4. INTRODUCTION
Any changes producing
pain and swelling of
salivary glands leads to
Salivary Gland Disorders.
5. Embryology
The parotid anlagen are the first to
develop, followed by the submandibular
gland, and finally the sublingual gland.
Parenchymal tissue (secretory) of the
glands arises from the proliferation of
oral epithelium.
6. Embryology
The stroma (capsule and septae) of the
glands originates from mesenchyme that
may be mesodermal or neural crest in
origin.
14. Parotid development
Although the parotid anlagen are the
first to develop, they become
encapsulated after the SMG and SLG.
This delayed encapsulation is critical
because after the encapsulation of the
SMG and SLG but before encapsulation
of the parotid, the lymphatic system
develops.
15. Parotid development
Therefore, there are intraglandular
lymph nodes and lymphatic channels
entrapped within the parotid gland (PG).
PG is also unique because its epithelial
buds grow, branch and extend around
the divisions of the facial nerve.
16. Embryology
The epithelial buds of each gland
enlarge, elongate and branch initially
forming solid structures.
Branching of the glandular mass
produces arborization.
Each branch terminates in one or two
solid end bulbs.
17. Embryology
Elongation of the end bulb follows and
lumina appears in their centers,
transforming the end bulbs into terminal
tubules.
These tubules join the canalizing ducts
to the peripheral acini.
19. Striated & Intercalated ducts well
developed in serous, than in mucous
glands
Striated duct: HCO3 taken in , Cl
taken out from lumen
Intercalated duct: K into lumen, Na
from lumen, producing hypotonic
fluid
Excretory ducts do NOT modify
saliva
20.
21.
22. Duct Canalization
Canalization results from mitotic activity
of the outer layers of the cord outpacing
that of the inner cell layers
Canalization is complete by 6th month
post conception.
23. Acinar cells
At around the 7-8th month in utero,
secretory cells (acini) begin to develop
around the ductal system.
24. Acinar cells of Salivary Glands
Classified as either:
Serous cells: produce a thin watery
secretion
Mucous cells: produce a more viscous
secretion
25. Major glands/Secretions
Major SG are paired structures and
include the parotid, submandibular and
sublingual
Parotid: serous
Submandibular: mucous & serous
Sublingual: mucous
26.
27. Anatomy: Parotid Gland
Nearly 80% of the
parotid gland (PG) is
found below the level
of the external
auditory canal,
between the
mandible and the
SCM.
Superficial to the
posterior aspect of
the masseter .
28. Anatomy:Parotid Gland
Extensions of PG project to mastoid
process
Down the anterior aspect of the SCM for a
short distance
Around the posterior border of the mandible.
Superiorly to the to inferior margin of the
zygomatic arch
29. Anatomy:Parotid Gland
CN VII branches
roughly divide the PG
into superficial
(lateral) and deep
lobes while coursing
anteriorly from the
stylomastoid foramen
to the muscles of
facial expression.
30.
31. Anatomy: Deep Lobe
The remaining 20% extends medially
through the stylomandibular tunnel,
which is formed
ventrally by the posterior edge of the ramus
dorsally by the anterior border of the SCM &
posterior digastric muscle
deeply and dorsally by the stylomandibular
ligament.
32. Parotid : Deep lobe lies on...
V: internal jugular vein
A: external and internal carotid arteries
N: glossopharyngeal N
vagus N
spinal accesory N
hypoglossal N
S: styloid process
styloglossus m
stylohyloid m
33. Anatomy: Parotid Duct
Small ducts coalesce at the anterosuperior
aspect of the PG to form Stensen’s duct.
Runs anteriorly from the gland and lies
superficial to the masseter muscle
Follows a line from the EAM to a point just
above the commissure.
Is inferior to the transverse facial artery
It is 1-3 mm in diameter
6cm in length
34.
35. Anatomy: Parotid Duct
At the anterior edge of the masseter
muscle, Stensen’s duct turns sharply
medial and passes through the
buccinator muscle, buccal mucosa and
into the oral cavity opposite the maxillary
second molar.
36. Anatomy: Parotid Fascia
Gland encapsulated by a fascial layer
that is continuous w/the deep cervical
fascia (DCF).
The stylomandibular ligament (portion of
the DCF) separates the parotid and
submandibular gland.
37. Anatomy: Parotid Lymphatics
Lymphatic drainage is to the superficial
and deep cervical nodes
Preauricular lymph nodes (LN) in the
superficial fascia drain the temporal
scalp, upper face, anterior pinna
LN within the gland drain the parotid
gland, nasopharynx, palate, middle ear
and external auditory meatus
38. Parotid: Parasympathetic
Innervation
Preganglionic parasympathetic (from
CN9) arrives at otic ganglion via lesser
petrosal n.
Postganglionic parasympathetic leaves
the otic ganglion and distributes to the
parotid gland via the auriculotemporal
nerve.
39.
40. Parotid: Sympathetic
Innervation
Postganglionic innervation is provided by
the superior cervical ganglion and
distributes with the arterial system
41. Parotid Anatomy: Great Auricular
Nerve (C2,C3)
Emerges from the
posterior border of the
SCM at Erb’s point.
It crosses the mid-portion
of the SCM about 6.5cm
beneath the EAM.
Passes parallel and
superior to the external
jugular vein to supply the
ear and pre-auricular
region.
42. Parotid Anatomy:
Auriculotemporal Nerve
Branch of V3
Traverses the upper part of the parotid
gland and emerges from the superior
surface with the superficial temporal
vessels.
It carries sensory fibers from the
trigeminal and post-ganglionic
parasympathetic (secretory)fibers.
43. Parotid Anatomy: Facial
Nerve
Emerges at the level of the digastric
muscle, through the stylomastoid
foramen.
Main trunk divides at the pes anserinus
(intraparotid plexus of CN7) into the
upper temporofacial and lower
cervicofacial divisions.
Before it enters gland, gives off 3
branches:
Posterior auricular, posterior digastric,
stylohyoid
44.
45.
46.
47.
48.
49.
50. Parotid Anatomy: Vessels
Retromandibular Vein: located within the
substance of the gland
External carotid : at the inferior level of the
gland, the external carotid divides into the
superficial temporal and internal maxillary
artery.
51. Anatomy:Submandibular gland
Located in the
submandibular triangle
of the neck, inferior &
lateral to mylohyoid
muscle.
The posterior-superior
portion of the gland
curves up around the
posterior border of the
mylohyoid and gives
rise to Wharton’s duct.
56. Anatomy: Submandibular Duct
Wharton’s duct passes forward along the
superior surface of the mylohyoid adjacent
to the lingual nerve.
The nerve winds around the duct, first
being lateral, then inferior, and finally
medial.
57. Anatomy: Submandibular duct
2-4mm in diameter & about 5cm in length.
It opens into the floor of the mouth through
a punctum.
The punctum is a constricted portion of
the duct to limit retrograde flow of
bacteria-laden oral fluids.
58. Anatomy: Sublingual glands
Lie on the superior
surface of the
mylohyoid muscle
and are separated
from the oral cavity
by a thin layer of
mucosa.
59. Anatomy: Sublingual glands
The ducts of the sublingual glands are
called Bartholin’s ducts.
In most cases, Bartholin’s ducts consists
of 8-20 smaller ducts of Rivinus. These
ducts are short and small in diameter.
60. Anatomy: Sublingual glands
The ducts of Rivinis either open…
individually into the FOM near the
punctum of Wharton’s duct
on a crest of sublingual mucosa
called the plica sublingualis
open directly into Wharton’s duct
61. Function of Saliva
Moistens oral mucosa
Moistens & cool food
Medium for dissolved food
Mineralization
Buffer (HCO3)
Protective Pellicle
Digestion (Amylase, Lipase)
Antibacterial (Lysozyme, IgA,
Peroxidase,
74. Exam: Palpation
Palpate for cervical lymphadenopathy
Bimanual palpation of floor of mouth in a
posterior to anterior direction
Have patient close mouth slightly & relax
oral musculature to aid in detection
Examine for duct purulence
Bimanual palpation of the gland (firm or
spongy/elastic).
77. Sialolithiasis
Sialolithiasis results in
a mechanical
obstuction of the
salivary duct
Is the major cause of
unilateral diffuse
parotid or
submandibular gland
swelling
78. Sialolithiasis Incidence
Escudier & McGurk 1:15-20 000
Marchal & Dulgurerov 1:10-20 000
Sialolithiasis remains the most frequent
reason for submandibular gland
resection
79.
80. Sialolithiasis
The exact pathogenesis of sialolithiasis
remains unknown.
Thought to form via….
an initial organic nidus that progressively
grows by deposition of layers of inorganic
and organic substances.
May eventually obstruct flow of saliva from
the gland to the oral cavity.
81. Sialolithiasis
Acute ductal obstruction may
occur at meal time when saliva
producing is at its maximum, the
resultant swelling is sudden and
can be painful.
MEAL TIME SYNDROME
82. Gradually reduction of the swelling
can result but it recurs repeatedly
when flow is stimulated.
This process may continue until
complete obstruction and/or
infection occurs.
83. Etiology
Hypercalcemia…
Xerostomic meds
Tobacco smoking
Smoking has an increased cytotoxic
effect on saliva, decreases PMN
phagocytic ability and reduces salivary
proteins
84. Etiology
Gout is the only systemic disease
known to cause salivary calculi and
these are composed of uric acid.
85. Stone Composition
Organic; often predominate
in the center
Glycoproteins
Mucopolysaccarides
Bacteria
Cellular debris
Inorganic; often in the
periphery
Calcium carbonates & calcium
phosphates in the form of
hydroxyapatite
86. Parotid (PG) vs. Submandibular
Gland (SMG)….
Obstructive phenomemnon such as mucous
plugs and sialoliths are most commonly
found in the SMG
Parotid glands are not most commonly
affected
87. Reasons sialolithiasis may occur
more often in the SMG
Saliva more alkaline
Higher concentration of calcium and
phosphate in the saliva
Higher mucus content
Longer duct
Anti-gravity flow
88. Other characteristics:
Despite a similar chemical make-up,
80-90% of SMG calculi are radio-
opaque
50-80% of parotid calculi are radiolucent
30% of SMG stones are multiple
60% of Parotid stones are multiple
89. Diagnostics: Plain occlusal film
Effective for
intraductal stones,
while….
intraglandular,
radiolucent or
small stones may
be missed.
90. Diagnostic approaches
CT Scan:
large stones or small CT slices done
also used for inflammatory disorders
Ultrasound:
operator dependent, can detect small
stones (>2mm), inexpensive, non-
invasive
91. Diagnostic approaches:
Sialography
Consists of opacification of the ducts by
a retrograde injection of a water-soluble
or oil based dye.
Provides image of stones and duct
morphological structure
May be therapeutic, but success of
therapeutic sialography never
documented
92. Sialography
Disadvantages:
irradiation dose
pain with procedure
infection dye reaction
push stone further
contraindicated in active infection
93. Diagnostic approach:
Radionuclide Studies
Useful to image the parenchyma
T99 is an artificial radioactive element
(atomic #43, atomic weight 99) that is used
as a tracer in imaging studies.
T99 is a radioisotope that decays and
emits a gamma ray. Half life of 6 hours.
94. Diagnostic Approaches:
Radionuclide Studies
Some authors say T99 is useful
preoperatively to determine if gland is
functional.
However, no evidence to suggest gland
won’t recover function after stone
removed. Not advised for pre-op
decision making.
95. Diagnostic approach:
Diagnostic Sialendoscopy
Allows complete exploration of the ductal
system, direct visualization of duct
pathology
Success rate of >95%
Disadvantage: technically challenging,
trauma could result in stenosis,
perforation
97. Sialolithiasis Treatment
None: antibiotics and anti-inflammatories,
hoping for spontaneous stone passage.
Stone excision:
Lithotripsy
Interventional sialendoscopy
Simple removal (20% recurrence)7
Gland excision
98. Sialolithiasis Treatment
If patients donot undergo treatment, they
need to know:
Stones will likely enlarge over time
Seek treatment early if infection
develops
Salivary gland massage and hyper-
hydration when symptoms develop.
99. Calculi excision
External lithotripsy
Stones are fragmented and expected to
pass spontaneously
The remaining stone may be the ideal nidus
for recurrence
Interventional Sialendoscopy
Can retrieve stones, may also use laser to
fragment stones and retrieve.
100. Transoral vs. Extraoral Removal
Some authors say:
if a stone can be palpated through the
mouth, it can be removed trans-orally .
Or if it can be visualized on a true central
occlusal radiograph, it can be removed
Trans orally .
Finally, if it is no further than 2cm from the
punctum, it can be removed Trans orally.
101. Posterior Stones
Deeper submandibular stones (~15-20% of
stones) may best be removed via
sialadenectomy or excision of the gland
has to be done .
Floor of mouth (FOM) opened opposite the
first premolar, duct dissected out, lingual
nerve identified.
Duct opened & stone removed, FOM
approximated.
103. Gland excision
After SMG excision, 3% cases have
recurrence via:
Retention of stones in intraductal portion or
new formation in residual Wharton's duct
106. Mucocele
Mucus is the exclusive secretory product
of the accessory minor salivary glands
and the most prominent product of the
sublingual gland.
The mechanism for mucus cavity
development is extravasation or
retention
107. Mucocele
Mucoceles, exclusive of the irritation
fibroma, are most common of the
benign soft tissue masses in the oral
cavity.
Muco: mucus , coele: cavity. When in
the oral floor, they are called ranula.
108. Mucocele
Extravasation is the leakage of fluid from the
ducts or acini into the surrounding tissue.
Extra: outside, vasa: vessel
Retention: narrowed ductal opening that
cannot adequately accommodate the exit
of saliva produced, leading to ductal
dilation and surface swelling. Less
common phenomenon
109. Mucocele
Consist of a circumscribed cavity in the
connective tissue and submucosa
producing an obvious elevation in the
mucosa
110. Mucocele
The majority of the mucoceles result
from an extravasation of fluid into the
surrounding tissue after traumatic break
in the continuity of their ducts.
Lacks a true epithelial lining.
111. Ranula
Is a term used for
mucoceles that occur
in the floor of the
mouth.
The name is derived
form the word rana,
because the swelling
may resemble the
translucent
underbelly of the frog.
112. Ranula
Although the source is usually the
sublingual gland,
may also arise from the submandibular duct
or possibly the minor salivary glands in the
floor of the mouth.
113. Ranula
Presents as a blue dome shaped
swelling in the floor of mouth (FOM).
They tend to be larger than
mucoceles & can fill the FOM &
elevate tongue.
Located lateral to the midline, helping
to distinguish it from a midline
dermoid cyst.
114. Plunging or Cervical Ranula
Occurs when spilled mucin dissects
through the mylohyoid muscle and
produces swelling in the neck.
Concomitant FOM swelling may or may
not be visible.
115. Treatment of Mucoceles
in Lip or Buccal mucosa
Excision with strict removal of any
projecting peripheral salivary glands
Avoid injury to other glands during primary
wound closure
118. Sialadenitis
Sialadenitis represents inflammation mainly
involving the acinoparenchyma of the
gland.
119. Sialadenitis
Awareness of salivary gland infections
was increased in 1881 when President
Garfield died from acute parotitis
following abdominal surgery and
associated systemic dehydration.
120. Sialadenitis
Acute infection more
often affects the
major glands than
the minor glands
121. Pathogenesis
1. Retrograde contamination of the
salivary ducts and parenchymal tissues
by bacteria inhabiting the oral cavity.
2. Stasis of salivary flow through the ducts
and parenchyma promotes acute
suppurative infection.
122. Acute Suppurative
More common in parotid gland.
Suppurative parotitis, surgical parotitis,
post-operative parotitis, surgical mumps,
and pyogenic parotitis.
The etiologic factor most associated with
this entity is the retrograde infection
from the mouth.
20% cases are bilateral
123. Predilection for Parotid
Salivary Composition
The composition of parotid secretions
differs from those in other major
glands.
Parotid is primarily serous, the others
have a greater proportion of
mucinous material.
124. Parotid Predilection
Anatomic factors
Minor role in formation of infections
Stensen’s duct lies adjacent to the
maxillary molars and Wharton’s near
the tongue.
It is thought that the mobility of the tongue
may prevent salivary stasis in the area of
Wharton's that may reduce the rate of
infections in SMG.
126. Risk Factors
Neoplasms
Sialectasis (salivary duct dilation)
increases the risk for retrograde
contamination. Is associated with cystic
fibrosis and pneumoparotitis
Extremes of age
Poor oral hygiene
Calculi, duct stricture
NPO status (stimulatory effect of mastication on
salivary production is lost)
127. Complex picture
Sialolithiasis can produce mechanical
obstruction of the duct resulting in salivary
stasis and subsequent gland infection.
Calculus formation is more likely to occur in
SMG duct (85-90% of salivary calculi are in
the SMG duct) However, the parotid gland
remains the Main site of acute suppurative
infection
128. Acute Suppurative Parotitis -
History
Sudden onset of erythematous swelling of
the pre/post auricular areas extend into
the angle of the mandible.
Is bilateral in 20%.
129. Bacteriology
Purulent saliva should be sent for
culture.
Staphylococcus aureus is most common
Streptococcus pnemoniae and S.pyogenes
Haemophilus Influenzae also common
130. Lab Testing
Parotitis is generally a clinical diagnosis
However, in critically ill patients further
diagnostic evaluation may be required
Elevated white blood cell count
Serum amylase generally within normal
If no response to antibiotics in 48 hrs can
perform MRI, CT or ultrasound to exclude
abscess formation
Can perform needle aspiration of abscess
131. Treatment of Acute
Sialadenitis
Reverse the medical condition that may
have contributed to formation
Discontinue anti-sialogogues if possible
Warm compresses, give sialogogues
(lemon drops)
External salivary gland massage if
tolerated
132. Treatment of Acute
Sialadenitis/Parotitis
Antibiotics!
70% of organisms produce B-lactamase
or penicillinase
Need B-lactamase inhibitor like
Augmentin or Unasyn or second
generation cephalosporin
Can also consider adding metronidazole
or clindamycin to broaden coverage
133. Failure to respond
After 48 hours the patient should
respond
Consider adding a third generation ceph
Possibly add an aminoglycoside
The preponderance of MRSA in nursing
homes and nosocomial environments
has prompted the recommendation of
vancomycin in these groups
134. Surgery for Acute Parotitis
Limited role for surgery
When a discrete abscess is identified,
surgical drainage is undertaken
Approach is anteriorly based facial flap
with multiple superficial radial incisions
created in the parotid fascia parallel to
the facial nerve
Close over a drain
135. Complications of Acute
Parotitis
Direct extension
Abscess ruptures into external auditory
canal and TMJ .
Hematogenous spread
Thrombophlebitis of the retromandibular
or facial veins are rare complications
136. Complications
Fascial capsule around parotid displays
weakness on the deep surface of the gland
adjacent to the loose areolar tissues of the
lateral pharyngeal wall (Achilles’heel of
parotid)
Extension of an abscess into the
parapharyngeal space may result in airway
obstruction, mediastinitis, internal jugular
thrombosis and carotid artery erosion
137. Complications
Dysfunction of one or more branches of
the facial nerve is rare.
Occurs secondary to perineuritis or
direct neural compression ; but resolves
with adequate treatment of the parotitis.
These patients need to be followed to
ensure resolution….must rule out
TUMOR.
138. Chronic Sialadenitis
Causative event is thought to be a
lowered secretion rate with subsequent
salivary stasis.
More common in parotid gland.
Damage from bouts of acute sialadenitis
over time leads to sialectasis, ductal
ectasia and progressive acinar
destruction combined with a lymphocyte
infiltrate.
139. Chronic Sialadenitis
Workup…
The clinician should look for a treatable
predisposing factor such as a calculus
or a stricture.
140. No treatable cause found:
Initial management should be
conservative and includes the use of
sialogogues, massage and antibiotics
for acute exacerbations.
Should conservative measures fail,
consider removing the gland.
141. Acute viral infection (AVI)
Mumps classically designates a viral
parotitis caused by the paramyxovirus
However, a broad range of viral
pathogens have been identified as
causes of AVI of the salivary glands.
142. Acute Viral infection
Derived from the Danish word
“mompen”
Means mumbling, the name given to
describe the characteristic muffled
speech that patients demonstrate
because of glandular inflammation and
trismus.
143. Viral Infections
As opposed to bacterial sialadenitis, viral
infections of the salivary glands are
SYSTEMIC from the onset!
144. Viral infection
Mumps is a non-suppurative acute
sialadenitis
Is endemic in the community and spread
by airborne droplets
Communicable disease
Enters through upper respiratory tract
145. Mumps
2-3 week incubation after exposure (the
virus multiplies in the URI or parotid
gland)
Then localizes to biologically active
tissues like salivary glands, germinal
tissues and the CNS.
146. Epidemiology
Occurs world wide and is highly
contagious
Prior to the widespread use of the Jeryl
Lynn vaccine (live attenuated), cases
were clustered in epidemic fashion
Sporadic cases are observed today
likely resulting from non-paramyxoviral
infection, failure of immunity or lack of
vaccination
147. Virology
Classic mumps syndrome is caused by
paramyxovirus, an RNA virus
Others can cause acute viral parotitis:
Coxsackie A & B, ECHO virus,
cytomegalovirus and adenovirus
HIV involvement of parotid glands is a
rare cause of acute viral parotitis, is
more commonly associated with chronic
cystic disease.
148. Clinical presentation
30% experience prodromal symptoms
prior to development of parotitis
Headache, myalgias, anorexia, malaise
Onset of salivary gland involvement is
heralded by earache, gland pain,
dysphagia and trismus
149. Physical exam
Glandular swelling (tense, firm) Parotid
gland involved frequently, SMG & SLG
can also be affected.
May displace ispilateral pinna
75% cases involve bilateral parotids,
may not begin bilaterally (within 1-5
days may become bilateral) 25%
unilateral
Low grade fever
150. Diagnostic Evaluation
Leukocytopenia, with relative
lymphocytosis
Increased serum amylase (normal by 2-
3 week of disease)
Viral serology essential to confirm:
Complement fixing antibodies appear
following exposure to the virus
151. Serology
“S” or soluble antibodies directed
against the nucleoprotein core of the
virus appear within the first week of
infection, peak in 2 weeks.
Disappear in 8-9 months and are
therefore associated with active or
recent infection
152. Serology
“V”, or viral antibodies directed against
the outer surface hemagglutinin, appear
several weeks after the S antibodies and
persist at low levels for about 5 years
following exposure.
V antibodies are associated with past
infection, prior vaccination and the late
stages of active infection
153. Serology
If the initial serology is noncontributory,
then a non-paramyxovirus may be
responsible for the infection.
Blood HIV tests should also be obtained
The mumps skin test is not useful in
diagnosis an acute infection because
dermal hypersensitivity does not
develop until 3 or 4 weeks following
exposure.
154. Treatment
Supportive
Fluid
Anti-inflammatories and analgesics
155. Prevention
The live attenuated vaccine became
available in 1967
Commonly combined with the measles
and rubella vaccines, the mumps
vaccine is administered in a single
subcutaneous dose after 12 months of
age. Booster at 4-6yr
156. Complications
Orchitis, testicular atrophy and sterility in
approximately 20% of young men
Oophoritis in 5% females
Aseptic meningitis in 10%
Pancreatitis in 5%
hearing loss <5%
Usually permanent
80% cases are unilateral
157. Immunologic Disease
Sjögren’s Syndrome
Most common immunologic disorder
associated with salivary gland disease.
Characterized by a lymphocyte-mediated
destruction of the exocrine glands leading
to xerostomia and keratoconjunctivitis
sicca
158. Sjögren’s syndrome
90% cases occur in women
Average age of onset is 50y
Classic monograph on the disease
published in 1933 by Sjögren, a
Swedish ophthalmologist
159. Sjögren’s Syndrome
Two forms:
Primary: involves the exocrine glands
only
Secondary: associated with a definable
autoimmune disease, usually
rheumatoid arthritis.
80% of primary and 30-40% of secondary
involves unilateral or bilateral salivary glands
swelling
160. Sjögren’s Syndrome
Unilateral or bilateral salivary gland
swelling occurs, may be permanent or
intermittent.
Rule out lymphoma
161. Sjögren’s Syndrome
Keratoconjuntivitis sicca: diminished
tear production caused by lymphocytic
cell replacement of the lacrimal gland
parenchyma.
Evaluate with Schirmer test. Two 5 x
35mm strips of red litmus paper placed
in inferior fornix, left for 5 minutes. A
positive finiding is lacrimation
of 5mm or less.
Approximately 85% specific &
sensitive
162. Sjögren’s Lip Biopsy
Biopsy of SG mainly used to aid in the
diagnosis
Can also be helpful to confirm sarcoidosis
163. Sjögren’s Lip Biopsy
Single 1.5 to 2cm horizantal incision labial
mucosa.
Not in midline, fewer glands there.
Include 5+ glands for identification
Glands assessed semi-quantitatively to
determine the number of foci of lymphocytes
per 4mm2/gland
164. Sjögren’s Treatment
Avoid xerostomic meds if possible
Avoid alcohol, tobacco (accentuates
xerostomia)
Sialogogue (eg:pilocarpine) use is limited by
other cholinergic effects like bradycardia &
lacrimation
Sugar free gum or diabetic confectionary
Salivary substitutes/sprays
165. Sialadenosis
Non-specific term used to describe a
non-inflammatory non-neoplastic
enlargement of a salivary gland, usually
the parotid.
May be called sialosis
The enlargement is generally
asymptomatic
Mechanism is unknown in many cases.
166. Related to…
a. Metabolic “endocrine sialendosis”
b. Nutritional “nutritional mumps”
a. Obesity: secondary to fatty hypertrophy
b. Malnutrition: acinar hypertrhophy
c. Any condition that interferes with the
absorption of nutrients (celiac dz, uremia,
chronic pancreatitis, etc)
167. Related to…
a. Alcoholic cirrhosis: likely based on
protein deficiency & resultant acinar
hypertrophy
b. Drug induced: iodine mumps
e. HIV
168. Radiation Injury
Low dose radiation (1000cGy) to a
salivary gland causes an acute tender
and painful swelling within 24hrs.
Serous cells are especially sensitive and
exhibit marked degranulation and
disruption.
169. Continued irradiation leads to complete
destruction of the serous acini and
subsequent atrophy of the gland7.
Similar to the thyroid, salivary neoplasm
are increased in incidence after radiation
exposure7.
170. Granulomatous Disease
Primary Tuberculosis of the salivary
glands:
Uncommon, usually unilateral, parotid most
common affected
Believed to arise from spread of a focus of
infection in tonsils
Secondary TB may also involve the
salivary glands but tends to involve the
SMG and is associated with active
pulmonary TB.
171. Granulomatous Disease
Sarcoidosis: a systemic disease
characterized by noncaseating granulomas
in multiple organ systems
Clinically, SG involvement in 6% cases
Heerfordts’s disease is a particular form of
sarcoid characterized by uveitis, parotid
enlargement and facial paralysis. Usually
seen in 20-30’s. Facial paralysis transient.
172. Granulomatous Diseases
Cat Scratch Disease:
Does not involve the salivary glands
directly, but involves the periparotid and
submandibular triangle lymph nodes
May involve SG by contiguous spread.
Bacteria is Bartonella Henselae(G-R)
Also, toxoplasmosis and actinomycosis.
173. Cysts
True cysts of the parotid account for 2-5% of
all parotid lesions
May be acquired or congenital
Type 1 Branchial arch cysts are a
duplication anomaly of the membranous
external auditory canal (EAC)
Type 2 cysts are a duplication anomaly of
the membranous and cartilaginous EAC
174. Cysts
Acquired cysts include:
Mucus extravasation vs. retention
Traumatic
Benign epithelial lesions
Association with tumors
Pleomorphic adenoma
Adenoid Cystic Carcinoma
Mucoepidermoid Carcinoma
Warthin’s Tumor
175. Other: Pneumoparotitis
In the absence of gas-producing bacterial
parotitis, gas in the parotid duct or gland is
assumed to be due to the reflux of
pressurized air from the mouth into
Stensen’s duct.
May occur with episodes of increased
intrabuccal pressure
Glass blowers, trumpet players
Aka: pneumosialadenitis, wind parotitis,
pneumatocele glandulae parotis
176. Pneumoparotitis
Crepitation, on palpation of the gland
Swelling may resolve in minutes to
hours, in some cases, days.
US and CT show air in the duct and
gland
Consider antibiotics to prevent
superimposed infection
177. Other: Necrotizing
Sialometaplasia
Cryptogenic origin, possibly a reaction to
ischemia or injury
Manifests as mucosal ulceration, most
commonly found on hard palate.
May have prodrome of swelling or
feeling of “fullness” in some.
Pain is not a common complaint
178. Necrotizing Sialometaplasia
Self limiting lesion, heals by secondary
intention over 6-8 weeks
Histologically may be mistaken for SCC
180. Pleomorphic Adenoma
Most common of all salivary gland neoplasms
○ 70% of parotid tumors
○ 50% of submandibular tumors
○ 45% of minor salivary gland tumors
○ 6% of sublingual tumors
4th-6th decades
F:M = 3-4:1
181. Pleomorphic Adenoma
Slow-growing, painless mass
Parotid: 90% in superficial lobe, most in
tail of gland
Minor salivary gland: lateral palate,
submucosal mass
Solitary vs. synchronous/metachronous
neoplasms
190. 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
191. Oncocytoma
Electron
microscopy:
Mitochondrial
hyperplasia
60% of cell volume
192. Monomorphic Adenomas
Basal cell, canalicular, sebaceous,
glycogen-rich, clear cell
Basal cell is most common: 1.8% of
benign epithelial salivary gland neoplasms
6th decade
M:F = approximately 1:1
Caucasian > African American
Most common in parotid
193. 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
198. Myoepithelioma
<1% of all salivary neoplasms
3rd-6th decades
F>M
Minor salivary glands > parotid >
submandibular gland
Presentation: asymptomatic mass
199. Myoepithelioma
Histology
Spindle cell
○ More common
○ Parotid
○ Uniform, central nuclei
○ Eosinophilic granular
or fibrillar cytoplasm
Plasmacytoid cell
○ Polygonal
○ Eccentric oval nuclei
200. Mucoepidermoid Carcinoma
Most common salivary gland malignancy
5-9% of salivary neoplasms
Parotid 45-70% of cases
Palate 18%
3rd-8th decades, peak in 5th decade
F>M
Caucasian > African American
201. 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
202. Mucoepidermoid Carcinoma
Gross pathology
Well-circumscribed
to partially
encapsulated to
unencapsulated
Solid tumor with
cystic spaces
206. Mucoepidermoid Carcinoma
Treatment
Influenced by site, stage, grade
Stage I & II
○ Wide local excision
Stage III & IV
○ Radical excision
○ +/- neck dissection
○ +/- postoperative radiation therapy
207. Adenoid Cystic Carcinoma
Overall 2nd most common malignancy
Most common in submandibular,
sublingual and minor salivary glands
M=F
5th decade
Presentation
Asymptomatic enlarging mass
Pain, paresthesias, facial weakness/paralysis
212. Acinic Cell Carcinoma
2nd most common parotid and pediatric
malignancy
5th decade
F>M
Bilateral parotid disease in 3%
Presentation
Solitary, slow-growing, often painless mass
216. Adenocarcinoma
Rare
5th to 8th decades
F>M
Parotid and minor
salivary glands
Presentation:
Enlarging mass
25% with pain or facial weakness
217. Adenocarcinoma
Histology
Heterogeneity
Presence of glandular
structures and
absence of epidermoid
component
Grade I
Grade II
Grade III
218. 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%
219. 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
220. Carcinoma Ex-Pleomorphic
Adenoma
2-4% of all salivary gland neoplasms
4-6% of mixed tumors
6th-8th decades
Parotid > submandibular > palate
Risk of malignant degeneration
○ 1.5% in first 5 years
○ 9.5% after 15 years
Presentation
○ Longstanding painless mass that undergoes sudden
enlargement
227. 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
228. Squamous Cell Carcinoma
1.6% of salivary gland neoplasms
7th-8th decades
M:F = 2:1
MUST RULE OUT:
○ High-grade mucoepidermoid carcinoma
○ Metastatic SCCA to intraglandular nodes
○ Direct extension of SCCA
238. REFERENCES
Oral anatomy & histology – K . Avery
Oral pathology – Shaffers
Oral medicine – Burkit
Grays anatomy – Grays
Head and neck otolaryngology
Lore and Medina Atlas
Dental Clinics of north america
Textbook of Hupp
Internet