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Inflammatoryand
Infectious diseases of salivary gland
SEMINAR NO. 10
Dr Sanjana RavindraOral Medicine and RadiologyRajarajeswari dental college, Bangalore
SALIVARY GLAND
Introduction Classification Composition of saliva Properties of Saliva Functions of Saliva Salivary gland
examination Classification of
Salivary gland diseases
INFLAMMATORY and INFECTIOUS DISEASES OF SALIVARY GLAND
Introduction Classification Various diseases
Summary References
Dr sanjana ravindra
INTRODUCTION
Salivary glands are compound, tubuloacinar, merocrine, exocrine glands whose ducts open into the oral cavity
It has more
than one tubule
entering the main
duct
Morphology
of the secreting
cells
Only the secretion
of the cell is
released
Secretes fluid
onto a free
surface
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302 Dr sanjana ravindra
CLASSIFICATION A
cco
rdin
g to
th
e si
ze
Major salivary glands.
Minor salivary glands.
Acc
ord
ing
to t
he
typ
e o
f se
cret
ion
:
Serous secreting
- Parotid - von ebners
Mucous secreting
- Glossopalatine - palatine.
Mixed
Submandibular – sublingual - labial and buccal - glands of blandin and
nuhn
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302 Dr sanjana ravindra
TYPES
Parotid: largest, anterior to ear, serous,25% of total saliva.
Submandibular: Intermediate, angle of mandible,60% of total saliva.
Sublingual: Smallest, anterior floor of mouth, 5% of total saliva.
Major salivary Glands
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302 Dr sanjana ravindra
Labial (lips) – mixed
Buccal (cheeks) - mixed
Palatine - mucous
Lingual:
• Anterior – mixed
• Middle – serous
• Posterior – mucous.
Minor salivary Glands
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302
TYPES
anterior glands of blandin and nuhn
posterior von ebner glands
Dr sanjana ravindra
Parotid glands are the largest of all salivary
glands, situated at the side of the face just
below and in front of the ear. Each gland
weighs about 20 to 30 g in adults.
Secretions from these glands are emptied into
the oral cavity by Stensen duct.
This duct is about 35 mm to 40 mm long and opens inside the cheek
against the upper second molar tooth
Parotid Glands
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302
TYPES
Dr sanjana ravindra
Submaxillary glands or submandibular glands are
located in submaxillary triangle, medial to
mandible.
Each gland weighs about 8 to 10 g.
Saliva from these glands is emptied into the oral cavity by Wharton duct, which is
about 40 mm long.
The duct opens at the side of frenulum of tongue, by means of a small opening on the summit of papilla
called caruncula sublingualis.
Submandibular Glands
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302
TYPES
Dr sanjana ravindra
Sublingual glands are the smallest salivary glands situated in the mucosa at the floor of the
mouth.
Each gland weighs about 2 to 3 g. Saliva from these glands is
poured into 5 to 15 small ducts called ducts of Rivinus.
These ducts open on small papillae beneath the tongue.
One of the ducts is larger and it is called Bartholin duct.
It drains the anterior part of the gland and opens on caruncula
sublingualis near the opening of submaxillary duct.
Sublingual Glands
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302
TYPES
Dr sanjana ravindra
1. Lingual Mucus Glands Lingual mucus glands are situated in posterior one third of the tongue, behind circumvallate papillae and at the tip and margins of tongue.
2. Lingual Serous Glands Lingual serous glands are located near circumvallate papillae and filiform papillae.
3. Buccal Glands Buccal glands or molar glands are present between the mucus membrane and buccinator muscle. Four to five of these are larger and situated outside buccinator, around the terminal part of parotid duct.
4. Labial Glands Labial glands are situated beneath the mucus membrane around the orifice of mouth.
5. Palatal Glands Palatal glands are found beneath the mucus membrane of the soft palate.
Minor salivary glands
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302
TYPES
anterior glands of blandin and nuhn
posterior von ebner glands
Dr sanjana ravindra
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302
COMPOSITION OF SALIVA
Dr sanjana ravindra
PROPERTIES OF SALIVA
1.Volume: 1000 mL to 1500 mL of saliva is secreted per day and it is approximately about 1 mL/minute.
2.Reaction: Mixed saliva from all the glands is slightly acidic with pH of 6.35 to 6.85
3. Specific gravity: It ranges between 1.002 and 1.012
4. Tonicity: Saliva is hypotonic to plasma.
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302 Dr sanjana ravindra
FUNCTIONS OF SALIVA
1. PREPARATION OF FOOD FOR SWALLOWING
• Food - moistened and dissolved by saliva. • Mucous membrane - moistened by saliva. It
facilitates chewing.
• Mucin of saliva lubricates the bolus and
facilitates swallowing.
2. APPRECIATION OF TASTE
• Taste is a chemical sensation. By its solvent action, saliva dissolves the solid food substances, so that the dissolved substances can stimulate the taste buds.
• The stimulated taste buds recognize the taste.
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302 Dr sanjana ravindra
3. DIGESTIVE FUNCTION
Saliva has three digestive enzymes, namely salivary amylase, maltase and lingual lipase
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302
FUNCTIONS OF SALIVA
Dr sanjana ravindra
4. CLEANSING AND PROTECTIVE FUNCTIONS
Due to the constant secretion of saliva, the mouth and teeth - rinsed - free off food debris, shed epithelial cells and foreign particles., saliva prevents bacterial growth by removing materials
Enzyme lysozyme of saliva kills bacteria such as staphylococcus, streptococcus and brucella.
Proline-rich proteins present in saliva posses antimicrobial property and neutralize the toxic substances such as tannins. Tannins are present in many food substances including fruits.
Lactoferrin of saliva also has antimicrobial property.
Proline-rich proteins and lactoferrin protect the teeth by stimulating enamel formation.
Immunoglobulin IgA in saliva also has antibacterial and antiviral actions.
Mucin present in the saliva protects the mouth by lubricating the mucus membrane of mouth.
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302
FUNCTIONS OF SALIVA
Dr sanjana ravindra
ROLE IN SPEECHBy moistening and lubricating soft parts of mouth and lips, saliva helps in speech. If the mouth becomes dry, articulation and pronunciation becomes difficult.
„REGULATION OF WATER BALANCEWhen the body water content decreases, salivary excretion also decreases. This causes dryness of the mouth and induces thirst. When water is taken, it quenches the thirst and restores the body water content.
EXCRETORY FUNCTIONMany substances, both organic and inorganic, are excreted in saliva. It excretes substances like mercury, potassium iodide, lead, and thiocyanate.
Sembulingam k., Sembulingam P. Digestive System. In: Essentials of Medical Physiology. 6th ed. Jaypee Brothers Medical Publishers (P) Ltd.
2012; 220-302
FUNCTIONS OF SALIVA
Dr sanjana ravindra
Salivary
Families
Anti-
BacterialBuffering
Digestion
Mineral-
ization
Lubricat-
ion &Visco-
elasticity
Tissue
Coating
Anti-
Fungal
Anti-
Viral
Carbonic anhydrases,
Histatins
Amylases,
Mucins, Lipase
Cystatins,
Histatins, Proline-
rich proteins,
Statherins
Mucins, Statherins
Amylases,
Cystatins, Mucins,
Proline-rich proteins, Statherins
Histatins
Cystatins,
Mucins
Amylases, Cystatins,
Histatins, Mucins,
Peroxidases
FUNCTIONS OF SALIVA
Dr sanjana ravindra
SALIVARY GLAND EXAMINATION
INSPECTION OF PAROTID GLAND
The parotid gland region between the
ramus of the mandible and the mastoid
process is examined for any swelling
Parotid swelling lifts the ear lobe
The skin over the region is observed for
any changes
In case of infection, the skin is distended, and in
the absence of inflammation there will
be no hyperaemia.
I/O, the orifrice of the duct is checked for
inflammation, swelling or fluid escape
Dr sanjana ravindra
SALIVARY GLAND EXAMINATION
PALPATION OF PAROTID GLAND
Palpated with thumb and
index/middle finger.
Margins of the gland are felt
externally for any warmth or
tenderness over the skin
Consistency of the gland is checked
whether soft, firm, nodular or indurated
Dr sanjana ravindra
SALIVARY GLAND EXAMINATION
INSPECTION OF SUBMANDIBULAR OR SUBLINGUAL GLAND
Inspected for any
abnormalities both I/o
and E/o
I/o one side of the floor
of the mouth is isolated
and dried –sterile
cotton rolls.
Swelling and colour
change in the
surrounding mucosa is
noted
Orifrice of the ducts of the glands
are observed for any
inflammatory changes and fluid
escape
Dr sanjana ravindra
SALIVARY GLAND EXAMINATION
PALPATION OF SUBMANDIBULAR AND SUBLINGUAL GLAND
Bimanually
Index finger of one hand is
placed along the lingual
surface of the mandible, and
one or two fingers of the
other hand used to palpate the gland from
outside.
Margins of the gland are felt externally for
any warmth or tenderness
over the skin
Consistency of the gland is
checked whether soft or
hard
Dr sanjana ravindra
INFLAMMATORY AND INFECTIOUS DISEASES OF
SALIVARY GLAND
Dr sanjana ravindra
CLASSIFICATION
CLASSIFICATION
SALIVARY GLAND DISEASES
Neoplastic
Benign
Malignant
Non- neoplastic
Developmental
Aplasia / Agenesis
Hyperplasia of minor salivary
glands
Infectious
Bacterial
Viral
Systemic
Sarcoidosis
Sjogrens’
Sialosis
Obstructive
Sialolith
Mucocele
Ranula
Autoimmune
Sjogrenssyndrome
Mikulicz’sdisease
CLASSIFICATION
Dr sanjana ravindra
Infl
am
ma
tory
Bacterial
Acute
Chronic
Viral
Mumps
HIV infection
Cytomegalovirus infection
Autoimmune
Sjogren’s Syndrome
Mikulicz’s Disease
Uveoparotid fever
CLASSIFICATION
Infl
am
ma
tory
Bacterial
Acute
Chronic
Viral
Mumps
HIV infection
Cytomegalovirus infection Allergic sialadenitis
Benign inflammatory condition
Necrotising sialometaplasia
CLASSIFICATION
Inflammatory diseases of salivary
gland
Acute
Acute Sialadenitis
Epidemic parotitis/ Mumps
Chronic
Chronic Sialadenitis
Sjogrens’ syndrome
Chronic Sclerosing Sialadenitis
Mickulicz disease
Stomatitis palatinii
Cheilitis glandularis
CLASSIFICATION
BACTERIAL SIALADENITIS
Dr sanjana ravindra
BACTERIAL SIALADENITIS
Staphylococcus aureus
Streptococcus viridans
Streptococcus pneumoniae
Escherichia coli
HaemophilusinfluenzaeAcute
Chronic
Sialadenitis, a generic term to describe infection of the salivary glands, has
a diverse range of signs and symptoms and predisposing factors.
Dr sanjana ravindra
ACUTE BACTERIAL SIALADENITIS
• Acute Suppurative Parotitis
• Surgical Parotitis
• Acute Bacterial Parotitis
PAROTID GLAND
• Acute SuppurativeSubmandibular Sialadenitis
• Acute Bacterial Submandibular Sialadenitis
SUBMANDIBULAR GLAND
Dr sanjana ravindra
ACUTE BACTERIAL SIALADENITISM
ICR
OO
RG
AN
ISM
S Most commonly caused by penicillin resistant Staph. Aureus or Strept. viridians
HO
ST F
AC
TO
RS May be caused
due to decreased host resistance, decreased salivary secretion and decreased bactericidal effects of saliva
SUR
GIC
AL
PR
OC
ED
UR
E
When major surgical procedure is carried out in patients with poor oral hygiene
DR
UG
S
Few reports suggests that drugs
ETIOLOGY
TRUMPET BLOWER’S SYNDROME: a pneumoparotitis associated with tissue
emphysema and crepitus, does not have the symptoms of acute infection. Swelling is
present because of collection of air within the tissue
Dr sanjana ravindra
SIALOLITHIASIS is the most common disorder of major salivary glands characterized by the development
of calculi within the parenchyma or ductal system.
It is the cause of 42–77% cases of salivary duct obstruction.
AGE GROUP
30 to 60 years.
SITE
Submandibular salivary gland – 80%.
Parotid gland - 10–20%
Sublingual gland - 1–5%
Greek word: sialon (saliva) and lithos (stone), and the Latin -iasis meaning "process" or "morbid condition
Dr sanjana ravindra
Composition
The salivary stones are comprised primarily of calcium carbonates and phosphate with traces of magnesium and ammonia. The organic matrix consists of carbohydrates and amino acids.
Sizes
0.1 to 30 mm
Number
In 25% of cases, the stones are multiple.
Dr sanjana ravindra
It produces a viscous, mucous and more alkaline saliva, with a relatively high concentration
of hydroxyapatites and phosphates This predisposes
to the precipitation of salts
Opening of Wharton’s duct is narrower than the diameter of
the whole duct
Gland and ductal system lies in a dependant position i.e. the
duct ascends towards its opening, which is also
conducive to saliva retention
Submandibular gland is the most common site for calculi formation
Dr sanjana ravindra
The nidus subsequently becomes bathed in a solution supersaturated with respect to calcium and phosphate and slowly
calcifies
Stagnation of saliva enhances the development of the sialolith and occurs secondary to either the nidus itself or due to the tortuosity
of the ductal system
Progression occurs once the nidus becomes lodged within the salivary ductal system
Salivary gland calculi develop around a central nidus made of desquamated epithelial cells, foreign bodies, bacteria or mucus
plugs
(Bodner 1993)
ETIOPATHOGENESIS
Dr sanjana ravindra
Static flow of saliva leading to migration of oral flora up to the Stensen duct
The reduced flow of saliva may be caused by duct stricture, obstruction (most commonly from sialoliths), or decreased saliva production secondary to illness or medication
The decline in saliva flow creates stasis- which potentiates bacterial growth
loss of saliva’s bacteriostatic effects-
PRONE prone to bacterial infection
ACUTE BACTERIAL SIALADENITIS
PATHOPHYSIOLOGY
Dr sanjana ravindra
HO
SPIT
AL
-AC
QU
IRE
D • Staphylococcus aureus • Common in debilitated and
immunocompromised patients
CO
MM
UN
ITY
-AC
QU
IRE
D • Staphylococcus and streptococcus• Salivary flow stasis Because of
• Medications that decrease salivary flow,
• Cheek biting• Medical conditions such as
diabetes, malnutrition, and dehydration from gastrointestinal disorders associated with loss of intravascular volume such as diarrhea and vomiting.
TYPES
ACUTE BACTERIAL SIALADENITIS
Dr sanjana ravindra
• Mostly in adults (male) but neonates and childhood form of disease may occur
AGE
• Unilateral parotid gland/ Submandibular gland
SITE
• Begins with elevation of body temperature and sudden onset of pain at the angle of the jaw which is intense when the extensive infection is contained within the confines of the parotid capsule
PRODROMAL SYMPTOMS
• Localized symptoms are accompanied by fever, leucocytosis
SYMPTOMS
• Gland is tender, enlarged and overlying skin is warm and red. Swelling causes elevation of earlobule and the overlying skin is characteristically warm and erythematous
SIGNS
SIGNS
SYMPTOMS
CLINICAL FEATURES
ACUTE BACTERIAL SIALADENITIS
Dr sanjana ravindra
SIGNS
SYMPTOMS
CLINICAL FEATURES
ACUTE BACTERIAL SIALADENITIS
salivary duct: initially flecks of purulent material –salivary duct orifrice,
surrounding erythematous
lymph nodes: cervical lymphadenopathy
Downwards into the deep facial plane of
neck
Backwards into the external
auditory canal
Outwards into the skin of
face
SPREAD OF INFECTION
Dr sanjana ravindra
Complete blood count with differential, and Gram stain
and culture sensitivity of the suppurative discharge
Direct aspiration of any abscess that is identified or aspiration of the parotid is
more likely to identify a causative pathogen
USG,CT and MRI -effective imaging modality to
• Assess for parotid inflammation
• Sialoliths• Cystic lesions • Abscesses
DIAGNOSIS
ACUTE BACTERIAL SIALADENITIS
• Leukocytosiswith immature polymorphoneuclear leukocytes
• increased haemacrit due to dehydration
• Elevated urine specific gravity
• Decreased urine flow rate
Dr sanjana ravindra
SONOGRAPHY: the affected gland shows swelling, increased vascularity
CT features: when the glands are involved in cellulitis, swelling of the glands and obscuration of the glands’ contour can be observed.
On enhanced CT, the affected glands are seen with a higher CT values compared with the normal side because of the increased vascularity
ACUTE BACTERIAL SIALADENITIS
DIAGNOSIS
Ultrasonogram of the right and left
submandibular glands. The right
submandibular gland with the
features of inflammatory process –
hypoechogenic parenchyma with
increased blood flow in Power
Doppler. The left submandibular
gland normal
Dr sanjana ravindra
ACUTE BACTERIAL SIALADENITIS
TREATMENT
Treatment of ASP is focused on rehydration (intravenous or oral) and emperic antibiotic therapy
Stabilization of underlying acute and chronic conditions, and minimizing medications that cause xerostomia
Treatments that may increase salivary flow are also helpful, including warm compresses, sialagogues, and/or parotid massage
Removal of sialolith
Dr sanjana ravindra
COMPLICATIONS
ACUTE BACTERIAL SIALADENITIS
Dr sanjana ravindra
ACUTE BACTERIAL SIALADENITIS
FOLLOW-UP
Dr sanjana ravindra
CHRONIC SIALADENITIS
Defined as “repeat episodes of Acute bacterial sialadenitis that are separated by intervening periods of remission.”
Long history of intermittent exacerbations of unilateral parotid swelling, with asymptomatic periods in between exacerbations
The periods of illness may last weeks or even months at a time with a spectrum of severity
There is generally less pain with eating and less purulent drainage
ADULT FORM
( Staphylococcus aureus )
JUVENILE FORM
( Streptococcus viridans )
Dr sanjana ravindra
TREATMENT
CHRONIC SIALADENITIS
Reduction or elimination of inflammation in the gland
• short term corticosteroids-tapering dosage of Dexamethasone
• 0.75 mg four times daily for 3 days
• Followed by 0.75 mg three times daily for 3 days
• Followed by 0.75 mg two times daily for 3 days
• One-half tablet twice daily for 3 days
Clear the preciptated serum protiens within the intraductal system
• Lozenges • Appropriate medication
management• Warm compresses
Dr sanjana ravindra
CHRONIC SIALADENITIS
Dr sanjana ravindra
Dr sanjana ravindra
CHRONIC SCLEROSING SIALADENITIS
Etiology. The etiopathogenesis is unknown, but it has been suggested to be the result of an immune process triggered by intraductal agents.
Clinical Presentation. Patients present with clinical features simulating a salivary tumor with enlarged, firm, and painful unilateral or bilateral submandibular salivary glands.
Diagnosis. This condition requires biopsy for histologic diagnosis since, clinically, it cannot be differentiated from a neoplasm. It is characterized by progressive periductal fibrosis, dilated ducts with a dense lymphocyte infiltration, and lymphoid follicle formation, with acinaratrophy. Sonographic findings include duct dilatation and calculi and prominent intraglandular vessels.
(Kuttner ’s Tumor)
Chronic sclerosing sialadenitis is a rare chronic inflammatory disease of the submandibular salivary gland, although it has been reported to occur in
parotid and minor salivary glands.
Dr sanjana ravindra
ALLERGIC SIALADENITIS
Description and Etiology Enlargement of the salivary glands - exposure to various pharmaceutical agents and allergens. Unclear - true allergic reactions or whether some represent secondary infections - medications that reduced salivary output.
Clinical Description The characteristic feature - acute salivary gland enlargement -itching over the gland. Cases have been reported of salivary gland enlargement without rash or other signs of allergy.
Diagnosis The diagnosis of allergic reaction should be made judiciously, especially when salivary gland enlargement is not accompanied by other signs of an allergic reaction. The possibility of infection or autoimmune disease should also be considered.
Dr sanjana ravindra
SIALOGRAPHY
• Sialography is defined as the radiographic demonstration of the major salivary glands by introducing a radiopaque contrast medium into their ductal system.
Sialography visualises the ducts and the parenchyma of the salivary gland, after contrast administration into the main salivary duct.
The preoperative
phase
The filling phase
The emptying
phase.
The procedure is divided into three phases.
Dr sanjana ravindra
PREOPERATIVE PHASE
This involves taking preoperative
(scout) radiographs, if not already taken,
before the introduction of the contrast
medium, for the following reasons:
• To note the position and/or presence of
any radiopaque obstruction
• To assess the position of shadows cast
by normal anatomical structures that
may overlie the gland, such as the hyoid
bone
• To assess the exposure factors.
Dr sanjana ravindra
FILLING PHASE
• Having obtained the scout films,
the relevant duct orifice needs to
be found, probed and dilated and
then cannulated. The contrast
medium can then be introduced.
• When this is complete, the filling
phase radiographs are taken,
ideally at least two different views
at right angles to one another.
EMPTYING PHASE
• The cannula is removed and the
patient allowed to rinse out.
• The use of lemon juice at this stage to
aid excretion of the contrast medium
is often advocated but is seldom
necessary.
• After 1 and 5 minutes, the emptying
phase radiographs are taken, usually
oblique laterals. These films can be
used as a crude assessment of
function.
Dr sanjana ravindra
Contrast media
• IONIC AQUEOUS SOLUTIONS— Diatrizoate (Urografin®)— Metrizoate (Triosil®)
• NON-IONIC AQUEOUS SOLUTIONS— lohexol (Omnipaque®)
• OIL-BASED SOLUTIONS— Iodized oil, [ Lipiodol®]
• WATER-INSOLUBLE ORGANIC IODINE COMPOUNDS,
-Pantopaque®.
Dr sanjana ravindra
Simple injection technique
Oil-based or aqueous contrast
medium is introduced using
gentle hand pressure until the
patient experiences tightness or
discomfort in the gland, (about
0.7 ml for the parotid gland,
0.5 ml for the submandibular
gland).
Hydrostatic technique
Aqueous contrast media is
allowed to flow freely into
the gland under the force of
gravity until the patient
experiences discomfort.
Continuous infusion
pressure-monitored
technique
Using aqueous contrast
medium, a constant flow
rate is adopted and the
ductal pressure monitored
throughout the procedure.
Advantages • The controlled introduction of contrast
medium is less likely to cause damage or give an artefactual
picture • Simple • Inexpensive.
Disadvantages • Reliant on the patient's responses • Patients
have to lie down during the procedure, so they need to be positioned in advance for the
filling-phase radiographs.
Advantages
• Simple
• Inexpensive
Disadvantages
• The arbitrary pressure which is applied may cause damage to the
gland
• Reliance on patient's responses may lead to underfilling or
overfilling of the gland.
Advantages • The controlled introduction of contrast media
at known pressures is not likely to cause damage • Does
not cause overfilling of the gland • Does not rely on the
patient's responses.
Disadvantages • Complex equipment is required • Time
consuming.
Dr sanjana ravindra
SIALOGRAPHIC APPEARANCES
Normal – Parotid gland: Tree in winter appearance
Submandibular gland: Bush in winter
Salivary gland calculi
Dr sanjana ravindra
Sjogrens’ syndrome : snowstorm appearance
SIALOGRAPHIC APPEARANCES
Sialadenitis – blobs/ dots
Dr sanjana ravindra
VIRAL SIALADENITIS
Dr sanjana ravindra
EPIDEMIC PAROTITIS MumpsAcute viral parotitis
Paramyxovirus
Coxsackie A virus
Cytomegalovirus
Epstein-Barr virusInfluenza A
Parainfluenza virus type 3
Human herpes virus 6
“ Acute, contagious, self limiting viral infection usually affecting the parotid glands and sometimes submandibular and sublingual salivary glands”
Dr sanjana ravindra
EPIDEMIC PAROTITIS
Incidence has decreased due to immunisation
programs- MMR (measles, Mumps, Rubella) vaccines
Spread of infection-direct contact,: saliva,
fomites and respiratory tract droplets
Incubation period: 2-3 weeks
Age: 5-6 years
Rare- adults
CLINICAL FEATURES
90% parotid gland
10% submand
ibular and
sublingual
Dr sanjana ravindra
EPIDEMIC PAROTITIS
Bilateral (75%) or unilateral (25%) swelling of the parotid glands with pain, tenderness to palpation, erythema, malaise, and fever
Patients often complain of pain with speech, swallowing, and eating
Trismus may be present if there is inflammation involving the pterygoid muscles
CLINICAL FEATURES
Enlargement is sudden and
often bilateral
Skin over the gland is
oedematous, gland is tender
No discharge, although
ductal orifrice is inflamed.
Dr sanjana ravindra
EPIDEMIC PAROTITIS
DIAGNOSIS
Serum amylase level
Specific IgM level
Proteins levels
Leukopenia with lymphocytosis
Glucose level( less than normal) SEROLOGICAL STUDIES
Complement fixing antibodies to paramyxovirus S antigen or soluble
antibodies directed against viral neucleoprotein appear
Titres peak within 2wks and persist for
8 or 9 months
Antibodies directed against the surface haemagglutination
appear -------
1st week of infection
Weeks but persist up to 5 years
Dr sanjana ravindra
EPIDEMIC PAROTITIS
TREATMENT
• MMR vaccine at the age of 12-15 months
• Booster dose at 4-12 years of age
• Symptomatic treatment : controlling the pain and swelling
MMR VACCINE
• The MMR vaccine is
an immunization vaccine
against measles, mumps,
and rubella (German measles).
• It is a mixture of live attenuated
viruses of the three diseases,
administered via injection.
• It was first developed by Maurice
Hilleman while at Merck.
"Measles, Mumps, and Rubella -- Vaccine Use and Strategies for Elimination of Measles, Rubella, and Congenital Rubella Syndrome and
Control of Mumps: Recommendations of the Advisory Committee on Immunization Practices (ACIP)Dr sanjana ravindra
EPIDEMIC PAROTITIS
COMPLICATIONS
Mild meningitis
Encephalitis : marked decrease in level of consciousness, convulsions,
paresis, involuntary movements and high fever
Pancreatitis
Myocarditis
Oophoritis : associated with fever, nausea, vomiting, low abdominal pain,
impaired fertility and early menopause
Orchitis and epididymitis : may result in testicular atrophy
Fetal deaths in the 1st trimester of pregnancy
Dr sanjana ravindra
CYTOMEGALOVIRUS INFECTION
MAJOR MANIFESTATION
• Fever and malaise
LESS COMMON
• Pharyngitis, tonsillitis, sphenomegaly and lymphadenopathy
Xerostomia and reduced saliva production were found with the presence of CMV and salivary gland
dysfunction
COMPLICATIONS: Interstitial pneumonia,
hepatitis, meningoencephalopathyand haemolytic anaemia
Dr sanjana ravindra
HIV INFECTION
Characterized by – xerostomia with unilateral or bilateral salivary gland enlargement
Reactivation of a latent
virus
ETIOLOGY
Frequency of salivary gland enlargement is
more among homosexuals
and Intravenous
drug users than those infected
by other routes of transmission
If enlargement increases, biopsy of gland is indicated as
chances of development of lymphoma and Kaposi
sarcoma are high
Dr sanjana ravindra
HEPATITIS C VIRUS ( HCV) INFECTION
Salivary gland enlargement is one of the extrahepatic manifestations of HCV infection
Sialadenitisappears to be more frequent in women with
chronic HCV infection than
men
Patients may complain of
salivary gland enlargement
with xerostomiabut not
commonly dryness of eyes
57-77% of HCV infected
persons were found to have
sialadenitisresembling SS
Detection of HCV-DNA and anti- HCV antibodies helps to confirm the diagnosis
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NECROTIZING SIALOMETAPLASIA
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NECROTIZING SIALOMETAPLASIA
“Benign self-limiting reactive inflammatory disorder of the salivary tissue”
ETIOLOGY
Clinically, this lesion mimics a malignancy, and failure to recognize this lesion has resulted in unnecessary radical surgery. Etiology - unknown, - local ischemic event, infectious process, or perhaps an immune response to an unknown allergen
describedby Abrams - 1973
Traumatic injury
Dental injections
Ill-fitting denture
Upper respiratory
tract infections
Previous surgeries
PREDISPOSING FACTORS
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Vasoconstriction Sluggish blood
flow
Compromised vascular blood
supply from trauma
Likely etiopathogenesis
It also reported in patients with other conditions, such
as sickle cell disease, Buerger disease, Raynaud
phenomenon, lymphoma and bulimia
NECROTIZING SIALOMETAPLASIA
Carlson DL. Necrotizing sialometaplasia: a practical approach to the diagnosis. Arch Pathol Lab Med 2009;133:692-8.Dr sanjana ravindra
Trauma was noted in 2%-9% of cases
Pain reported in 22%-45% of cases, and up
to 12% reported
numbness.
Approximately 12% of cases involve the
palate bilaterally
Other oral sites include buccal
mucosa, lip, retromolar
pad, and major salivary glands.
The lesion also occur at extra salivary sites including lungs, breast, and skin.
Lesion occurring outside the salivary glands - designated as adenometaplasia
Skin was affected, lesion termed as syringometaplasia or metaplasia of sweat ducts
The average age is 40 years, with a 2:1 male predilection
NECROTIZING SIALOMETAPLASIA
Commonly affects the mucoserous glands of hard palate but can occur anywhere, with 10% of cases affecting the major salivary glands
Affects hard palatal mucosa in 40%-60% of cases; Junction of hard and soft palate in 13% of cases ; Soft palate in 3%-10% of cases; Tongue affected in only 3% of cases
Dr sanjana ravindra
Necrotizing sialometaplasiapresents initially as a swelling.
Subsequent ulceration innecrotizing sialometaplasia
NECROTIZING SIALOMETAPLASIA
Classically, NS presents initially as slight unilateral swelling
that over a few days develops into a 1-3-cm ulcer on the
posterior hard palate or at the junction of hard and soft palate.
The initial swelling suggest the diagnosis of an abscess, the
subsequent ulceration suggests a malignancy, such as a
squamous cell carcinoma or salivary gland malignancy.
The ulcerated and necrotic tissue separates from the
adjacent vital tissue, and it is common for the former to
sequestrate
Carlson DL. Necrotizing sialometaplasia: a practical approach to the diagnosis. Arch Pathol Lab Med 2009;133:692-8.Dr sanjana ravindra
Anneroth and Hansen described histopathogenesis of NSby proposing five histological stages: infarction, sequestration,
ulceration, repair, and healing.
A reactive inflammatory infiltrate composed of neutrophils, chronic inflammatory cells, & histiocytes develops, with
squamous metaplasia of ducts & acini
Small acini-sized pools of mucus bordered by basement membrane and delicate fibrous septa
Infarcted salivary lobules in the earliest stages exhibit escape of mucus into the parenchyma
NECROTIZING SIALOMETAPLASIA
Carlson DL. Necrotizing sialometaplasia: a practical approach to the diagnosis. Arch Pathol Lab Med 2009;133:692-8.Dr sanjana ravindra
• Metaplasia of salivary ducts in NS – extensive, to be mistaken for
islands of invasive squamous cell carcinoma
However, maintenance of lobular architecture, lack of significant
cytologic atypia and lack of overlying dysplasia rule out a squamous
cell carcinoma
NECROTIZING SIALOMETAPLASIA
Treatment is directed toward
symptom relief, and spontaneous
resolution occurs within 2-3 months
after biopsy
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GRANULOMATOUS CONDITIONS
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TUBERCULOSIS
Tuberculosis (TB) is a chronic bacterial infection, caused by Mycobacterium tuberculosis, leading to the formation of granulomas in the infected tissues.
“First case of parotid gland tuberculosis – DePaoli – 1893
Sinve then only 100 cases have been reported in the literature”
1st mode
• It may begin as infection of tonsillar tissue or by autoinoculation with infected sputum, which reaches the parenchyma or lymphatic system of the parotid gland by the afferent lymphatics or by ducts
2nd mode
• Gland may be infected by metastasis from the lungs by a haematogenous or lymphatic route
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TUBERCULOSIS
Diffuse, parenchymatiusdisease resembling common parotid inflammation
Nodal involvement-acute inflammatory reaction with diffuse generalised glandular swelling
Involvement of intraglandular lymph nodes.
Presents with chronic, slow-growing, painless and firm parotid lump simulating a neoplasm
Glandular parenchymal involvement- presents as an encapsulated, chronic mass.
The mass is typically unilateral and associated with matted lymph nodes.
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SARCOIDOSIS
Sarcoidosis is a chronic condition in which T lymphocytes, mononuclear phagocytes, and granulomas cause destruction of involved tissue.
represents an infection or a hypersensitivity response to atypical mycobacteria
The parotid is affected in less than 10% of cases of sarcoidosis
Clinically- bilateral painless enlargement of the parotids that has a diffuse or multinodular character may be seen
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SARCOIDOSIS
Heerfordt syndrome - also known as uveoparotid fever-Pathognomonic for sarcoidosis-it consists of
Parotid enlargement,Bilateral uveitis, andFacial nerve palsy.
TREATMENT• Primarily palliative
• Chloroquine alone or in combination with corticosteroids
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CHEILITIS GLANDULARIS
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CHEILITIS GLANDULARIS
Rare inflammatory disorder of the minor salivary glands affecting mostly those of the lower lip
Self- inflicted trauma such as
biting and excessive wetting
habitual licking
Actinic exposure
ETIOLOGY
SIMPLE: Lesions are multiple superficial papules with central
depression and dilated ducts
SUPERFICIAL SUPPURATIVE: (Baelz disease) : indurated
swelling of the lip with painless shallow ulcers and crusting
DEEP SUPPURATIVE: (Cheilitisglandularis apostematosa):
abscesses, sinus tracts, fistulas and in few cases scarring
TYPES
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CHEILITIS GLANDULARIS
Progressive chronic condition, most often diagnosed 3-12 months after onset
Early stages: Asymptomatic lower lip swelling with clear viscous secretion on the mucosal surface
Patient may complain of discomfort or a raw sensation at the vermilion border
Pain which may be transient or recurrent – mucopurulentdischarge through the opening of inflamed salivary gland ducts
With increasing in swelling- lip gets everted, demarcation by the vermilion border vanishes,
Exposed labial mucosa –susceptible to drying,
erosion, ulceration and fissuring
When exposed to actinic rays, the chances of
development of SCC also increases.
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NICOTINIC STOMATITIS
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NICOTINIC STOMATITIS
M>F, 5th-7th decade of life
Seen commonly in reverse smokers.
Minor SG of hard palate is affected
Palatal mucosa becomes diffusely grey or numerous elevated papules with punctate centres maybe seen
‘Dried mud appearance’ - keratinized palatal epithelium
Seen in cigar smokers and pipe smokers
ETIOLOGY- inflammation of minor salivary
glands and their orifices due to chronic
irritation from tobacco smoke
TREATMENT
Completely
reversible with
smoking cessation
within 2-5 weeks
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MIKULICZ’S DISEASE
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MIKULICZ’S DISEASE
Symmetric or bilateral, chronic, painless lacrimal, parotid, and submandibular gland enlargement with associated lymphocytic infiltrations
1st coined by Mikulicz -
1888
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MIKULICZ’S DISEASEAGE AND SEX
Commonly in women in middle and later life
SITE
Unilateral or bilateral enlargement of parotid and/or submandibular gland
PRODOMAL SYMPTOMS
Associated with fever, upper respiratory tract infection, oral infection, tooth extraction or some local inflammatory disorders
Mild local discomfort, occasional pain and xerostomia
Dr sanjana ravindra
MIKULICZ’S DISEASESI
GN
S Often diffuse, poorly outlined enlargement of salivary gland rather than formation of a discrete tumor nodule.The enlargement varies in sizes but generally few centimeters in diameter
H/O alternating increase and decrease in size of mass, from time to time
DU
RA
TIO
N Few months or many
years
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MIKULICZ’S DISEASE
DIAGNOSIS
Clinical diagnosis
• Unilateral or bilateral enlargement of parotid and lacrimal gland
Laboratory diagnosis
• Biopsy shows solid nest or clumps of poorly defined epithelial which termed as “ epimyoepithelialisland”
TREATMENT:Surgical excision of involved gland
Good prognosis
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SJOGRENS’ SYNDROME
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Sjogren syndrome (SS) is an autoimmune disorder in which immunocytes damage the salivary, lacrimal and other exocrine glands and is thus termed an autoimmune exocrinopathy
SJOGRENS’ SYNDROME
SS has two major forms
Primary Sjögrensyndrome (SS-1)
• dry eyes and dry mouth are seen in the absence of a connective tissue disease.
• Uncommon and sometimes termed ‘sicca syndrome’, but the latter term is also used non-specifically for dry mouth and eyes.
Secondary Sjögrensyndrome (SS-2)
• is more common: dry eyes and dry mouth are seen together with other autoimmune diseases,
• usually primary biliary cirrhosis (PBC) or a connective tissue –most usually (in descending order of frequency)
■ Rheumatoid arthritis (RA)■ Systemic lupus erythematosus■ Polymyositis■ Scleroderma■ Mixed connective tissue disease.
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SJOGRENS’ SYNDROME
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SJOGRENS’ SYNDROME
AGE can affect any age, but the onset is
most common in middle-age or older.
GENDER The majority of patients
affected by SS are women.
GEOGRAPHIC There is no known
geographic incidence to SS.
Estimated to affect 1–3% of the general
population.
Menopausal women in the fourth and fifth
decades of life.
More prevalent in women than men, with a ratio
of 9:1.
EPIDEMIOLOGY
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SJOGRENS’ SYNDROME
AETIOLOGY
Initiation by an exogenous factor
disruption of salivary gland epithelial cells
T lymphocyte migration and lymphocytic infiltration of exogenous glands
B lymphocyte hyper-reactivity and production of rheumatoid factor and antibodies to Ro(SS-A) and La(SS-B)
Konttinen Y, Kasna-Ronkainen L. Sjogren’s syndrome viewpoint on pathogenesis. Scand J Rheumatol 2002;116:15–22.Dr sanjana ravindra
SJOGRENS’ SYNDROME
RISK FACTORS
A genetic predisposition to SS has been suggested because of multiple reports of two or more members of the same family developing the syndrome.
A family history of the disease puts people at an increased risk of developing SS compared to the general population.
This is also supported by the development of SS in twins.
It has been suggested that a genetic susceptibility is required for the development of autoantibodies which are found in SS and this may be associated with a link between polymorphic major histocompatibility complex (MHC) genes and the
development of autoimmune diseases.
This area needs further exploration before a definitive link can be found.
GENETIC PREDISPOSITION
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SJOGRENS’ SYNDROME
VIRAL INITIATING FACTORRISK FACTORS
Cytomegalovirus infection led to the development of SS-like symptoms
Other viruses potentially involved in the aetiology of SS are Epstein-Barr virus, hepatitis C virus (HCV) and human T-cell Leukaemia virus-1
It is hypothesized that viruses can promote autoantibody production through molecular mimicry, resulting in cross-reactivity of immune reagents with host antigens.
The amino-acid sequence and structural similarities between foreign and self-peptides (molecules from dissimilar genes) allows an immune response directed against the virus to concurrently elicit a tissue-specific immune response via the creation of cytotoxic cross-reactive lymphocytes and antibodies which result in cell and tissue destruction
Dr sanjana ravindra
SJOGRENS’ SYNDROME
The early manifestations may be non-specific, such as fatigue, arthralgia, and Raynaud phenomenon, and it can be 8–10 years from the initial symptoms to
full-blown disease.
CLINICAL FEATURES
It presents with a clinical spectrum that ranges from an organ-specific autoimmune process to a systemic disorder
Systemic lupus erythematosus
Scleroderma
mixed connective tissue
disease
primary biliary cirrhosis
hyperthyroidism (Graves disease)
hypothyroidism (Hashimoto thyroiditis).
Mothers with SS can pass autoantibodiesacross the placenta into the foetal circulation –leading to foetal heart block
Dr sanjana ravindra
SJOGRENS’ SYNDROME
CLINICAL FEATURES
Sensations of grittiness, soreness, itching, dryness, blurred vision or light intolerance.
The eyes may be red with infection of the conjunctivae and soft crusts at the angles (keratoconjunctivitis sicca).
The lacrimal glands may swell.
EYE
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SJOGRENS’ SYNDROME
CLINICAL FEATURES
Xerostomia: often the most frequent although not all patients complain of dry mouth
Soreness or burning sensation
Difficulty eating dry foods, such as biscuits (the cracker sign)
Difficulties in controlling dentures
Difficulties in speech: there may be a clicking quality of the speech as the tongue tends to stick to the palateDifficulties in swallowing
Complications such as unpleasant taste or loss of sense of taste; oral malodour; caries; candidiasis; sialadenitis.
ORAL
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SJOGRENS’ SYNDROME
Hyposalivation
Tendency of the mucosa to stick to a dental mirror
Food residues
Lack of salivary pooling
Frothiness of saliva and absence of frank salivation from
Major gland duct orifices
A characteristic tongue appearance; lobulated, usually
red, surface with partial or complete depapillation
In advanced cases – obviously dry and glazed oral
mucosae.
OBJECTIVE SIGNS
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SJOGRENS’ SYNDROME
■ Raynaud phenomenon
■ arthralgia
■ myalgia ■ fatigue
■ skin ulceration or
rash
■ dyspnoea ■ dry vagina
■ bruising, bleeding and
purpura
numbness
EXTRAORAL (EXTRA-GLANDULAR) COMPLICATIONS OF SS
Connective tissue disease in SS usually precedes the onset of dry eyes and dry mouth, and, therefore, patients presenting
With dry eyes and dry mouth alone probably have Primary SS
■ Other neurological features, including orofacial sensory loss, orofacial pain or facial palsy, and other cranial neuropathies.
Dr sanjana ravindra
A non-productive cough secondary to dryness of tracheobronchial mucosa (xerotrachea) or dyspnea due to small airway obstruction is
relatively common
High-resolution CT of the lungs often demonstrate wall thickening at the segmental bronchi, and bronchial biopsy shows peribronchial
and/or peribronchiolar mononuclear inflammation.
Interstitial lung disease in Sjogren’s syndrome is less common.
Pleural effusions are infrequently found in primary Sjogren’s syndrome. Lymphoma should always be suspected when lung
nodules or hilar or mediastinal lymphadenopathy are present in chest radiographs.
SJOGRENS’ SYNDROME
RESPIRATORY TRACT DISEASE
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SJOGRENS’ SYNDROME
MUSCULOSKELETON SYMPTOMS
Polyarthralgias
polymyalgias
morning stiffness
intermittent inflammatory
synovitis
chronic polyarthritis.
Despite myalgia and easy fatigue, frank myositis is unusual.
Inflammatory arthritis is observed in 50% of patients but, in contrast to RA, there are usually no erosive changes.
Rare cases of inflammatory myositis have been reported.
Dr sanjana ravindra
SJOGRENS’ SYNDROME
Pseudolymphoma,
Monoclonal gammopathies (such as waldenstrom's macroglobulinaemia)
Mixed monoclonal cryoglobulins
Non-hodgkin lymphoma of the diffuse large b-cell type
Extranodal marginal zone b-cell lymphomas of the mucosa-associated lymphoid tissue type.
LYMPHOPROLIFERATIVE DISEASES
Mostly seen in primary SS, as b-cell lymphoproliferation in mucosal- associated lymphoid tissue (MALT)
Patients with SS have a 15–40-fold increased risk of the development of B-cell non-Hodgkin lymphoma.
This is < 1 case per 100 patients per year; 2% of cases at 5 years and up to 5% of cases with time.
Dr sanjana ravindra
SJOGRENS’ SYNDROME
o Most lymphomas complicating SS arise in mucosal extranodal sites, especially the
salivary glands.
o Most lymphomas are low-grade marginal zone B-cell lymphoma with long-term
survival.
Pseudolymphoma or frank lymphoma should be suspected when:■ persistent salivary gland enlargement■ lymphadenopathy■ hepatosplenomegaly
Lymphomas may be predicted if there are features such as:■ fever■ palpable purpura■ leg ulcers■ peripheral neuropathy■ lymphopenia with low CD4 counts■ hypocomplementaemia■ cryoglobulinaemia.
Dr sanjana ravindra
SJOGRENS’ SYNDROME
• Benign lymphoepithelial lesions of the salivary glands do not necessarily require surgical treatment.
• For lymphomas,; chemotherapy or rituximab.(or) radioimmunotherapy using (90)Y-ibritumomab tiuxetan.
Dr sanjana ravindra
SJOGRENS’ SYNDROME
DIAGNOSIS OF SJOGREN SYNDROME
History
Clinical examination
Investigation findings
A subjective feeling of dry mouth (xerostomia) is common in the general population, although reduced salivary flow (hyposalivation) is not always confirmed by objective studies
ocular symptoms oral symptoms ocular signs autoantibodies and other
blood tests salivary gland studies
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SJOGRENS’ SYNDROME DIAGNOSTIC CRITERIA
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SJOGRENS’ SYNDROME
INVESTIGATIONS
Dr sanjana ravindra
SJOGRENS’ SYNDROME
SIALOMETRY
To measure salivary flow rate (resting /
stimulated)
Provide essential information for diagnostic and
research purposes
Calculated from the individual major salivary gland or
from a mixed sample of the oral
fluids, termed “whole saliva”.
Passive drool
sialometricsoral swab
Infant swabSpitting method
Suction method
INVESTIGATIONS
Dr sanjana ravindra
SJOGRENS’ SYNDROME
SIALOMETRY
• Avoid having alcohol,caffenine,prescribed medication 12 hours before collection of saliva.
• Avoid eating major meal within 60 min of sample collection
• Avoid dairy products for 20 min before sample collection
• Participants should not brush their teeth within 45 minutes prior to sample collection.
• Rinse mouth with water to remove food residue before sample collection. Wait at least 10
minutes after rinsing before collecting saliva to avoid sample dilution.
• Also while pipetting saliva, greater accuracy is obtained by aspirating slowly in order to
avoid formation of bubbles.
PRECAUTIONS
INVESTIGATIONS
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SJOGRENS’ SYNDROME
SIALOMETRY
PASSIVE DROOL• Passive drool - highly recommended
because it is both cost effective and approved for use with almost all analytes.
• To avoid problems with introduction of contaminants, use only high quality polypropylene vials for collection .
• The vials used must seal tight and be able to withstand temperatures down to -80ºC.
• Should allow saliva to pool in the mouth.
• Unwrap the saliva collection aid (SCA) and insert it into the top of the cryovial .
• With head tilted forward, drool down the SCA to collect saliva in the cryovial.
INVESTIGATIONS
Dr sanjana ravindra
SJOGRENS’ SYNDROME
SIALOMETRY
SALIMETRICS ORAL SWAB (SOS)
• An excellent alternative to passive drool
• SOS also helps filter large macro molecules and other particulate matter from the sample.
• Not recommended for children below 6 yrs of age
INVESTIGATIONS
Dr sanjana ravindra
SJOGRENS’ SYNDROME
AUTOANTIBODIES AND OTHER BLOOD TESTS
Serology is used to establish the presence of anti-SS-A/Ro and
anti-SS-B/La auto-antibodies,based on (enzyme-linked immunosorbent assay).
Anti-SS-A/Ro antibodies can also be detected in other autoimmune
processes such as rheumatoid arthritis and systemic lupus
erythematosus; for this reason, anti-SS-B/La antibodies are
considered to be more specific of SS.
Anti- SS-A/Ro can be isolated in 25-65% of cases, and anti- SS-
B/La in 13-48%
INVESTIGATIONS
SEROLOGIC TESTS
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SJOGRENS’ SYNDROME
AUTOANTIBODIES AND OTHER BLOOD TESTSINVESTIGATIONS
SEROLOGIC TESTS
Erythrocyte Sedimentation Rate (ESR),
C-reactive Protein (CRP)
Plasma Viscosity (PV
Dr sanjana ravindra
SJOGRENS’ SYNDROME
The sialography typically shows sialectasias in contrast to the fine arborization seen in normal parotid ductules.
Diagnosis is generally based on the classification
Sjogrens’ syndrome : snowstorm appearance
SIALOGRAPHY
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SJOGRENS’ SYNDROME
SS is a mixture of increased inflammatory proteins and decreased acinar proteins when compared with healthy controls.
SIALOCHEMISTRY
Analysis of saliva composition (sialochemistry) for the diagnosis and monitoring of salivary disease
■ lactoferrin
■ beta 2 -microglobulin
■ interleukin-6
■ lysozyme
■ sodium, chloride, albumin, IgA and IgG
Dr sanjana ravindra
SJOGRENS’ SYNDROME
• In the scintigraphic test, 99mTc-pertechnate is given intravenously, and
in SS patients the typical finding is decreased uptake in response to
stimulation of the parotid and submandibular salivary glands.
• This test is a sensitive and valid method to measure abnormalities in
salivary gland function
SCINTIGRAPHY
Dr sanjana ravindra
SJOGRENS’ SYNDROME
However, the lymphocytic foci are
not present in all minor salivary
glands, and multiple glands should be
examined to secure an accurate diagnosis
Focal aggregates of at least 50
lymphocytes and plasma cells and adjacent to ducts
and replacing aciniare seen in patients
with Sjogren’ssyndrome.
Lip biopsy confirms lymphocytic
infiltration of the minor salivary
glands.
LIP BIOPSY
Dr sanjana ravindra
SJOGRENS’ SYNDROME
1. Schirmer test
2. Rose Bengal
Staining
3. Tear break up
time (BUT)
OCULAR DIAGNOSTIC TESTS
Dr sanjana ravindra
SJOGRENS’ SYNDROME
SCHIRMER’S TEST
• The tip of a strip of filter paper 30 mm
long is slipped beneath the inferior lid,
with the remainder of the paper
hanging out.
• After 5 minutes, the length of paper
wetted is measured.
• Wetting of less than 5 mm is a strong
indication of diminished tearing.
Dr sanjana ravindra
SJOGRENS’ SYNDROME
• Rose bengal is stains the devitalized or damaged
epithelium of both the cornea and conjunctiva.
• In Sjogren’s syndrome, slit lamp examination after
rose bengal staining shows a punctate pattern of
filamentary keratitis.
ROSE BENGAL STAINING
Dr sanjana ravindra
SJOGRENS’ SYNDROME
• A drop of fluoroscein is instilled into the eye,
and the time between the last blink and
appearance of dark, nonfluorescent areas in the
tear film is measured.
• An overly rapid break-up of the tear film
indicates an abnormality of either the mucin or
the lipid layer.
TEAR BREAK-UP TIME
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SJOGRENS’ SYNDROME
Dr sanjana ravindra
SJOGRENS’ SYNDROME
Dr sanjana ravindra
SJOGRENS’ SYNDROME
Dr sanjana ravindra
SJOGRENS’ SYNDROME
Dr sanjana ravindra
SJOGRENS’ SYNDROME
NOTABLE CASES
CARRIE ANN INABA(SINGER-ACTRESS)
VENUS WILLIAMS(WORLD CHAMPION TENNIS PLAYER)
Dr sanjana ravindra
Dr sanjana ravindra
SJOGRENS’ SYNDROME
Dr sanjana ravindra
REFERENCES
Dr sanjana ravindra
REFERENCES
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Salivary Glands - Development, adaptations and diseases 2nd Ed. Krager, Switzerland, 2010.p.01-24.
2. Tucker A.S., Miletich I. Salivary Gland diseases. In: Salivary Glands - Development, adaptations and diseases 2nd
Ed. Krager, Switzerland, 2010.p.129-146.
3. Scully C. Common and important oral conditions .p. 183-406.
4. Lynch MA. Salivary Gland Diseases. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine:
Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
5. Cumming CG. Salivary Gland diseases. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine:
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Oral Medicine. 10th ed. Spain: BC Decker Inc; 2003. 563-577.
7. Silvermann S., Eversole R.L., Truelove E.L. Salivary gland diseases. In: Essentials of Oral Medicine. 3rd ed. London:
BC Decker Inc; 2011. p. 260-281.
8. Harris P.J., Weisman M. H. Rheumatic diseases. In: Head and Neck manifestations of systemic diseases. USA:
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Medical Publishers (P) Ltd. 2012; 220-302
10. Waites E. Essentials of Dental Radiography and Radiology, 3rd Ed. Churchill Livingstone. 2003;304-341.
Dr sanjana ravindra
REFERENCES
11.Regezi JJ. Sciubba JA, Jordan RJ. Salivary gland Disease. In: Oral Pathology- Clinical Pathologic correlation. 6th ed. USA:
Elseveir; 2012.p. 186-225.
12.Meyers EN, Ferris RL. Anatomy, Function, and Evaluation of the Salivary Glands. In: Salivary gland disorders. 2nd Ed.
NewYork: Springer-Verlag Berlin Heidelberg; 2007.p. 1-16.
13.Meyers EN, Ferris RL. Infections of Salivary Glands. In: Salivary gland disorders. 2nd Ed. NewYork: Springer-Verlag Berlin
Heidelberg; 2007.p. 167-177.
14.Meyers EN, Ferris RL. Diagnosis and Management of Autoimmune Salivary Gland Disorders. In: Salivary gland disorders.
2nd Ed. NewYork: Springer-Verlag Berlin Heidelberg; 2007.p. 201-220.
15.Bruch M., Treister NS. Salivary gland diseases. In: Oral medicine and Oral pathology. New York : Springer Dordrecht
Heidelberg London; 2012. p.103-113.
16.Scully C. Sjogrens Syndrome. In: Oral and Maxillofacial Medicine THE BASIS OF DIAGNOSIS AND TREATMENT. p.321-330.
17.Montes C , Ortiz M, Garcia JF, Hermandez F. Review of the literature on necrotizing sialometaplasia Review of the
literature on necrotizing sialometaplasia . Quintessence Int. 2015;46(1):67-72.
18.Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and Maxillofacial Pathology. 2nd ed. Philadelphia: Saunders; 2002.
19.Rajendran R. Textbook of oral pathology.6th edition, 2011 Elsevier
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