salivary gland diseases

1. by: dr nikil
Salivary Glands
& Disease

2. 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.

3. Embryology
The stroma (capsule and septae) of the glands
originates from mesenchyme that may be
mesodermal or neural crest in origin.

4. 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.

5. 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.

6. 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.

7. 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.

8. 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.

9. Acinar cells
At around the 7-8th
month in utero, secretory cells
(acini) begin to develop around the ductal system.

10. Acinar cells of Salivary Glands
Classified as either:
Serous cells: produce a thin watery secretion
Mucous cells: produce a more viscous secretion

11. Salivary gland secretory unit
Composed of terminal acini
Intercalated, striated and excretory ducts
Myoepithelial cells

12. Major glands/Secretions
Major SG are paired structures and include the
parotid, submandibular and sublingual
Parotid: serous
Submandibular: mucous & serous
Sublingual: mucous

13. Salivary Function
Aid is mastication, deglutination
Salivary lysozyme, IgA and other antibacterial
substances protect against caries and oral cavity
infections
Saliva also aids in speech

14. 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
mm

15. 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

16. Anatomy:Parotid Gland
CN VII branches
roughly divide the PG
into superficial and deep
lobes while coursing
anteriorly from the
stylomastoid foramen to
the muscles of facial
expression.

17. 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.

18. 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

19. 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.

20. 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.

21. 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

22. 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.

23. Parotid: Sympathetic Innervation
Postganglionic innervation is provided by the
superior cervical ganglion and distributes with
the arterial system

24. 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.

25. 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.

26. 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

27. 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.

28. Parotid Bed: 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 mm
stylohyloid mm

29. 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.

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

31. 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.

32. Anatomy: Submandibular duct
2-4mm in diameter & about 5cm in length.
It opens into the floor of the mouth thru a
punctum.
The punctum is a constricted portion of the duct
to limit retrograde flow of bacteria-laden oral
fluids.

33. 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.

34. 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.

35. 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

36. Physiology
Physiologic control of the SG is almost entirely by
the autonomic nervous system; parasympathetic
effects predominate.
If parasympathetic innervation is interrupted,
glandular atrophy occurs.
Normal saliva is 99.5% water
Normal daily production is 1-1.5L

37. Obstructive
Salivary Gland Disorders
Sialolithiasis
Mucous retention/extravasation

38. Obstructive SG Disorders:
Sialolithiasis
Sialolithiasis results in a mechanical obstuction
of the salivary duct
Is the major cause of unilateral diffuse parotid
or submandibular gland swelling2

39. Sialolithiasis Incidence
Escudier & McGurk 1:15-20 0003
Marchal & Dulgurerov 1:10-20 0002
Sialolithiasis remains the most frequent reason for
submandibular gland resection5

40. 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.

41. 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.

42. 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.

43. Etiology
Water hardness ↑likelihood? …Maybe….
Hypercalcemia…in rats only
Xerostomic meds
Tobacco smoking, positive correlation
Smoking has an increased cytotoxic effect on saliva,
decreases PMN phagocytic ability and reduces
salivary proteins

44. Etiology
Gout is the only systemic disease
known to cause salivary calculi and
these are composed of uric acid.

45. 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

46. Parotid (PG) vs. Submandibular Gland (SMG)….
Most authorities agree obstructive
phenomemnon such as mucous plugs and
sialoliths are most commonly found in the SMG
 Escudier et al3
 Lustmann et al4
 Rice7
Others note that parotid glands are most
commonly affected2

47. 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

48. Other characteristics:
Despite a similar chemical make-up,
80-90% of SMG calculi are radio-opaque7
50-80% of parotid calculi are radiolucent7
30% of SMG stones are multiple
60% of Parotid stones are multiple

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

50. 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?

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

52. 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).

53. Diagnostics: Plain occlusal film
Effective for
intraductal stones,
while….
intraglandular,
radiolucent or
small stones may be
missed.

54. 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

55. Diagnostic approaches: Sialography
Consists of opacification of the ducts by a retrograde
injection of a water-soluble dye.
Provides image of stones and duct morphological
structure
May be therapeutic, but success of therapeutic
sialography never documented

56. Sialography continued…
Disadvantages:
 irradiation dose
 pain with procedure
 poss.perforation
 infection dye reaction
 push stone further
 contraindicated in active infection.

57. 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.
Helman & Fox 1987, found that Technitium-99
shares the Na-K-Cl transport system on the
basement membrane of the parotid acinar cells

58. Diagnostic Approaches: Radionuclide Studies
Some 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!

59. Diagnostic Approach:
MR Sialography
T2 weighted fast spin echo slides in sagittal and
axial planes. Volumetric reconstruction allows
visualization of ducts
ADV: No dye, no irradiation, no pain
DIS: Cost, possible artifact

60. Diagnostic approach:
Diagnostic Sialendoscopy
Allows complete exploration of the ductal
system, direct visualization of duct
pathology
Success rate of >95%2
Disadvantage: technically challenging,
trauma could result in stenosis,
perforation

61. Sialolithiasis Treatment
None: antibiotics and anti-inflammatories,
hoping for spontaneous stone passage.
Stone excision:
 Lithotripsy
 Interventional sialendoscopy
 Simple removal (20% recurrence)7
Gland excision

62. Sialolithiasis Treatment
If patients DO defer 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.

63. Stone 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.

64. Transoral vs. Extraoral Removal
Some say:
 if a stone can be palpated thru the mouth, it can be removed
trans-orally (TO)
 Or if it can be visualized on a true central occlusal radiograph,
it can be removed TO.
 Finally, if it is no further than 2cm from the punctum, it can
be removed TO.

65. Posterior Stones
Deeper submandibular stones (~15-20% of stones)
may best be removed via sialadenectomy.
Some surgeons say can still remove transorally, but
should be done via general anesthetic.
Floor of mouth (FOM) opened opposite the first
premolar, duct dissected out, lingual nerve
identified.
Duct opened & stone removed, FOM approximated.

66. Submandibular Sialoliths: Transoral Advantages
Preserves a functional gland
Avoids neck scar
Possibly less time from work
No overnight stay in hospital
Avoids risk to CN 7 & 12

67. Gland excision
After SMG excision, 3% cases have recurrence via:
 Retention of stones in intraductal portion or new formation in
residual Wharton's duct
No data regarding recurrence after parotidectomy

68. Gland excision indicated
Very posterior stones
Intra-glandular stones
Significantly symptomatic patients
Failed
transoral
approach

69. Gland excision
While some believe that a gland with sialolithiasis is
no longer functional, a recent study on SMGs removed
due to sialolithiasis found there was no correlation
between the degree of gland alteration and the number
of infectious episodes.
50% of the glands were histopathologically normal or
close to normal
A conservative approach to the gland/stone seems to
be justified

70. Obstructive
Salivary Gland Disorders
Sialolithiasis
Mucous
retention/extravasation

71. 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

72. 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.

73. 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

74. Mucocele
Consist of a
circumscribed cavity in
the connective tissue
and submucosa
producing an obvious
elevation in the mucosa

75. 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.

76. 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.

77. 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.

78. 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.

79. 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.

80. 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

81. Ranula Treatment
Marsupialization has fallen into disfavor due to the
excessive recurrence rate of 60-90%
Sublingual gland removal via intraoral approach

82. Salivary Gland Infections
Acute bacterial sialdenitis
Chronic bacterial sialdenitis
Viral infections

83. Sialadenitis
Sialadenitis represents inflammation mainly
involving the acinoparenchyma of the gland.

84. Sialadenitis
Awareness of salivary gland infections was increased
in 1881 when President Garfield died from acute
parotitis following abdominal surgery and associated
systemic dehydration.

85. Sialadenitis
Acute infection more
often affects the
major glands than the
minor glands1

86. 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.

87. 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 bilateral7

88. 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.

89. Salivary Composition
Mucoid saliva contains elements that protect against
bacterial infection including lysozymes & IgA
antibodies (therefore, parotid has ↓ bacteriostatic activity)
Mucins contain sialic acid which agglutinates
bacteria and prevents its adherence to host tissue.
Specific glycoproteins in mucins bind epithelial cells
competitively inhibiting bacterial attachment to
these cells.

90. Parotid Predilection : Anatomic factors
Minor role in formation of infections
Stensen’s duct lies adjacent to the maxillary
mandibular 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.

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

92. Risk Factors continued…
Neoplasms (pressure occlusion of duct)
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)

93. Complex picture
There must be other factors at work…..
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 MC site of
acute suppurative infection!

94. Differential Diagnosis of Parotid Gland
Enlargement
Lymphoma
Actinomycoses
Cat-scratch disease
Sjogren’s syndrome
Wegener’s granulomatosis
Viral infection

95. 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%.

96. Bacteriology
Purulent saliva should be sent for culture.
 Staphylococcus aureus is most common
 Streptococcus pnemoniae and S.pyogenes
 Haemophilus Influenzae also common

97. 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

98. Treatment of Acute Sialadenitis
Reverse the medical condition that may have
contributed to formation
Discontinue anti-sialogogues if possible
Warm compresses, maximize OH, give sialogogues
(lemon drops)
External salivary gland massage if tolerated

99. 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

100. 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

101. 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

102. Complications of Acute Parotitis
Direct extension
 Abscess ruptures into external auditory canal and TMJ have
been reported
Hematogenous spread
Thrombophlebitis of the retromandibular or facial
veins are rare complications

103. 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

104. 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.

105. 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.

106. Chronic Sialadenitis
Of importance in the workup…
The clinician should look for a treatable predisposing
factor such as a calculus or a stricture.

107. 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.

108. 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.

109. AVI
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.

110. Viral Infections
As opposed to bacterial sialadenitis, viral
infections of the salivary glands are SYSTEMIC
from the onset!

111. 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

112. Mumps
2-3 week incubation after exposure (the virus
multiplies in the URI or parotid gland)
3-5day viremia
Then localizes to biologically active tissues like
salivary glands, germinal tissues and the CNS.

113. 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

114. 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 dz

115. 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

116. 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

117. 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

118. 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

119. 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

120. 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.

121. Treatment
Supportive
Fluid
Anti-inflammatories and analgesics

122. 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

123. Complications
Orchitis, testicular atrophy and sterility in
approximately 20% of young men
Oophoritis in 5% females
Aseptic meningitis in 10%
Pancreatitis in 5%
Sensorineural hearing loss <5%
 Usually permanent
 80% cases are unilateral

124. 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

125. Sjögren’s syndrome
90% cases occur in women
Average age of onset is 50y
Classic monograph on thediease published in 1933
by Sjögren, a Swedish ophthalmologist

126. 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

127. Sjögren’s Syndrome
Unilateral or bilateral salivary gland swelling
occurs, may be permanent or intermittent.
Rule out lymphoma

128. 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

129. Sjögren’s Lip Biopsy
Biopsy of SG mainly used to aid in the
diagnosis
Can also be helpful to confirm sarcoidosis

130. 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

131. 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

132. 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.

133. Related to…
a. Metabolic “endocrine sialendosis”
a. 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)

134. Related to
a. Alcoholic cirrhosis: likely based on protein
deficiency & resultant acinar hypertrophy
b. Drug induced: iodine mumps
c. HIV

135. 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.

136. Continued irradiation leads to complete destruction
of the serous acini and subsequent atrophy of the
gland.
Similar to the thyroid, salivary neoplasm are
increased in incidence after radiation exposure.

137. 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.

138. 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.

139. Granulomatous Disease
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.

140. 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

141. 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

142. 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

143. 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

144. 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

145. Necrotizing Sialometaplasia
Self limiting lesion, heals by secondary
intention over 6-8 weeks
Histologically may be mistaken for SCC

146. References
1. Tex book of oral surgery- Peter wardbooth
2. Principles of oral surgery – Peterson
3. Salivary glands disorder – Mayors