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Februray 29, 2009

Salivary Glands
Classification, General Considerations
&
Tumors Like Conditions
By Louay Jaber DDS, MSc, MSD, PhD
The Normal Salivary Gland


The system is comprised of
major & minor salivary glands





Major: Parotid, submandibular &
sublingual.
Minor:

They produce the fluid that
constitute oral saliva




Parotid: serous
Submandibular: serous & mucous
Sublingual: mucous & serous





Palate: mucous
Tongue: mucous & serous
Lip: mucous
Buccal mucosa: mucous

Oral
mucosa

Acinus

Intercalaetd-Striated-Excretory
“ducts”
The Normal Salivary Gland (Cont.)
“Parotid gland”

Lymph node
Serous Acini
& striated duct

Facial nerve
The Normal Salivary Gland (Cont.)
“Submandibular, sublingual & minor glands”

Submandibular

Sublingual

Minor
Mucocele
70% in the lower lip
 The remainders




floor of the mouth, tongue & buccal
mucosa

Third decades of life
 Men > women (slight)
 Small dome-shaped swelling
 Size 0.2-1.0 cm
 Mucoceles of the floor of the
mouth can be a large size
(several centimeters-Ranula)


Mucocele

Ranula
Mucocele







Pts might report a
fluctuation in size related to
meals or rupture
They are generally soft &
fluctuant (older becomes
firmer)
They are painless
They develop rapidly within
hours to days

Ruptured mucocele

Mucocele
Mucocele
Microscopically
Pool of mucus



It is a rounded pool of mucus
within fibrous connective tissue



Inflammatory reaction
(Macrophages that contain
phagocytized mucus)
Phagocytic macrophages
Mucus Retention Cyst


Etiology:
It results from obstruction of salivary
flow because of sialolith, periductal
scar or impinging tumor



Clinical features:
it is commonly found in the upper lip,
palate, cheek and floor of the mouth.
It represents asymptomatic swelling

Microscopically
 Retention cyst: Epithelial-lined
fibrous tissue wall surrounds the
mucus pool


Little or no inflammatory reaction (no
epithelial rupture

Cuboidal epithelium
Ranula





It is a clincial term that includes mucus extravasation
phenomenon and mucus retention cyst
Occur specifically in the floor of t he mouth
Etiology:


Trauma & ductal obstruction




Clinical features:




Sialolith: represents precipitation of calcium salts
around the central nidus of cellular debris

it is fluctuant, unilateral soft tissue mass in the floor of the mouth

Histopathology:


It is similar to mucus retention cyst
Necrotizing Sialometaplasia









Clinically
It is a reactive inflammatory
condition of the salivary glands
Average age is 46 years
Male predominence 2:1
Palatal location preference
Deep crater-like ulcer, develops
rapidly & slow to heal
Size 1-5 cm.
Unilateral ulcer of necrotizing sialometaplasia
Necrotizing Sialometaplasia


Pathogenesis: Ischemic
necrosis or infarction







Traumatic injury
Dental injection
Denture use
Adjacent tumor & cyst
Surgery
Upper respiratory
infection or allergy

Swelling but no ulceration of necrotizing sialometaplasia
Necrotizing Sialometaplasia


Histologically
The principle
characteristics are:








Lobular coagulative
necrosis of acini
Squamous metaplasia of
ducts
Pseudoepitheliomatous
hyperplasia
inflammation

Acini necrosis

Necrotizing sialometaplasia
Necrotizing Sialometaplasia

Necrotic mucous acini &
mild inflammatory infiltrate

Squamous metaplasia (ducts)
Infectious Conditions


Mumps:
 It is an infectious , acute viral sialadenitis primarily
affected the parotid glands
 It is the most common salivary gland diseases
 Etiology:
 The causative agent is a paramyxovirus
 2-3 weeks incubation period
 Transmission by direct contact with salivary droplets
Mumps


Clinical features:
 Fever
 Malaise
 Headache
 Chills
 Preauricular pain
 Parotid swelling
 Male = female
 Young adults & children
Mumps


Complications:
 Serious complication in adults can occur:
 Oophoritis
 Orchitis
 Widspread involvement can include
 Liver
 Pancreas
 Kindney
 Nervous system
Mumps


Differential diagnosis
 Bacterial infection (suppurative parotitis)
 Salivary calculi
 Lymphoma
 Lymphoepithelial lesion
 Metabolic diseases
Mumps


Treatment & Prognosis
 Symptomatic therapy
 Bed rest
 Analgesics
 Corticosteroids (variable success)
 Vaccination is now available
Metabolic Conditions
Sialadenosis



It is non-neoplastic & non-inflammatory salivary gland
enlargement
 It is related to metabotic factor or
secretory dysfunction
Painless bilateral swellings
Peak incidence: 5th & 6th decades of life



Slight female predominence



Swelling develops slowly, painless & accompanied by
decreasing salivary secretion




Metabolic Conditions
Sialadenosis


It is usually associated
with systemic
conditions:







Diabetes mellitus
Malnutrition
Liver cirrhosis (Chronic
Alcoholism)
Hyperlipidemia
Acromegaly
Enlargement of parotid associated with
chronic alcoholism & liver cirrhosis
Metabolic Conditions
Sialadenosis
Microscopically


As the disease persistsAtrophy of the paranchymal
tissue but compensatory
increase in the amount of
adipose tissue



Inflammatory cell infiltrates
are absent

Atrophy of parotid parenchymal tissue &
increase of intraglandular fat
Sjögren Syndrome


It is the expression of an autoimmune process that principally
results in
 Rheumatoid arthritis
 Dry eyes (keratoconjunctivitis sicca)
 Dry mouth (xerostomia)
 Lymphocytic replacement of lacrimal
and salivary glands
Sjögren Syndrome




Clinical features:
 Peak age: 50 yo
 Parotid gland enlargment
Treatment:
 Artificial saliva and tears & preventive oral measures
Sjögren Syndrome

Focal aggregates of lymphocytes, periductal lymphocytes & dilated ducts
Mixed Tumors
“Pleomorphic Adenoma”


It is the most common benign neoplasm
of salivary glands origin



It represents 45-74% of all salivary gland
tumors



Slow growing & asymptomatic,



Average age is about 43 yo.



Recurrent lesion occurs as multiple
nodules & are less mobile than initial
lesion.
Mixed Tumors
“Pleomorphic Adenoma”


CT revealed a mixed tumor
medial to the mandibular
ramus



It has prominent cartilagenous
& osseous elements that led
initially to diagnosis of
osteochondroma
Mixed Tumors
“Pleomorphic Adenoma”


The most common intraoral site is
the palate followed by the upper
lip & buccal mucosa



Mobility is limited for palatal
tumors.



Large intraoral tumors are
susceptible to trauma
Mixed Tumors
“Pleomorphic Adenoma”

Submandibular
Small glistening
capsular surface


Gross finding: It is
irregular round to ovoid
mass & well defined
borders
Parotid
Homogeneous tan
or tan white surface
Mixed Tumors
“Pleomorphic Adenoma”

Gross findings
Translucent central zone
represents myxochondroid
tissue

The presence of multiple
individual nodules are typical
of recurrent mixed tumor
Mixed Tumors
“Pleomorphic Adenoma”
Microscopic findings


Composed of epithelial
& mesenchymal like
tissue



Present or absent of
fibrous capsule
Mixed Tumors
“Pleomorphic Adenoma”
Cystic
degeneration

Prominent osseous
differentiation in
mixed tumor

Epithelial cell in
mixed tumor

Cytokeratin
immunoteactivity
in epithelial cells
Mixed Tumors
“Pleomorphic Adenoma”

Microscopic findings


In the absence of surgical
intervention, viable epithelial cells
within necrotic tissue suggest a
malignant transformation



Rarely tumor cells are seen within
vascular spaces
Mixed Tumor
“Treatment”


Parotidectomy & excision of the scar tissue with
preservation of the facial nerve are recommended
(specially recurrent)



Long term follow up is recommended more than 5 years



The risk of malignant degeneration increases with time



Radiotherapy has been found by some investigators to be
useful in some recurrent mixed tumor
Carcinoma Ex-Mixed Tumor
“Clinical Features”


It arises from a benign mixed tumor (diagnosis requires
identification of mixed tumor)



20% of patients had previous operation for mixed tumor



The risk for malignant transformation correlates with the
duration of mixed tumor



Painless mass or sometimes associated with facial nerve
pain or palsy



Tumor is freely movable or sometime fixed to underlying
tissue (especially with recurrent tumors)
Carcinoma Ex-Mixed Tumor
“Microscopic Findings”

Capsular
invasion

Myxochondoid bening elements &
carcinomatous elements
Carcinoma Ex-Mixed tumor
“Treatment”


38-53% develop recurrence



Distant metastasis to lung, bone, brain, liver &
subcutaneous tissue



Radiotherapy alone has proven ineffective, although
it may have a beneficial role when combined with
surgery
Basal Cell Adenoma




It is composed of cells
predominantly of one type
Basal cell adenoma:
 Occurs mainly in parotid
 Slow growing & painless
 Can be multinodular
 Age 35-80
 Male predominence
Well circumscribed mass near
the inferior pole of the parotid
Basal Cell Adenoma

Solid

Trabecular

Solid
Basal Cell Adenoma
Immunostaining for cytokeratin

Histology:
Ultrastructure shows ductal cells
Basal Cell Adenoma
Basal cell adenoma usually
lack cribriform pattern

Histology:

Adenoid cystic carcinoma with
clear cytoplasm & angular nuclei
Basal Cell Adenoma
 Treatment & prognosis:

Conservative surgical
excision including a margin
of normal uninvolved tissue
 Prognosis is good and
recurrence rate is so low


Small cells in the periphery of the epithelial islands
And larger cells adjacent to the tumor islands
Malignant Epithelial Tumors
“Mucoepidermoid Carcinoma”


It is the most common
malignant salivary
glands tumor



It represents 15.5% of all
benign & malignant
tumors at all sites
resemble a mucoceles.
Size varies from 1-12cm



Mucoepidermoid Carcinoma


It is believed to arise from
salivary duct system

Normal duct-lining epithelium
Neoplastic transformation
Mucoepidermoid Carcinoma


Ionizing radiation increases the risk for its developing



Occurrence:



7% Submandibular gland



1% Sublingual gland





45% Parotid gland

21% in the palate and 19% for the rest of the minor
salivary glands.

Mean age is about 47 years with the age range between
8 to 92 yo.



Women > men
Mucoepidermoid Carcinoma


Typically, it is a solitary painless mass



2/3 of pts. are asymptomatic


if growing rapidly, usually accompanied with pain &
mucosal ulceration, and sometimes a discharge of fluid
resemble abscess.



6 years average between onset & diagnosis (high grade
lesions demonstrate a 1.5-year interval before diagnosis).
Mucoepidermoid Carcinoma


According to cytologic features, it is divided into:
- Low
- Intermediate
- High grade types.
 All grades of this neoplasm are carcinomas and
have the potential to metastasize.
 They are epithelial mucin-producing tumor
Mucoepidermoid Carcinoma (Central)



This lesion may also arise centrally within the mandible
(Differential diagnosis: giant cell granuloma & odontogenic tumors).



Asymptomatic radiolucencies



Mandibule > maxilla



Third molar region is the
most likely to be involved
Mucoepidermoid Carcinoma (Central)
It arises from either:

Ectopic salivary gland tissue
Neoplastic transformation of epithelial lining of odontogenic cysts
Glandular odontogenic cyst

Mayer’s mucicarmine stain
highlights numerous mucus
cells in a dentigerous cyst
Mucoepidermoid Carcinoma


Treatment & Prognosis:
 low grade usually follow a benign course.
However, in several instances low grade lesions
have metastasize widely.
 High grade metastasize widely (60% of cases).
 Surgical, or surgery plus postoperative
radiotherapy (high grade)
 Central mucoepidermoid carcinoma is usually of
low grade (40% recurrence rate).
Adenoid Cystic Carcinoma
Oral mucosa overlying this palatal mucosa is ulcerated

Clinical Features


50-70% starts in the
minor salivary glands.



If major salivary gland
(parotid is the most affected)



Age: 5th and 7th decades

This tumor appears
deceptively well circumscribed
Adenoid Cystic Carcinoma


No gender predilection


(slight female predominance).



Unilocular mass



Firm on palpation



Occasional pain or tenderness



Slow growth rate



Bone invasion occurs



Lung metastasis
Sublingual gland tumor.
Adenoid Cystic Carcinoma


Treatment & prognosis:


Surgery is the treatment of choice



Radical resection is justified to obtain surgical
margins that are free of tumor



Multiple-agent chemotherapy showed some
promise for postoperative treatment



High recurrence rate
Acinic Cell Carcinoma
Clinical features
 Age: 5th to 6th decades of life
 No gender predilection
 It represents 14% of parotid

gland tumor
 9% of total salivary gland

carcinoma of all sites
 50% of cases, the clinical

appearance is a benign lesion
Acinic Cell Carcinoma





Usually less than 3 cm in
diameter
Pain
The interval between the
initial appearance &
treatment is 6 months to 5
years

The origin is the ductal cells
Acinic Cell Carcinoma


Treatment & prognosis:


Surgery is the preferred treatment



Seldom metastasize



Tendency to recur
Polymorphous Low-Grade Adenocarcinoma











It is considered to be low grade malignancy and low risk
of metastasis
Age: 5th to 8th decades
No gender predilection
Occurs in minor salivary
glands (palate)
Firm, non-ulcerated &
non tender
Size between 1-4 cm
Slow growth
Well circumscribed mass at the junction of the hard &
soft palate
Polymorphous Low-Grade Adenocarcinoma

Partially circumscribed but lack encapsulation
Polymorphous Low-Grade Adenocarcinoma
 Treatment & prognosis:



Conservative surgical excision
Prognosis is good
Carcinoma Ex-Mixed Tumor
“Microscopic Findings”
The carcinomatous elements appeared
separated from benign element
Apparent malignant transformation
Carcinomatous & benign Components of ExMixed


w
Mucoepidermoid Carcinoma


Fluctuant because of cyst formation

Mucin filled cystic spaces
Mucoepidermoid Carcinoma



Microscopic features:
The name is a contraction of
epidermoid and mucus-secreting carcinoma

A close association of mucous
& epidermoid cells

Mayer’s mucicarmine
hightlights the extracellular &
Intracytoplasmic mucin
Mucoepidermoid Carcinoma

Mucoepidermoid carcinoma incites
secondary lymphoid proliferation

The lymphoid response extends
along the periphery of the tumor
Mucoepidermoid Carcinoma
Low grade. Note
Intracystic spaces

Intermediate grade.
hyperchromatic nuclei
& several microcystic spaces

High grade
Focal necrosis
Epidermoid &
mucus cells

Epidermoid cells
solid & infiltrative

Central Mucoepidermoid
Carcinoma
Cyst
Solid & cystic
neoplastic area

Characteristic variety
of cell types
Adenoid Cystic Carcinoma

Tubular pattern in the top
& bottom. A cribriform pattern
in the center

Epithelial cells have a clear
Cytoplasm, poorly defined
border & irregular shaped nuclei

Immunoreactivity of the
tumor cells for cytokeratin
Adenoid Cystic Carcinoma

Mitotic figures

The tumor appears
well circumscribed

Myoepithelial &
ductal cells
Adenoid Cystic Carcinoma

Neural invasion

Comedo-type necrosis
Acinic Cell Carcinoma
 Well differentiated acinar cell
 Cytoplasmic granules.
 Slightly

basophilic cytoplasm
 Eccentricaly located nuclei

Acinar cells
Acinic Cell Carcinoma

Papillary cystic growth pattern
Follicular pattern
Acinic Cell Carcinoma

Cluster of neoplastic epithelial cells & numerous
electron dense cytoplasmic granules
Polymorphous Low-Grade Adenocarcinoma

The nuclei are round or ovoid
& have a slightly irregular contour

Tumor cells are often
concentrically arranged
October 11, 2005

Oral Pathology II
0701441
Connective Tissue Lesions
Connective Tissue Lesions


Fibrous lesions:
 Reactive hyperplasia: Fibrous hyperplasia or exuberant
proliferation of granulation tissue
 Peripheral fibroma
 Generalized gingival hyperplasia
 Denture induced fibrous hyperplasia
 Neoplasms: heterogeneous that form complex collection of
disease
 Myxoma
 Fibrosarcoma
Connective Tissue Lesions
“Fibrous Lesions”


Peripheral fibroma
 Etiology: Reactive (secondary to overexuberant repair)
 Origin: Connective tissue of the submucosa
 Clinical features:
 Predilection for young adults
 Female>male
 Location: commonly at the gingiva anterior to molars
 Similar in color to the surrounding tissue
Connective Tissue Lesions
“Fibrous Lesions”


Peripheral Odontogenic fibroma
Connective Tissue Lesions
“Fibrous Lesions”


Focal fibrous hyperplasia:
 It is common in frequently
traumatized area
Connective Tissue Lesions
“Fibrous Lesions”


Peripheral fibroma
 Histopathology:
 Focal fibrous hyperplasia: Highly collagenous and relatively
avascular
 Mild to moderate inflammatory cell infiltrate
 Subtypes:
 Peripheral ossifying fibroma
 Peripheral odontogenic fibroma
 Giant cell fibroma
 Differential diagnosis: Pyogenic granuloma & peripheral giant
cell granuloma
 Treatment: Local excision
Connective Tissue Lesions
“Fibrous Lesions”


Peripheral Ossifying Fibroma
Connective Tissue Lesions
“Fibrous Lesions”


Generalized gingival hyperplasia:
 Definition: Overgrowth of the gingiva
 Etiology:
 Non-specific: Response to chronic inflammation
associated with local factor
 Hormonal changes (imbalance)
 Drugs (Phenytoin, Cyclosporine, Nifidipine)
 Leukemia
Connective Tissue Lesions
“Fibrous Lesions”


Generalized gingival hyperplasia:


Clinical features: Increase in the bulk of free and attached gingiva.






Stippling is lost
Color: red to blue
Associated inflammation: non-specific factors & hormonal imbalance
appears more inflamed than drug induced hyperplasia

Histopathology:






Abundance in collagen
Increased number of fibroblasts
Various degree of chronic inflammation
Increased capillaries (hormonal)
Immature & atypical white blood cells with leukemic type
Connective Tissue Lesions
“Fibrous Lesions”


Gingival fibromatosis
Connective Tissue Lesions
“Fibrous Lesions”


Generalized gingival hyperplasia:



Treatment: Attentive oral hygiene is necessary
Gingivoplasty or gingivectomy in combination with prophylaxis
Connective Tissue Lesions
“Fibrous Lesions”


Denture-induced fibrous hyperplasia
 Etiology: Chronic trauma produced by an ill-fitting denture
 Clinical features: Occurs in the vestibular mucosa
 Overexuberant fibrous connective tissue reparative
response
 Painless folds of fibrous tissue
 Treatment: Surgical excision is usually required
Epulis Fissuratum
Connective Tissue Lesions
“Fibrous Lesions”


Neoplasms:
 Myxoma: Benign proliferation of spindle cells
 Clinical features: It is a soft neoplasms composed of
gelatinous material
 Slow growing
 Asymptomatic
 Location: Palate
 Occurs at any age

Soap bubble multilocular area
Connective Tissue Lesions
“Fibrous Lesions”


Myxoma:


Histopathology:
 Not encapsulated (may exhibit
infiltration into surrounding soft tissue)
 Dispersed stellate & spindle-shaped fibroblasts
 Loose myxoid stroma
Connective Tissue Lesions
“Fibrous Lesions”


Myxoma:
 Treatment: Surgical excision
 Recurrence is not uncommon
Pluripotential Mesenchymal Stem Cells
Connective Tissue Lesions
“Fibrous Lesions”


Fibrosarcoma: It is a malignant spindle
cell tumor showing interlacing fascicular
pattern
 Clinical features
 Can arise in bone
 Young adults most commonly affected
 It is considered as infiltrative neoplasms
Connective Tissue Lesions
“Fibrous Lesions”


Fibrosarcoma:
 Histopathology:
 Collagen sparse
 Frequent mitotic figures
 Ill defined periphery
Connective Tissue Lesions
“Fibrous Lesions”


Treatment of Fibrosarcoma


Wide surgical excision
 Recurrence is not uncommon
 Metastasis is infrequent
 5 years survival rate is 3050%
Vascular Lesion



Reactive & Congenital Lesions
Lymphangioma




Etiology:
 It is regarded as congenital lesion
 Appears within the first 2 decades of life
Clinical features:
 Painless nodular, vesicle like swelling
 Crepitant sound
 Tongue is the most common
intraoral site
Vascular Lesion


Histopathology:
 Endothelium-lined lymphatic channels
 Eosinophilic lymph that occasionally
include red blood cells
 Lymphatic channels directly adjacent
to overlying epithelium



Treatment: Surgical removal but because
of lack of encapsulation, recurrences are
common
Vascular lesion



Neoplasms:
Angiosarcoma
 It is a neoplasm of endothelial cell origin
 Scalp is the usual location
 The lesion consists of an unencapsulated
proliferation of endothelial cells enclosing
irregular luminal spaces
 It has an aggressive clinical course and
poor prognosis
Neural lesions



Reactive lesion:
Traumatic neuroma:
 Etiology: It is caused by injury of peripheral nerve
 Oral surgery procedure
 Local anesthetic injection
 Accident
 Clinical features:
 Pain
 Wide age range
 Mental foramen is the most common location
Neural lesion


Traumatic neuroma (Cont.)
 Histopathology:
 Bundles of nerves admixed
with dense collagenous fibrous
tissue
 Treatment: Surgical excision
Neural Lesion


Neoplasms:



Granular cell tumors
 Etiology: It is an uncommon benign tumor of unknown cause
 The granular cell that make this tumor is believed to originate
from Schwann cells
Clinical features:
 Wide age range
 Tongue is the most common location
 Uninflamed asymptomatic mass
 < 2 cm in diameter
 Overlying epithelium is intact


Neural lesion



Neoplasms:
Granular cell tumors
 Histopathologically:


Unencapsulated sheets of
large polygonal cells with pale
granular or grainy cytoplasm



Pseudoepitheliomatous hyperplasia





Treatment: Surgical removal
Neural lesion



Neoplasms:
Schwannoma:



Etiology: It is derived from schwann cells
Clinical features:
 It is an encapsulated submucosal mass
 Asymptomatic lump
 Occurs at any age
 Tongue is the most common location
 Bony lesion produce a well-defined
radiolucent lesion
 Slow growing but may undergoe
a sudden increase (hemorrhage)
Neural lesion



Neoplasms:
Schwannoma:
 Histopathology:
 Spindle cells either organized
(palisaded waves) or
haphazardly distributed
 Treatment: Surgical excision
Neural lesion



Neoplasms:
Neurofibroma:





It mat appear as solitary or multiple lesions
Etiology: - Solitary type is unknown
- Neurofibromatosis is inherited
Clinical features: Solitary type
 Uniflamed asymptomatic submucosal mass
 Location: Tongue, vestibule & buccal mucosa
Neural lesion
Neurofibroma
Neural lesion


Neurofibroma:


Clinical features: Neurofibromatosis:
 Multiple
 Café-au-lait macules
 Bone abnormalities (cortical erosion
or medullary resorption)
 Central nervous system changes
 Pain or parasthesia may be seen
 Malignant degeneration into
neurogenic sarcoma is seen in
5% to 15%
Neurofibromatosis

(JADA, 1988)
Neural lesion


Neurofibroma:


Histopathology:
 Spindle-shaped cells in connective
tissue matrix
 It may be well circumscribed or blended
into surrounding connective tissue
 Mast cells are scattered
 Immunohistochemistry with S-100 is a
useful tool to confirm diagnosis
 Treatment: Surgical excision for solitary lesion

Lack of encapsulation
Neural lesion


Malignant peripheral nerve sheet tumor
 The cell of origin is believed to be the schwann cells and
possibly other nerve sheath cells
 It appears as expansile mass (soft tissue)
 Asymptomatic
 Dilation of the mandibular canal (bone)
 Pain or parasthesia
Neural lesion


Malignant peripheral nerve sheet tumor
 Histopathologically:
 Abundant spindle cells
 Mitotic figures
 Nuclear pleomorphism
 Treatment: Wide surgical exicion
 Recurrence is common
 Metastases are frequently seen
Muscle Lesions


Neoplasms (Leiomyoma & leiomyosarcoma):





Smooth muscle neoplasms are relatively common
They may arise anywhere in the body

Leiomyoma








Leiomyomas are commonly arise in the
muscularis of the gut and uterus
Oral leiomyoma is slow growing &
asymptomatic submucosal masses
Appears in the tongue, hard palate
or buccal mucosa
Spindle cells
Appears at any age

Pterygo-mandibular space
Muscle Lesions


Leiomyoma
 Histopathology:
 Immunohistochemical demonstration of actin and
desmin protein expression can confirm diagnosis

Obvious vascular origin

Vascular leiomyoma

Limited & uniform proliferation
around each of the vascular spaces
Muscle Lesions



Neoplasms
Leiomyosarcoma








It is commonly arise in the retroperitoneum,
mesentery, or subcutaneous and deep tissue
of the limbs
It may appear at any age
Immunohistocemistry can be a valuable
diagnostic tool
Treatment: wide surgical excision
Metastasis is not uncommon
Blunt ended nuclei
Muscle Lesions


Rhabdomyoma:







Predilection for the soft tissues
of the head and neck
 Floor of the mouth, soft palate,
tongue & buccal mucosa
Mean age: 50 years (children to older adults)
Asymptomatic
Well defined submucosal mass Well demarcated but
unencapsulated
The neoplastic cells mimic their
normal counterpart (adult)
Large eosinophilic granular cell
with peripheral nuclei
Muscle Lesions


Rhabdomyosarcoma:






When occurs in head and neck is
primarily found in children
It is a rapidly growing mass
May cause pain and parasthesia
Common location: Tongue and soft palate
Muscle Lesions
Rhabdomyosarcoma


Histopathology:
 Embryonal type (children) consists
of primitive round cells in which
striations are rarely found
 Immunohistochemistry demonstrates
desmin, actin and myogenin
Muscle Lesions
Rhabdomyosarcoma


Treatment: Combination of surgery,
radiation and chemotherapy



Survival rate incraese from 10% to 70%
with this aggressive treatment approach
Fat Lesion


Lipoma:






Location: Buccal mucosa, tongue
& floor of the mouth
Asymptomatic, yellowish submucosal mass
Overlying epithelium is intact
Superficial blood vessels are usually evident
Fat Lesion


Lipoma:


Well circumscribed, lobulated mass
of mature fat cells
Fat Lesion


Lipomyosarcoma:






It is a lesion of adulthood
It may occur at any site
Slow growing (mistaken for a benign process)
Treatment: surgery or radiation
Prognosis is fair to good

Well differentiated

Myxoid type
Mumps




It is an acute viral sialadenitis affecting primarily the parotid
glands
Etiology & pathogenesis:



Paramyxovirus, incubation period is 2-3 weeks
Transmission is by direct contact with salivary droplets

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Salivary gland pathology

  • 1. Februray 29, 2009 Salivary Glands Classification, General Considerations & Tumors Like Conditions By Louay Jaber DDS, MSc, MSD, PhD
  • 2. The Normal Salivary Gland  The system is comprised of major & minor salivary glands    Major: Parotid, submandibular & sublingual. Minor: They produce the fluid that constitute oral saliva    Parotid: serous Submandibular: serous & mucous Sublingual: mucous & serous     Palate: mucous Tongue: mucous & serous Lip: mucous Buccal mucosa: mucous Oral mucosa Acinus Intercalaetd-Striated-Excretory “ducts”
  • 3. The Normal Salivary Gland (Cont.) “Parotid gland” Lymph node Serous Acini & striated duct Facial nerve
  • 4. The Normal Salivary Gland (Cont.) “Submandibular, sublingual & minor glands” Submandibular Sublingual Minor
  • 5. Mucocele 70% in the lower lip  The remainders   floor of the mouth, tongue & buccal mucosa Third decades of life  Men > women (slight)  Small dome-shaped swelling  Size 0.2-1.0 cm  Mucoceles of the floor of the mouth can be a large size (several centimeters-Ranula)  Mucocele Ranula
  • 6. Mucocele     Pts might report a fluctuation in size related to meals or rupture They are generally soft & fluctuant (older becomes firmer) They are painless They develop rapidly within hours to days Ruptured mucocele Mucocele
  • 7. Mucocele Microscopically Pool of mucus  It is a rounded pool of mucus within fibrous connective tissue  Inflammatory reaction (Macrophages that contain phagocytized mucus) Phagocytic macrophages
  • 8. Mucus Retention Cyst  Etiology: It results from obstruction of salivary flow because of sialolith, periductal scar or impinging tumor  Clinical features: it is commonly found in the upper lip, palate, cheek and floor of the mouth. It represents asymptomatic swelling Microscopically  Retention cyst: Epithelial-lined fibrous tissue wall surrounds the mucus pool  Little or no inflammatory reaction (no epithelial rupture Cuboidal epithelium
  • 9. Ranula    It is a clincial term that includes mucus extravasation phenomenon and mucus retention cyst Occur specifically in the floor of t he mouth Etiology:  Trauma & ductal obstruction   Clinical features:   Sialolith: represents precipitation of calcium salts around the central nidus of cellular debris it is fluctuant, unilateral soft tissue mass in the floor of the mouth Histopathology:  It is similar to mucus retention cyst
  • 10. Necrotizing Sialometaplasia       Clinically It is a reactive inflammatory condition of the salivary glands Average age is 46 years Male predominence 2:1 Palatal location preference Deep crater-like ulcer, develops rapidly & slow to heal Size 1-5 cm. Unilateral ulcer of necrotizing sialometaplasia
  • 11. Necrotizing Sialometaplasia  Pathogenesis: Ischemic necrosis or infarction       Traumatic injury Dental injection Denture use Adjacent tumor & cyst Surgery Upper respiratory infection or allergy Swelling but no ulceration of necrotizing sialometaplasia
  • 12. Necrotizing Sialometaplasia  Histologically The principle characteristics are:     Lobular coagulative necrosis of acini Squamous metaplasia of ducts Pseudoepitheliomatous hyperplasia inflammation Acini necrosis Necrotizing sialometaplasia
  • 13. Necrotizing Sialometaplasia Necrotic mucous acini & mild inflammatory infiltrate Squamous metaplasia (ducts)
  • 14. Infectious Conditions  Mumps:  It is an infectious , acute viral sialadenitis primarily affected the parotid glands  It is the most common salivary gland diseases  Etiology:  The causative agent is a paramyxovirus  2-3 weeks incubation period  Transmission by direct contact with salivary droplets
  • 15. Mumps  Clinical features:  Fever  Malaise  Headache  Chills  Preauricular pain  Parotid swelling  Male = female  Young adults & children
  • 16. Mumps  Complications:  Serious complication in adults can occur:  Oophoritis  Orchitis  Widspread involvement can include  Liver  Pancreas  Kindney  Nervous system
  • 17. Mumps  Differential diagnosis  Bacterial infection (suppurative parotitis)  Salivary calculi  Lymphoma  Lymphoepithelial lesion  Metabolic diseases
  • 18. Mumps  Treatment & Prognosis  Symptomatic therapy  Bed rest  Analgesics  Corticosteroids (variable success)  Vaccination is now available
  • 19. Metabolic Conditions Sialadenosis  It is non-neoplastic & non-inflammatory salivary gland enlargement  It is related to metabotic factor or secretory dysfunction Painless bilateral swellings Peak incidence: 5th & 6th decades of life  Slight female predominence  Swelling develops slowly, painless & accompanied by decreasing salivary secretion  
  • 20. Metabolic Conditions Sialadenosis  It is usually associated with systemic conditions:      Diabetes mellitus Malnutrition Liver cirrhosis (Chronic Alcoholism) Hyperlipidemia Acromegaly Enlargement of parotid associated with chronic alcoholism & liver cirrhosis
  • 21. Metabolic Conditions Sialadenosis Microscopically  As the disease persistsAtrophy of the paranchymal tissue but compensatory increase in the amount of adipose tissue  Inflammatory cell infiltrates are absent Atrophy of parotid parenchymal tissue & increase of intraglandular fat
  • 22. Sjögren Syndrome  It is the expression of an autoimmune process that principally results in  Rheumatoid arthritis  Dry eyes (keratoconjunctivitis sicca)  Dry mouth (xerostomia)  Lymphocytic replacement of lacrimal and salivary glands
  • 23. Sjögren Syndrome   Clinical features:  Peak age: 50 yo  Parotid gland enlargment Treatment:  Artificial saliva and tears & preventive oral measures
  • 24. Sjögren Syndrome Focal aggregates of lymphocytes, periductal lymphocytes & dilated ducts
  • 25. Mixed Tumors “Pleomorphic Adenoma”  It is the most common benign neoplasm of salivary glands origin  It represents 45-74% of all salivary gland tumors  Slow growing & asymptomatic,  Average age is about 43 yo.  Recurrent lesion occurs as multiple nodules & are less mobile than initial lesion.
  • 26. Mixed Tumors “Pleomorphic Adenoma”  CT revealed a mixed tumor medial to the mandibular ramus  It has prominent cartilagenous & osseous elements that led initially to diagnosis of osteochondroma
  • 27. Mixed Tumors “Pleomorphic Adenoma”  The most common intraoral site is the palate followed by the upper lip & buccal mucosa  Mobility is limited for palatal tumors.  Large intraoral tumors are susceptible to trauma
  • 28. Mixed Tumors “Pleomorphic Adenoma” Submandibular Small glistening capsular surface  Gross finding: It is irregular round to ovoid mass & well defined borders Parotid Homogeneous tan or tan white surface
  • 29. Mixed Tumors “Pleomorphic Adenoma” Gross findings Translucent central zone represents myxochondroid tissue The presence of multiple individual nodules are typical of recurrent mixed tumor
  • 30. Mixed Tumors “Pleomorphic Adenoma” Microscopic findings  Composed of epithelial & mesenchymal like tissue  Present or absent of fibrous capsule
  • 31. Mixed Tumors “Pleomorphic Adenoma” Cystic degeneration Prominent osseous differentiation in mixed tumor Epithelial cell in mixed tumor Cytokeratin immunoteactivity in epithelial cells
  • 32. Mixed Tumors “Pleomorphic Adenoma” Microscopic findings  In the absence of surgical intervention, viable epithelial cells within necrotic tissue suggest a malignant transformation  Rarely tumor cells are seen within vascular spaces
  • 33. Mixed Tumor “Treatment”  Parotidectomy & excision of the scar tissue with preservation of the facial nerve are recommended (specially recurrent)  Long term follow up is recommended more than 5 years  The risk of malignant degeneration increases with time  Radiotherapy has been found by some investigators to be useful in some recurrent mixed tumor
  • 34. Carcinoma Ex-Mixed Tumor “Clinical Features”  It arises from a benign mixed tumor (diagnosis requires identification of mixed tumor)  20% of patients had previous operation for mixed tumor  The risk for malignant transformation correlates with the duration of mixed tumor  Painless mass or sometimes associated with facial nerve pain or palsy  Tumor is freely movable or sometime fixed to underlying tissue (especially with recurrent tumors)
  • 35. Carcinoma Ex-Mixed Tumor “Microscopic Findings” Capsular invasion Myxochondoid bening elements & carcinomatous elements
  • 36. Carcinoma Ex-Mixed tumor “Treatment”  38-53% develop recurrence  Distant metastasis to lung, bone, brain, liver & subcutaneous tissue  Radiotherapy alone has proven ineffective, although it may have a beneficial role when combined with surgery
  • 37. Basal Cell Adenoma   It is composed of cells predominantly of one type Basal cell adenoma:  Occurs mainly in parotid  Slow growing & painless  Can be multinodular  Age 35-80  Male predominence Well circumscribed mass near the inferior pole of the parotid
  • 39. Basal Cell Adenoma Immunostaining for cytokeratin Histology: Ultrastructure shows ductal cells
  • 40. Basal Cell Adenoma Basal cell adenoma usually lack cribriform pattern Histology: Adenoid cystic carcinoma with clear cytoplasm & angular nuclei
  • 41. Basal Cell Adenoma  Treatment & prognosis: Conservative surgical excision including a margin of normal uninvolved tissue  Prognosis is good and recurrence rate is so low  Small cells in the periphery of the epithelial islands And larger cells adjacent to the tumor islands
  • 42. Malignant Epithelial Tumors “Mucoepidermoid Carcinoma”  It is the most common malignant salivary glands tumor  It represents 15.5% of all benign & malignant tumors at all sites resemble a mucoceles. Size varies from 1-12cm  
  • 43. Mucoepidermoid Carcinoma  It is believed to arise from salivary duct system Normal duct-lining epithelium Neoplastic transformation
  • 44. Mucoepidermoid Carcinoma  Ionizing radiation increases the risk for its developing  Occurrence:   7% Submandibular gland  1% Sublingual gland   45% Parotid gland 21% in the palate and 19% for the rest of the minor salivary glands. Mean age is about 47 years with the age range between 8 to 92 yo.  Women > men
  • 45. Mucoepidermoid Carcinoma  Typically, it is a solitary painless mass  2/3 of pts. are asymptomatic  if growing rapidly, usually accompanied with pain & mucosal ulceration, and sometimes a discharge of fluid resemble abscess.  6 years average between onset & diagnosis (high grade lesions demonstrate a 1.5-year interval before diagnosis).
  • 46. Mucoepidermoid Carcinoma  According to cytologic features, it is divided into: - Low - Intermediate - High grade types.  All grades of this neoplasm are carcinomas and have the potential to metastasize.  They are epithelial mucin-producing tumor
  • 47. Mucoepidermoid Carcinoma (Central)   This lesion may also arise centrally within the mandible (Differential diagnosis: giant cell granuloma & odontogenic tumors).  Asymptomatic radiolucencies  Mandibule > maxilla  Third molar region is the most likely to be involved
  • 48. Mucoepidermoid Carcinoma (Central) It arises from either: Ectopic salivary gland tissue Neoplastic transformation of epithelial lining of odontogenic cysts Glandular odontogenic cyst Mayer’s mucicarmine stain highlights numerous mucus cells in a dentigerous cyst
  • 49. Mucoepidermoid Carcinoma  Treatment & Prognosis:  low grade usually follow a benign course. However, in several instances low grade lesions have metastasize widely.  High grade metastasize widely (60% of cases).  Surgical, or surgery plus postoperative radiotherapy (high grade)  Central mucoepidermoid carcinoma is usually of low grade (40% recurrence rate).
  • 50. Adenoid Cystic Carcinoma Oral mucosa overlying this palatal mucosa is ulcerated Clinical Features  50-70% starts in the minor salivary glands.  If major salivary gland (parotid is the most affected)  Age: 5th and 7th decades This tumor appears deceptively well circumscribed
  • 51. Adenoid Cystic Carcinoma  No gender predilection  (slight female predominance).  Unilocular mass  Firm on palpation  Occasional pain or tenderness  Slow growth rate  Bone invasion occurs  Lung metastasis Sublingual gland tumor.
  • 52. Adenoid Cystic Carcinoma  Treatment & prognosis:  Surgery is the treatment of choice  Radical resection is justified to obtain surgical margins that are free of tumor  Multiple-agent chemotherapy showed some promise for postoperative treatment  High recurrence rate
  • 53. Acinic Cell Carcinoma Clinical features  Age: 5th to 6th decades of life  No gender predilection  It represents 14% of parotid gland tumor  9% of total salivary gland carcinoma of all sites  50% of cases, the clinical appearance is a benign lesion
  • 54. Acinic Cell Carcinoma    Usually less than 3 cm in diameter Pain The interval between the initial appearance & treatment is 6 months to 5 years The origin is the ductal cells
  • 55. Acinic Cell Carcinoma  Treatment & prognosis:  Surgery is the preferred treatment  Seldom metastasize  Tendency to recur
  • 56. Polymorphous Low-Grade Adenocarcinoma        It is considered to be low grade malignancy and low risk of metastasis Age: 5th to 8th decades No gender predilection Occurs in minor salivary glands (palate) Firm, non-ulcerated & non tender Size between 1-4 cm Slow growth Well circumscribed mass at the junction of the hard & soft palate
  • 57. Polymorphous Low-Grade Adenocarcinoma Partially circumscribed but lack encapsulation
  • 58. Polymorphous Low-Grade Adenocarcinoma  Treatment & prognosis:   Conservative surgical excision Prognosis is good
  • 59. Carcinoma Ex-Mixed Tumor “Microscopic Findings” The carcinomatous elements appeared separated from benign element Apparent malignant transformation
  • 60. Carcinomatous & benign Components of ExMixed  w
  • 61. Mucoepidermoid Carcinoma  Fluctuant because of cyst formation Mucin filled cystic spaces
  • 62. Mucoepidermoid Carcinoma   Microscopic features: The name is a contraction of epidermoid and mucus-secreting carcinoma A close association of mucous & epidermoid cells Mayer’s mucicarmine hightlights the extracellular & Intracytoplasmic mucin
  • 63. Mucoepidermoid Carcinoma Mucoepidermoid carcinoma incites secondary lymphoid proliferation The lymphoid response extends along the periphery of the tumor
  • 64. Mucoepidermoid Carcinoma Low grade. Note Intracystic spaces Intermediate grade. hyperchromatic nuclei & several microcystic spaces High grade Focal necrosis
  • 65. Epidermoid & mucus cells Epidermoid cells solid & infiltrative Central Mucoepidermoid Carcinoma Cyst Solid & cystic neoplastic area Characteristic variety of cell types
  • 66. Adenoid Cystic Carcinoma Tubular pattern in the top & bottom. A cribriform pattern in the center Epithelial cells have a clear Cytoplasm, poorly defined border & irregular shaped nuclei Immunoreactivity of the tumor cells for cytokeratin
  • 67. Adenoid Cystic Carcinoma Mitotic figures The tumor appears well circumscribed Myoepithelial & ductal cells
  • 68. Adenoid Cystic Carcinoma Neural invasion Comedo-type necrosis
  • 69. Acinic Cell Carcinoma  Well differentiated acinar cell  Cytoplasmic granules.  Slightly basophilic cytoplasm  Eccentricaly located nuclei Acinar cells
  • 70. Acinic Cell Carcinoma Papillary cystic growth pattern Follicular pattern
  • 71. Acinic Cell Carcinoma Cluster of neoplastic epithelial cells & numerous electron dense cytoplasmic granules
  • 72. Polymorphous Low-Grade Adenocarcinoma The nuclei are round or ovoid & have a slightly irregular contour Tumor cells are often concentrically arranged
  • 73. October 11, 2005 Oral Pathology II 0701441 Connective Tissue Lesions
  • 74. Connective Tissue Lesions  Fibrous lesions:  Reactive hyperplasia: Fibrous hyperplasia or exuberant proliferation of granulation tissue  Peripheral fibroma  Generalized gingival hyperplasia  Denture induced fibrous hyperplasia  Neoplasms: heterogeneous that form complex collection of disease  Myxoma  Fibrosarcoma
  • 75. Connective Tissue Lesions “Fibrous Lesions”  Peripheral fibroma  Etiology: Reactive (secondary to overexuberant repair)  Origin: Connective tissue of the submucosa  Clinical features:  Predilection for young adults  Female>male  Location: commonly at the gingiva anterior to molars  Similar in color to the surrounding tissue
  • 76. Connective Tissue Lesions “Fibrous Lesions”  Peripheral Odontogenic fibroma
  • 77. Connective Tissue Lesions “Fibrous Lesions”  Focal fibrous hyperplasia:  It is common in frequently traumatized area
  • 78. Connective Tissue Lesions “Fibrous Lesions”  Peripheral fibroma  Histopathology:  Focal fibrous hyperplasia: Highly collagenous and relatively avascular  Mild to moderate inflammatory cell infiltrate  Subtypes:  Peripheral ossifying fibroma  Peripheral odontogenic fibroma  Giant cell fibroma  Differential diagnosis: Pyogenic granuloma & peripheral giant cell granuloma  Treatment: Local excision
  • 79. Connective Tissue Lesions “Fibrous Lesions”  Peripheral Ossifying Fibroma
  • 80. Connective Tissue Lesions “Fibrous Lesions”  Generalized gingival hyperplasia:  Definition: Overgrowth of the gingiva  Etiology:  Non-specific: Response to chronic inflammation associated with local factor  Hormonal changes (imbalance)  Drugs (Phenytoin, Cyclosporine, Nifidipine)  Leukemia
  • 81. Connective Tissue Lesions “Fibrous Lesions”  Generalized gingival hyperplasia:  Clinical features: Increase in the bulk of free and attached gingiva.     Stippling is lost Color: red to blue Associated inflammation: non-specific factors & hormonal imbalance appears more inflamed than drug induced hyperplasia Histopathology:      Abundance in collagen Increased number of fibroblasts Various degree of chronic inflammation Increased capillaries (hormonal) Immature & atypical white blood cells with leukemic type
  • 82. Connective Tissue Lesions “Fibrous Lesions”  Gingival fibromatosis
  • 83. Connective Tissue Lesions “Fibrous Lesions”  Generalized gingival hyperplasia:   Treatment: Attentive oral hygiene is necessary Gingivoplasty or gingivectomy in combination with prophylaxis
  • 84. Connective Tissue Lesions “Fibrous Lesions”  Denture-induced fibrous hyperplasia  Etiology: Chronic trauma produced by an ill-fitting denture  Clinical features: Occurs in the vestibular mucosa  Overexuberant fibrous connective tissue reparative response  Painless folds of fibrous tissue  Treatment: Surgical excision is usually required
  • 86. Connective Tissue Lesions “Fibrous Lesions”  Neoplasms:  Myxoma: Benign proliferation of spindle cells  Clinical features: It is a soft neoplasms composed of gelatinous material  Slow growing  Asymptomatic  Location: Palate  Occurs at any age Soap bubble multilocular area
  • 87. Connective Tissue Lesions “Fibrous Lesions”  Myxoma:  Histopathology:  Not encapsulated (may exhibit infiltration into surrounding soft tissue)  Dispersed stellate & spindle-shaped fibroblasts  Loose myxoid stroma
  • 88. Connective Tissue Lesions “Fibrous Lesions”  Myxoma:  Treatment: Surgical excision  Recurrence is not uncommon
  • 90. Connective Tissue Lesions “Fibrous Lesions”  Fibrosarcoma: It is a malignant spindle cell tumor showing interlacing fascicular pattern  Clinical features  Can arise in bone  Young adults most commonly affected  It is considered as infiltrative neoplasms
  • 91. Connective Tissue Lesions “Fibrous Lesions”  Fibrosarcoma:  Histopathology:  Collagen sparse  Frequent mitotic figures  Ill defined periphery
  • 92. Connective Tissue Lesions “Fibrous Lesions”  Treatment of Fibrosarcoma  Wide surgical excision  Recurrence is not uncommon  Metastasis is infrequent  5 years survival rate is 3050%
  • 93. Vascular Lesion   Reactive & Congenital Lesions Lymphangioma   Etiology:  It is regarded as congenital lesion  Appears within the first 2 decades of life Clinical features:  Painless nodular, vesicle like swelling  Crepitant sound  Tongue is the most common intraoral site
  • 94. Vascular Lesion  Histopathology:  Endothelium-lined lymphatic channels  Eosinophilic lymph that occasionally include red blood cells  Lymphatic channels directly adjacent to overlying epithelium  Treatment: Surgical removal but because of lack of encapsulation, recurrences are common
  • 95. Vascular lesion   Neoplasms: Angiosarcoma  It is a neoplasm of endothelial cell origin  Scalp is the usual location  The lesion consists of an unencapsulated proliferation of endothelial cells enclosing irregular luminal spaces  It has an aggressive clinical course and poor prognosis
  • 96. Neural lesions   Reactive lesion: Traumatic neuroma:  Etiology: It is caused by injury of peripheral nerve  Oral surgery procedure  Local anesthetic injection  Accident  Clinical features:  Pain  Wide age range  Mental foramen is the most common location
  • 97. Neural lesion  Traumatic neuroma (Cont.)  Histopathology:  Bundles of nerves admixed with dense collagenous fibrous tissue  Treatment: Surgical excision
  • 98. Neural Lesion  Neoplasms:  Granular cell tumors  Etiology: It is an uncommon benign tumor of unknown cause  The granular cell that make this tumor is believed to originate from Schwann cells Clinical features:  Wide age range  Tongue is the most common location  Uninflamed asymptomatic mass  < 2 cm in diameter  Overlying epithelium is intact 
  • 99. Neural lesion   Neoplasms: Granular cell tumors  Histopathologically:  Unencapsulated sheets of large polygonal cells with pale granular or grainy cytoplasm  Pseudoepitheliomatous hyperplasia   Treatment: Surgical removal
  • 100. Neural lesion   Neoplasms: Schwannoma:   Etiology: It is derived from schwann cells Clinical features:  It is an encapsulated submucosal mass  Asymptomatic lump  Occurs at any age  Tongue is the most common location  Bony lesion produce a well-defined radiolucent lesion  Slow growing but may undergoe a sudden increase (hemorrhage)
  • 101. Neural lesion   Neoplasms: Schwannoma:  Histopathology:  Spindle cells either organized (palisaded waves) or haphazardly distributed  Treatment: Surgical excision
  • 102. Neural lesion   Neoplasms: Neurofibroma:    It mat appear as solitary or multiple lesions Etiology: - Solitary type is unknown - Neurofibromatosis is inherited Clinical features: Solitary type  Uniflamed asymptomatic submucosal mass  Location: Tongue, vestibule & buccal mucosa
  • 104. Neural lesion  Neurofibroma:  Clinical features: Neurofibromatosis:  Multiple  Café-au-lait macules  Bone abnormalities (cortical erosion or medullary resorption)  Central nervous system changes  Pain or parasthesia may be seen  Malignant degeneration into neurogenic sarcoma is seen in 5% to 15%
  • 106. Neural lesion  Neurofibroma:  Histopathology:  Spindle-shaped cells in connective tissue matrix  It may be well circumscribed or blended into surrounding connective tissue  Mast cells are scattered  Immunohistochemistry with S-100 is a useful tool to confirm diagnosis  Treatment: Surgical excision for solitary lesion Lack of encapsulation
  • 107. Neural lesion  Malignant peripheral nerve sheet tumor  The cell of origin is believed to be the schwann cells and possibly other nerve sheath cells  It appears as expansile mass (soft tissue)  Asymptomatic  Dilation of the mandibular canal (bone)  Pain or parasthesia
  • 108. Neural lesion  Malignant peripheral nerve sheet tumor  Histopathologically:  Abundant spindle cells  Mitotic figures  Nuclear pleomorphism  Treatment: Wide surgical exicion  Recurrence is common  Metastases are frequently seen
  • 109. Muscle Lesions  Neoplasms (Leiomyoma & leiomyosarcoma):    Smooth muscle neoplasms are relatively common They may arise anywhere in the body Leiomyoma     Leiomyomas are commonly arise in the muscularis of the gut and uterus Oral leiomyoma is slow growing & asymptomatic submucosal masses Appears in the tongue, hard palate or buccal mucosa Spindle cells Appears at any age Pterygo-mandibular space
  • 110. Muscle Lesions  Leiomyoma  Histopathology:  Immunohistochemical demonstration of actin and desmin protein expression can confirm diagnosis Obvious vascular origin Vascular leiomyoma Limited & uniform proliferation around each of the vascular spaces
  • 111. Muscle Lesions   Neoplasms Leiomyosarcoma      It is commonly arise in the retroperitoneum, mesentery, or subcutaneous and deep tissue of the limbs It may appear at any age Immunohistocemistry can be a valuable diagnostic tool Treatment: wide surgical excision Metastasis is not uncommon Blunt ended nuclei
  • 112. Muscle Lesions  Rhabdomyoma:      Predilection for the soft tissues of the head and neck  Floor of the mouth, soft palate, tongue & buccal mucosa Mean age: 50 years (children to older adults) Asymptomatic Well defined submucosal mass Well demarcated but unencapsulated The neoplastic cells mimic their normal counterpart (adult) Large eosinophilic granular cell with peripheral nuclei
  • 113. Muscle Lesions  Rhabdomyosarcoma:     When occurs in head and neck is primarily found in children It is a rapidly growing mass May cause pain and parasthesia Common location: Tongue and soft palate
  • 114. Muscle Lesions Rhabdomyosarcoma  Histopathology:  Embryonal type (children) consists of primitive round cells in which striations are rarely found  Immunohistochemistry demonstrates desmin, actin and myogenin
  • 115. Muscle Lesions Rhabdomyosarcoma  Treatment: Combination of surgery, radiation and chemotherapy  Survival rate incraese from 10% to 70% with this aggressive treatment approach
  • 116. Fat Lesion  Lipoma:     Location: Buccal mucosa, tongue & floor of the mouth Asymptomatic, yellowish submucosal mass Overlying epithelium is intact Superficial blood vessels are usually evident
  • 117. Fat Lesion  Lipoma:  Well circumscribed, lobulated mass of mature fat cells
  • 118. Fat Lesion  Lipomyosarcoma:      It is a lesion of adulthood It may occur at any site Slow growing (mistaken for a benign process) Treatment: surgery or radiation Prognosis is fair to good Well differentiated Myxoid type
  • 119. Mumps   It is an acute viral sialadenitis affecting primarily the parotid glands Etiology & pathogenesis:   Paramyxovirus, incubation period is 2-3 weeks Transmission is by direct contact with salivary droplets