parotid gland, minor salivary glands
 Presentation: Slow growing, asymptomatic
 Finger like extension into adjacent tissues
 LN involvement is common – pain
Lingual nerve
 HISTOPATHOLOGY
 Well circumscribed
 Serous acinar cell- granular basophilic cytoplasm, round darkly
stained eccentric nucleus
Solid:
 Numerous well-differentiated acinar cells
Microcystic :
 Multiple small cystic spaces containing mucinous/ eosinophilic
material
Papillary-cystic: large cystic areas are formed that are lined by
epithelium-papillary projections
Follicular: similar to thyroid tissue
HISTOPATHOLOGY
 TREATMENT

 Aggressive resection
 Radiotherapy
 Metastases-10-15%
MUCOEPIDERMOID CARCINOMA
 MC malignant tumor of salivary gland
 MC malignant tumor to occur in parotid
 Children-most common salivary gland tumor
 Arises from excretory ducts of glands
 Presence of mucin producing cells, squamous cells of
ducts or acini.
 CLINICAL FEATURES
 Age: 2nd – 7th decade
 Sex: F > M
 Presentation: Slow growing
 Asymptomatic. Pain/facial
palsy-high grade tumours
 GROSS PATHOLOGY
 Relatively well
circumscribed
 Partially encapsulated
 Cut surface: Firm,
pinkish/yellowish tan
 Cystic spaces- mucoid
material
 HISTOPATHOLOGY
 Mucous cells
 Epidermoid cells
 Intermediate cells
 Columnar/clear cells
 Mucous cells: relatively large cells pale foamy
cytoplasm
 Intermediate cells- smaller than squamous cells and
large than basal cells
 Epidermoid cells- squamoid in appearence
 HISTOPATHOLOGY
Low grade Intermediate grade High grade

Amount of cyst Prominent cyst Cyst formation occurs Solid islands of squamous
formation formation but less prominent- and intermediate cells
low grade tumours Cyst formation<20%
Degree of cytological Minimal cellular Cellular atypia may or Considerable
atypia atypia may not be observed pleomorphism and
mitotic activity
Relative number of Relatively high Intermediate cells- Mucous producing cells
mucous cells, proportion of predominate may be infrequent,
epidermoid cells and mucous cells predominantly squamous
intermediate cells cells
Mucoepidermoid carcinoma: Grading parameters and
point values
Parameter Point value
Intracystic component < 20% +2
Neural invasion +2
Necrosis +3
Four or mitoses per 10 HPF +3
Anaplasia present +4

Grade Total point score

Low 0-4
Intermediate 5-6
High 7-14
 Variants
 Sclerosing mucoepidermoid carcinoma: intense central
sclerosis

Tumour infarction Extravasation of mucous

Reactive fibrosis

Sclerosis
 Intraosseous MEC
 May originate within jaws
Dentigenous cyst
 Thought to arise from malignant transformation of odontogenic cysts

 Asymptomatic radiolucent lesion

 Mandible > maxilla

Mucus call in to serous cells

 TREATMENT
 Low grade can be managed similar to that of pleomorphic

adenoma. Positive margin- post op RT

 Intermediate grade- Total conservative parotidectomy

 High grade- more aggressive treatment. Total parotidectomy

with resection of involved facial nerve branch and nerve

grafting

 Neck dissection, full course of post op RT

 POLYMORPHOUS
LOW-GRADE ADENOCARCINOMA

 Evans and Batsakis coined the term

 Lobular carcinoma
 Terminal duct carcinoma
 Papillary carcinoma
 Trabecular carcinoma
 CLINICAL FEATURES
 Age: 6th-8th decade

 Sex: Female predilection

 Site: Minor salivary glands. Palate>Upper lip >

Buccal mucosa

 Presentation: Slow growing, painless mass

 Can erode/infiltrate underlying bone

Perineurial invasion
 HISTOPATHOLOGY
 Different growth patterns: solid
patterns/ cords, ducts or large
cystic spaces
 Cuboidal to columnar cells with
indistinct cell borders and pale
to eosinophilic cytoplasm
 Nuclei: round,ovoid/spindled,
pale staining
 Stroma: mucoid/hyalinised
 Perineural invasion
 TREATMENT
 Wide surgical excision
 Metastasis to lymph nodes - 10%
 Recurrence: 9-17%
 Necrosis

SALIVARY DUCT CARCINOMA

 Rare, high grade malignancy ≈ expanded
salivary glands
 Clinical features:
 Age: 7-8th decade
 Sex: Male
 Site: Parotid
 Presentation: swelling
 Facial nerve dysfunction or paralysis
 HISTOPATHOLOGICAL FEATURES
 Epithelium:
 Solid pattern/cribriform
 Cuboidal and polygonal cells with moderate eosinophilic material
 Stroma: may be hyalinised
 TREATMENT

 High grade: Complete local excision with radical neck

dissection and post radiotherapy
TUMOUR LIKE LESIONS:

 Sialadenosis
 Oncocytosis
 Necrotising sialometaplasia
 Benign lymphepithelial lesion
 Salivary gland cysts
 Chronic sclerosing sialadenitis of submandibular gland
 Cystic lymphoid hyperplasia in AIDS
SIALADENOSIS ( SIALOSIS )
 Unusual non-neoplastic, non inflammatory disorder

characterized by the salivary gland enlargement

 Frequently associated with Endocrine , Nutritional , Neurogenic

medication.
Atrophy of
myoepithelial
cell
Impaired exocitosis
of serous or
mucous acini
CONDITIONS ASSOCIATED WITH SIALADENOSIS

 Hormonal sialadenosis
 Sex hormonal sialadenosis
 Diabetic sialadenosis
 Thyroid sialadenosis
 Hypophyseal and adrenal cortical disorders

 Neurohumoral sialadenosis
 Peripheral neurohumoral sialadenosis
 Central neurogenous sialadenosis
CONDITIONS ASSOCIATED WITH SIALADENOSIS

 Dysenzymatic sialadenosis
 Pancreatogenic sialadenosis
 Nephrogenic sialadenosis
 Dysproteinemic sialadenosis

 Malnutritional sialadenosis
 Mucoviscidosis
 Drug-induced sialadenosis
 CLINICAL FEATURES
 Age: 4th decade or beyond
 Site : parotid gland
 Swelling slowly enlarges
 May or may not be painful
 Usually bilateral
 Decreased salivary secretion may occur
 “ leafless tree ” pattern

Sialography
 HISTOPATHOLOGICAL FEATURES
 Hypertrophy of the acinar cells.
Diameter-increases 2-3 times
 Nuclei are displaced to the cell base
and the cytoplasm is - engorged
Zymogen granules
 Inflammatory cells-absent
 Diabetes or alcoholism – acinar
atrophy and fatty infiltration
TREATMENT
 Control of the underlying cause
 Partial parotidectomy
 BENIGN LYMPHOEPITHELIAL LESION

 Mikulicz disease
 Mikulicz syndrome, dacryosialadenopathia, mikulicz-
Radecki syndrome, mikulicz-sjogren syndrome, von
mikulicz syndrome
 Chronic condition chracterised by- abnormal enlargement
of the salivary and lacrimal glands
 Etiology :
 Unknown
 Suspected to be an autoimmune disorder
IGg
CLINICAL FEATURES
 Age: Middle adults
 Sex: Female
 Site: Lacrimal glands, salivary
glands
 Presentation: Xerostomia,
Xerophthalmia, lacrimal gland
and parotid gland enlargement
HISTOPATHOLOGICAL FEATURES
 Lymphoid infiltration of
salivary gland tissue
 Epithelial cells islands: cellular
proliferation, loss of polarity
 Epimyoepithelial islands
 Hyaline material
 D.D: Lymphoepithelial
tumour, metastatic carcinoma,
chronic sialadenitis, warthins
tumour and uveoparotitis
 TREATMENT
 Symptomatic treatment:
 Artificial tears
 Artificial saliva
 Soft moist diet

 Complications: malignant
lymphoepithelial lesion
NECROTIZING SIALOMETAPLASIA
 Uncommon

 Locally destructive inflammatory condition of the salivary gland

 Mimics a malignant process – clinically and microscopically

 Result of ischemia of the salivary tissue that lead to the infarction

 Tobacco- possible etiologic risk factor

PREDISPOSING FACTORS
 Traumatic injuries

 Dental injection

 Iii fitting dentures

 Upper respiratory infections

 Adjacent tumors

 Previous surgery
 CLINICAL FEATURES
 Age: Any age ( mean age 46 yrs )
 Sex: Males are often effected than females
 Site: Most commonly – Palatal salivary gland (posterior palate)
 Hard palate is commonly effected than SP
 Unilateral or bilateral or midline
 Major salivary gland also effected
 Presentation: Non ulcerated swelling often associated with pain
and paresthesia
 CLINICAL FEATURES

 With in 2 – 3 weeks – necrotic

tissue sloughs out, leaving a crater
like ulcer
 Measuring about – less than 1 cm
to more than 5 cm in diameter
 “ A part of my palate fall out ”
 Destruction of the underlying
palatal bone.
HISTOPATHOLOGICAL FEATURES
 Acinar necrosis in early lesion
 Squamous metaplasia of the
salivary duct
 Mucous cells are necrotic
 Lobular architecture is still
preserved
 Liberation of the mucin and
inflammatory cells
HISTOPATHOLOGICAL FEATURES
 Squamous metaplasia are the
striking feature
 Easily misdiagnosed as
Squamous cell carcinoma or
Mucoepidermoid carcinoma
 Associated with Pseudo
epitheliomatous hyperplasia of
the overlying epithelium
 TREATMENT
 Clinical presentation

 Biopsy

 No specific treatment

 Lesion resolve on its own

 Average healing period – 5 to 6 weeks

 SJOGREN’S SYNDROME
 It is chronic, systemic auto immune disorders
 Characterized – lymphocytic infiltration and
acinar destruction of lacrimal and salivary
gland
 Xerostomia – dry mouth
 Xerophthalmia – dry eyes
 Both Xerostomia + Xerophthalmia =
Sicca syndrome
 CLASSIFICATION
Primary Secondary
Primary sjogren’s syndrome/sicca
complex
Sicca syndrome alone , no other
auto immune disorders
Secondary sjogren’s syndrome
Sicca syndrome + auto immune
diseases ( SLE , Systemic sclerosis ,
Rheumatoid arthritis )
 CAUSES
 Genetic, hormonal, infectious and immunologic
 Histo compatibility antigens ( HLA‟S) – greater
frequency
 HLA – DRw52 is associated with both the form
 HLA – B8 and HLA – DR 3 – increased frequency in the
primary form
 EBV and Human T cell lymph tropic virus
 MANIFESTATION
 Glandular ( Exocrine gland )

 Extra glandular
 Glandular ( Exocrine gland )
 Salivary gland – Xerostomia

 Lacrimal gland – Xerophthalmia

 Skin – Xeroderma

 Respiratory tract –

Nasal dryness ,
sinusitis
 Pharynx and GI tract – Dysphagia ,
atrophic gastritis
 Reproductive system – Vaginal dryness
 CLINICAL FEATURES
 Age: Middle aged adults

 Sex: Females

 Oral manifestation
o Xerostomia
o Saliva appear frothy
o Difficulty in swallowing
o Altered taste
o Difficulty in wearing denture
 Tongue – fissured and atrophy of the
papillae
 Mucosa – red and tender
 Secondary candidiasis
 Denture sore mouth and angular chelitis
 Diffuse, firm enlargement of the salivary
gland
 Swelling – bilaterally
 Non painful or slightly tender and may be
intermittent or persistent in nature
 SAILOGRAPHIC EXAMINATION
 Punctuate sialectasia and
lack of normal arborization
of the ductal system
 „Cherry blossom‟ / “
Fruit – laden branchless
tree ”
KERATO CONJUNCTIVITIS SICCA
 Reduced tear production- lacrimal gland

 Vision – blurred, aching pain

 Confirm the decreased tear secretion - Schirmer

test

 Schirmer test – measuring the length of wetting of

the filter paper

 Values below – 5mm --- 5 minute period

 Positive for Rose Bengal staining of cornea or

conjunctiva

 Higher values – kerato conjunctivitis Sicca

 Value from 0 – 2 mm – strong confirm a dry – eye

state.
HISTOPATHOLOGICAL FEATURES
 Three types:
1. Lymphocytic infiltration
– around intra lobular
ducts
2. Proliferation of ductal
epithelium and
myoepithelium -
Epimyoepithelial islands
3. Lymphocytic infiltration
is accompanied by
acinar atrophy
Advanced cases –
 sheets of lymphoid cells surrounding epimyoepithelial

islands

 Replacing entire salivary gland lobules

 Lymphoid cells consists of B and T lymphocytes

 Plasma cells and macrophages also seen

LABORATORY INVESTIGATIONS
 Erythrocytic sedimentation rate – high

 Ig G ( serum ) --- elevated

 Positive Rheumatoid factor

 Nuclear antibodies – anti – SS – A and Anti – SS – B ----

frequently found
 Biopsy – labial salivary gland biopsy

 More than one focus 50 or more cells with in a 4

mm 2 area of glandular tissue is considered

supportive of the diagnosis of Sjogren’s
syndrome
 TREATMENT
 Supportive

 Dry eyes ---- artificial tears

 Artificial saliva

 Sugar less candy or gum

 Oral hygiene products -- lactoperoxidase, lysozyme

and cevimeline

 Sialogogues -- pilocarpine

 Antifungal therapy
 ONCOCYTOSIS
 Reactive process characterised by focal replacement of

normal glandular tissue with enlarged eosinophilic

epithelial cells with granular cytoplasm

 Age: older

 Site: parotid
 HISTOPATHOLOGY
 Enlarged eosinophilic epithelial cells – sheets, trabecular/

ductlike
THANK YOU