This document provides an overview of salivary gland embryology, anatomy, functions, and disorders. It begins with the embryological development of the major salivary glands. It then describes the anatomy of the parotid, submandibular, and sublingual glands as well as their duct systems. The functions of saliva are discussed. Finally, salivary gland disorders are classified and two obstructive disorders, sialolithiasis and mucous retention, are introduced.

2. Mohammad Akheel
OMFS PG

3. CONTENTS
 INTRODUCTION
 EMBRYOLOGY
 ANATOMY
 FUNCTIONS OF SALIVA
 CLASSIFICATION
 SALIVARY GLAND DISORDERS

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.

8. STAGES OF DEVELOPMENT
STAGE 1
BUD STAGE

9. STAGE 2 CORD STAGE

10. STAGE 3 (TERMINAL BULB)

11. STAGE 4 ( LOBULE STAGE )

12. STAGE 5 ( DUCT
CANALISATION)

13. STAGE 6 ( CYTODIFFERENTIATION)

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.

18. Microanatomy
 The Secretory Unit
Acinus (serous, mucous, mixed)
 Myoepithelial cells
 Intercalated duct
 Striated duct
 Excretory duct

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

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

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.

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

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.

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

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.

55. Anatomy: Submandibular
Lymphatics
Submandibular
gland drains into
submandibular
nodes.

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,

62. Salivary hypofunction
 Candidiasis
 Lichen Planus
 Burning Mouth
 Aphthous ulcers
 Dental caries
 Xerostomia

63. Autonomic Innervation
 Parasympathetic
Abundant, watery saliva
Amylase down
 Sympathetic
Scant, viscous saliva
Amylase up

64. CLASSIFICATION OF
SALIVARY GLAND
DISORDERS

65. CLASSIFICATION
 Congenital
Agenesis
Hypoplasia
 Acquired
Inflammatory
Infection
 bacterial
 viral
 fungal

66. CLASSIFICATION
○ Autoimmune
 Sjogrens
 Sicca Syndromes
○ Idiopathic
 necrotizing sialometaplasia
 sarcoidosis
Traumatic
○ Mucocele
○ Ranula
○ Salivary fistula
○ Radiotherapy induced xerostomia

67. CLASSIFICATION
 Obstructive
Calculus disease
Ductal stenosis
Ductal atresia
 Benign
Adenomas
○ Pleomorpic adenoma
○ Basal cell adenoma
○ Adenolymphoma
○ Cystadenoma

68. Classification
Non epithelial
○ Angioma
○ Lipoma
○ Neural
 Malignant
Acinic cell carcinoma
Mucoepidermoid carcinoma
Polymorphous low grade adenocarcinoma
Squamous cell carcinoma
Squamous cell ex Pleomorphic Carcinoma
Adenoid cystic carcinoma
Lymphomas

69. Classification
 Tumor like lesions
Sialadenosis
Necrotising sialometaplasia
Benign lymphoepithelial lesions
Salivary gland cysts
Cystic lymphoid hyperplasia (HIV)

70. EXAMINATION OF SALIVARY
GLANDS

71. Clinical presentation
 Painful swelling (60%)
 Painless swelling (30%)
 Pain only (12%)
Sometimes described as recurrent salivary
colic and spasmodic pains upon eating

72. Clinical History
 History of swellings / change over time?
 Trismus?
 Pain?
 Variation with meals?
 Bilateral?
 Dry mouth? Dry eyes?
 Recent exposure to sick contacts
(mumps)?
 Radiation history?
 Current medications?

73. Exam: Inspection
 Asymmetry (glands, face, neck)
 Diffuse or focal enlargement
 Erythema extra-orally
 Trismus
 Medial displacement of structures
intraorally?
 Examine external auditory canal (EAC)

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).

75. SALIVARY GLAND DISORDERS.

76. Obstructive
Salivary Gland Disorders
 Sialolithiasis
 Mucous retention/extravasation

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

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

96. SIALOENDOSCOPY

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.

102. Submandibular Sialoliths:
Transoral Advantages
 Preserves a functional gland
 Avoids neck scar
 Possibly less time from work
 Avoids risk to CN 7 & 12

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

104. Gland excision Indications
 Very posterior stones
 Intra-glandular stones
 Significantly symptomatic patients
 Failed
transoral
approach

105. Obstructive
Salivary Gland Disorders
 Sialolithiasis
 Mucous
retention/extravasation

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

116. Ranula Treatment
Sublingual gland removal via intraoral
approach

117. Salivary Gland Infections
 Acute bacterial sialdenitis
 Chronic bacterial sialdenitis
 Viral infections

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.

125. Risk Factors for Sialadenitis
 Systemic dehydration (salivary stasis)
 Chronic disease and/or
immunocompromise
Liver failure
Renal failure
DM, hypothyroid
Malnutrition
HIV
Sjögren’s syndrome

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

179. SALIVARY GLAND
NEOPLASMS

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

182. Pleomorphic Adenoma
 Gross pathology
Smooth
Well-demarcated
Solid
Cystic changes
Myxoid stroma

183. Pleomorphic Adenoma
 Histology
Mixture of epithelial,
myopeithelial and
stromal components
Epithelial cells:
nests, sheets, ducts,
trabeculae
Stroma: myxoid,
chrondroid, fibroid,
osteoid
No true capsule
Tumor pseudopods

184. Pleomorphic Adenoma
 Treatment: complete surgical excision
Parotidectomy with facial nerve preservation
Submandibular gland excision
Wide local excision of minor salivary gland
 Avoid enucleation and tumor spill

185. Warthin’s Tumor
 papillary cystadenoma lymphomatosum
 6-10% of parotid neoplasms
 Older, Caucasian, males
 10% bilateral or multicentric
 3% with associated neoplasms
 Presentation: slow-growing, painless mass

186. Warthin’s Tumor
 Gross pathology
Encapsulated
Smooth/lobulated
surface
Cystic spaces of
variable size, with
viscous fluid, shaggy
epithelium
Solid areas with
white nodules
representing
lymphoid follicles

187. Warthin’s Tumor
 Histology
Papillary projections
into cystic spaces
surrounded by
lymphoid stroma
Epithelium: double
cell layer
○ Luminal cells
○ Basal cells
Stroma: mature
lymphoid follicles
with germinal centers

188. Oncocytoma
 Rare: 2.3% of benign salivary tumors
 6th decade
 M:F = 1:1
 Parotid: 78%
 Submandibular gland: 9%
 Minor salivary glands: palate, buccal
mucosa, tongue

189. Oncocytoma
 Presentation
Enlarging, painless mass
 Technetium-99m pertechnetate
scintigraphy
Mitochondrial hyperplasia

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

194. Basal Cell Adenoma
 Solid
Most common
Solid nests of tumor
cells
Uniform,
hyperchromatic,
round nuclei,
indistinct cytoplasm
Peripheral nuclear
palisading
Scant stroma

195. Basal Cell Adenoma
 Trabecular
Cells in elongated
trabecular pattern
Vascular stroma

196. Basal Cell Adenoma
 Tubular
Multiple duct-like
structures
Columnar cell lining
Vascular stroma

197. Basal Cell Adenoma
 Membranous
Thick eosinophilic
hyaline membranes
surrounding nests of
tumor cells
“jigsaw-puzzle”
appearance

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

203. Mucoepidermoid Carcinoma
 Histology—Low-
grade
Mucus cell >
epidermoid cells
Prominent cysts
Mature cellular
elements

204. Mucoepidermoid Carcinoma
 Histology—
Intermediate- grade
Mucus = epidermoid
Fewer and smaller cysts
Increasing pleomorphism
and mitotic figures

205. Mucoepidermoid Carcinoma
 Histology—High-
grade
Epidermoid > mucus
Solid tumor cell
proliferation
Mistaken for SCCA
○ Mucin staining

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

208. Adenoid Cystic Carcinoma
 Gross pathology
Well-circumscribed
Solid, rarely with
cystic spaces
infiltrative

209. Adenoid Cystic Carcinoma
 Histology—
cribriform pattern
Most common
“swiss cheese”
appearance

210. Adenoid Cystic Carcinoma
 Histology—tubular  Histology—solid
pattern pattern
 Layered cells forming  Solid nests of cells
duct-like structures without cystic or
 Basophilic mucinous tubular spaces
substance

211. Adenoid Cystic Carcinoma
 Treatment
Complete local excision
Tendency for perineural invasion: facial nerve
sacrifice
Postoperative XRT
 Prognosis
Local recurrence: 42%
Distant metastasis: lung
Indolent course: 5-year survival 75%, 20-year
survival 13%

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

213. Acinic Cell Carcinoma
 Gross pathology
Well-demarcated
Most often
homogeneous

214. Acinic Cell Carcinoma
 Histology
Solid and microcystic
patterns
○ Most common
○ Solid sheets
○ Numerous small cysts
Polyhedral cells
Small, dark, eccentric
nuclei
Basophilic granular
cytoplasm

215. Acinic Cell Carcinoma
 Treatment
Complete local excision
+/- postoperative XRT
 Prognosis
5-year survival: 82%
10-year survival: 68%
25-year survival: 50%

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

221. Carcinoma Ex-Pleomorphic
Adenoma
 Gross pathology
Poorly circumscribed
Infiltrative
Hemorrhage and
necrosis

222. Carcinoma Ex-Pleomorphic
Adenoma
 Histology
Malignant cellular
change adjacent to
typical pleomorphic
adenoma
Carcinomatous
component
○ Adenocarcinoma
○ Undifferentiated

223. Carcinoma Ex-Pleomorphic
Adenoma
 Treatment
Radical excision
Neck dissection (25% with lymph node
involvement at presentation)
Postoperative XRT
 Prognosis
Dependent upon stage and histology

224. Carcinosarcoma
 Rare: <.05% of salivary gland neoplasms
 6th decade
 M=F
 Parotid
 History of previously excised pleomorphic
adenoma, recurrent pleomorphic
adenoma or recurring pleomorphic treated
with XRT
 Presentation

225. Carcinosarcoma
 Gross pathology
Poorly circumscribed
Infiltrative
Cystic areas
Hemorrhage,
necrosis
Calcification

226. Carcinosarcoma
 Histology
Biphasic appearance
Sarcomatous
component
○ Dominant
○ chondrosarcoma
Carinomatous
component
○ Moderately to poorly
differentiated ductal
carcinoma
○ Undifferentiated

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

229. Squamous Cell Carcinoma
 Gross pathology
Unencapsulated
Ulcerated
fixed

230. Squamous Cell Carcinoma
 Histology
Infiltrating
Nests of tumor cells
Well differentiated
○ Keratinization
Moderately-well
differentiated
Poorly differentiated
○ No keratinization

231. Squamous Cell Carcinoma
 Treatment
Radical excision
Neck dissection
Postoperative XRT
 Prognosis
5-year survival: 24%
10-year survival: 18%

232. Polymorphous Low-Grade
Adenocarcinoma
 2nd most common
malignancy in minor
salivary glands
 7th decade
 F>M
 Painless, submucosal
mass
 Morphologic diversity
○ Solid, glandular, cribriform,
ductular, tubular, trabecular,
cystic

233. Polymorphous Low-Grade
Adenocarcinoma
 Histology
Isomorphic cells,
indistinct borders,
uniform nuclei
Peripheral “Indian-
file” pattern
 Treatment
Complete yet
conservative excision

234. Clear Cell Carcinoma
 AKA glycogen-rich
 Palate and parotid
 6th-8th decade
 M=F
 Histology
○ Uniform, round or
polygonal cells
○ Peripheral dark nuclei
○ Clear cytoplasm
 Treatment
○ Complete local
excision

235. Epithelial-Myoepithelial
Carcinoma
 < 1% of salivary
neoplasms
 6th-7th decades, F > M,
parotid
 ? Increased risk for 2nd
primary
 Histology
○ Tumor cell nests
○ Two cell types
○ Thickened basement
membrane
 Treatment

236. INCISIONS

237. FACE LIFT INCISION

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