Salivary glands /certified fixed orthodontic courses by Indian dental academy

Salivary Glands
& Disease

INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com


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.


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


Parotid development13
• 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.

Parotid development13
• 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.


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.

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.


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.


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


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


Salivary gland secretory unit12
• Composed of terminal acini
• Intercalated, striated and excretory ducts
• Myoepithelial cells


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

Salivary Function12
• Aid is mastication, deglutination
• Salivary lysozyme, IgA and other
antibacterial substances protect against
caries and oral cavity infections
• Saliva also aids in speech


Anatomy: Parotid Gland12,13
• 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


Anatomy:Parotid Gland12
• 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


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.

Anatomy: Deep Lobe13
• 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.

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

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.


Anatomy: Parotid Fascia12
• 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.


Anatomy: Parotid Lymphatics12
• 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

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.


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


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 preauricular region.

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.

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

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.

Parotid Bed: Deep lobe lies on...14
• 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

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.

Anatomy: Submandibular
Lymphatics
Submandibular gland drains into
submandibular nodes.


Anatomy: Submandibular Duct13
• 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.


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 bacterialaden oral fluids.

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.


• 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.


• 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


Physiology13
• 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

Obstructive
Salivary Gland Disorders
• Sialolithiasis
• Mucous retention/extravasation


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 swelling 2


Sialolithiasis Incidence2
• Escudier & McGurk 1:15-20 0003
• Marchal & Dulgurerov 1:10-20 0002
Sialolithiasis remains the most frequent
reason for submandibular gland resection 5


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.

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.


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.


Etiology2
•
•
•
•
•

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

Etiology7
Gout is the only systemic disease known
to cause salivary calculi and these are
composed of uric acid.


Stone Composition2
• 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

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

Reasons sialolithiasis may occur
7
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

Other characteristics:
• Despite a similar chemical make-up,
80-90% of SMG calculi are radio-opaque 7
50-80% of parotid calculi are radiolucent 7
• 30% of SMG stones are multiple
60% of Parotid stones are multiple

Clinical presentation10
• Painful swelling (60%)
• Painless swelling (30%)
• Pain only (12%)
– Sometimes described as recurrent salivary
colic and spasmodic pains upon eating


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?

Exam: Inspection12
•
•
•
•
•
•
•

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

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).

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

Diagnostic approaches2
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

Diagnostic approaches:
2
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


Sialography continued…
• Disadvantages:
–
–
–
–
–
–

irradiation dose
pain with procedure
poss.perforation
infection dye reaction
push stone further
contraindicated in active infection.


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

Diagnostic Approaches:
11
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!


Diagnostic Approach:
2
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


Diagnostic approach:
2
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


Sialolithiasis Treatment2
• None: antibiotics and anti-inflammatories,
hoping for spontaneous stone passage.
• Stone excision:
– Lithotripsy
– Interventional sialendoscopy
– Simple removal (20% recurrence)7

• Gland excision

Sialolithiasis Treatment11
• 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 hyperhydration when symptoms develop.


Stone excision2
• 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.

Transoral vs. Extraoral
11
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.


Posterior Stones11
• 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.

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


Gland excision11
• 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


Gland excision indicated11
•
•
•
•

Very posterior stones
Intra-glandular stones
Significantly symptomatic patients
Failed
transoral
approach


Gland excision

6

• 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

Obstructive
Salivary Gland Disorders
• Sialolithiasis

• Mucous retention/extravasation


Mucocele9
• 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


Mucocele

9

• 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.


Mucocele9
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

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


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.


Ranula9
• 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.

Ranula9
• 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.


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.


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.


Treatment of Mucoceles9
in Lip or Buccal mucosa
• Excision with strict removal of any
projecting peripheral salivary glands
• Avoid injury to other glands during primary
wound closure


Ranula Treatment9
• Marsupialization has fallen into disfavor
due to the excessive recurrence rate of 6090%
• Sublingual gland removal via intraoral
approach


Salivary Gland Infections
• Acute bacterial sialdenitis
• Chronic bacterial sialdenitis
• Viral infections


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


Sialadenitis1
Awareness of salivary gland infections was
increased in 1881 when President Garfield
died from acute parotitis following
abdominal surgery and associated systemic
dehydration.


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


Pathogenesis1
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.


Acute Suppurative1
• 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

Predilection for Parotid

1

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.


Salivary Composition1
• 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.

Parotid Predilection
Anatomic factors

1

• 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.

Risk Factors for Sialadenitis1
• Systemic dehydration (salivary stasis)
• Chronic disease and/or immunocompromise
–
–
–
–
–
–

Liver failure
Renal failure
DM, hypothyroid
Malnutrition
HIV
Sjögren’s syndrome

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)


Complex picture1
• 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!

Differential Diagnosis of Parotid
Gland Enlargement
•
•
•
•
•
•

Lymphoma
Actinomycoses
Cat-scratch disease
Sjogren’s syndrome
Wegener’s granulomatosis
Viral infection

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%.


Bacteriology1
• Purulent saliva should be sent for culture.
– Staphylococcus aureus is most common
– Streptococcus pnemoniae and S.pyogenes
– Haemophilus Influenzae also common


Lab Testing1
• 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

Treatment of Acute Sialadenitis1
• 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


Treatment of Acute
1
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

Failure to respond1
•
•
•
•

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

Surgery for Acute Parotitis1
• 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

Complications of Acute Parotitis1
• 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


Complications1
• 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

Complications1
• 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.

Chronic Sialadenitis7
• 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.

Chronic Sialadenitis7
• Of importance in the workup…
• The clinician should look for a treatable
predisposing factor such as a calculus or a
stricture.


No treatable cause found7:
• 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.


Acute viral infection (AVI)1
• 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.


AVI1
• 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.


Viral Infections1
As opposed to bacterial sialadenitis, viral
infections of the salivary glands are
SYSTEMIC from the onset!


Viral infection1
• Mumps is a non-suppurative acute
sialadenitis
• Is endemic in the community and spread by
airborne droplets
• Communicable disease
• Enters through upper respiratory tract


Mumps1
• 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.


Epidemiology1
• 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

Virology1
• 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

Clinical presentation1
• 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


Physical exam1
• 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

Diagnostic Evaluation1
• 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

Serology1
• “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


Serology1
• “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

Serology1
• 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.

Treatment
• Supportive
• Fluid
• Anti-inflammatories and analgesics


Prevention1
• 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


Complications1
• 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

Immunologic Disease
7
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


Sjögren’s syndrome7
• 90% cases occur in women
• Average age of onset is 50y
• Classic monograph on thediease published
in 1933 by Sjögren, a Swedish
ophthalmologist


Sjögren’s Syndrome7
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

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


Sjögren’s Syndrome15
• 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

Sjögren’s Lip Biopsy15
• Biopsy of SG mainly used to aid in the diagnosis
• Can also be helpful to confirm sarcoidosis


Sjögren’s Lip Biopsy15
• 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


Sjögren’s Treatment15
• 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


Sialadenosis7
• Non-specific term used to describe a noninflammatory 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.


Related to7…
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)

Related to7…
a. Alcoholic cirrhosis: likely based on
protein deficiency & resultant acinar
hypertrophy
b. Drug induced: iodine mumps
e. HIV


Radiation Injury7
• 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.


• 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.


Granulomatous Disease7
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.

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.

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.

Cysts7
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

Cysts7
Acquired cysts include:
• Mucus extravasation vs. retention
• Traumatic
• Benign epithelial lesions
• Association with tumors
–
–
–
–

Pleomorphic adenoma
Adenoid Cystic Carcinoma
Mucoepidermoid Carcinoma
Warthin’s Tumor

Other: Pneumoparotitis7,8
• 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

Pneumoparotitis8
• 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


Other: Necrotizing
7
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

Necrotizing Sialometaplasia15
• Self limiting lesion, heals by secondary
intention over 6-8 weeks
• Histologically may be mistaken for SCC


References
1.
2.
3.

4.

5.

McQuone, SJ: Acute viral and bacterial infections of the salivary
glands. Oto Clinics North America, 32:793,1999
Marchal F, Dulguerov P. Sialolithiasis Management. Arch Oto,
129:951, 2003
Escudier MP, McGurk M. Symptomatic sialodenitiis and
sialolithiasis in the english population:an estimate of the cost of
hospital treatment. Br Dent J. 1999;186:463
Lustmann J, Regev E, Melamed Y. Sialolithiasis: a survey on 245
patients and a review of the literature. Int J Oral Maxillofacial.
1990; 19, 135
Crabtree GM, Yartington CT. Submandibular gland excision.
Laryngoscope. 1988;98:1044

References
6. Marchal F, Kurt AM, Dulgeurov P, Becker M et al. Histopathology of
submandibular glands removed for sialolithiasis. Ann Oto
Rhinol.2001;110, 464
7. Rice DH. Salivary Gland Disorders. Med Clin North Am. 1999; vol 83,
197.
8. Kirsh CM, Shinn J, Porzio R et al. Chest. 1999, vol 116, 1476
9. Baurmash HD. Mucoceles and Ranulas. J Oral Maxillo Surg. 2003, vol
61, 369
10. Ellies M, Laskawi R, Arglebe C, et al. Surgical management of
nonneooplastic disease of the submandibular gland. Int J Oral
Maxillofac Surg. 25:1996, 285
11. Williams MF. Salivary gland diseases: sialolithiasis. Oto Clin North
America. Vol 32, 819, 1999

References
• 12: Krause GE, Meyers AD. Management of
parotid swelling. Comprehensive Therapy. 1996,
22:256.
• 13. Silvers AR, Som PM. Head and Neck
Imaging: the Salivary Glands. 1998, 36:941
• 14. Carlson GW. The salivary glands. Surgical
Clin North America. 2000, 80:261
• 15. Feinberg SE. Diagnosis and management of
salivary gland disorders. Ch.34

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