SALIVARY GLAND

DISORDERS
PRESENTED BY:
AMARINDER KAUR

 The term GLANDS with reference

to salivary gland structures was first
introduced Vesalius.

Three pairs of
Major Salivary
glands :
1) Parotid
2) Submandibular
3) Sublingual
Numerous Minor
Salivary glands :
In tongue , palate ,
cheeks and lips.

PAROTID GLAND
The ancient Greeks
referred parotid
glands as paraauricular swellings
Largest salivary
gland
Weighs 14-28 gm
Measures on an
average 5.8cm
craniocaudally and
3.4cm ventrodorsally

ANATOMY
Situated below external acoustic
meatus , between the ramus of the
mandible and sternocleidomastoid.
Overlaps these structures
Anteriorly also overlaps masseter
muscle

 PAROTID CAPSULE:
Formed by the investing layer of deep
cervical fascia
The fascia splits between the angle of
mandible and the mastoid process to enclose
the gland
Superficial lamina , thin and is attached
above to the zygomatic arch
Deep lamina is thin, attached to styloid
process, the mandible and the tympanic
plate

1)
2)
3)
4)

EXTERNAL FEATURES:
3 sided pyramid
Apex : directed downwards
Has 4 surfaces :
Superior
Superficial
Anteromedial
Posteromedial

 SURFACES:
Superior : forms upper end of the
gland , small and concave
Superficial :largest of the four surfaces
Anteromedial :grooved by the posterior
border of the ramus of the mandible
Posteromedial :moulded to the mastoid
and the structures attached to them

 STRUCTURES WITHIN THE PAROTID

GLAND :
Arteries: External Carotid Artery
Maxillary Artery
Superficial Temporal
vessels
Posterior Auricular Artery

 VEINS : Retromandibular vein

NERVES: Facial Nerve
LYMPH NODES :Parotid lymph
nodes

 PAROTID DUCT:
Stensons duct after Neil Stenson
Thick walled
5cm long
Emerges from the middle of the
anterior border of the gland
Opens into the buccal mucosa
opposite the crown of the maxillary
first molar

BLOOD SUPPLY :
Supplied by External Carotid Artery and
its branches that arise near the gland
VEINS :
Drain into External jugular vein
NERVE SUPPLY :
1) Auriculotemporal nerve
2) Plexus around the external carotid
artery
3) Great auricular nerve

 LYMPH NODES :
Drains first to the parotid lymph
nodes and from there to the upper
deep cervical lymph nodes.

SUBMANDIBULAR SALIVARY GLAND

Thomas Wharton of York
was the first to identify the
submandibular gland and
duct, thats why its duct
bears his name
Large salivary gland
Situated in the anterior
part of the digastric
triangle
Size of a walnut
Roughly J shape , being
indented by the posterior
border of the mylohyoid
which divides it into a
larger part superficial to
the muscle and a small
part lying deep to the
muscle

 SUPERFICIAL PART:
Fills the digastric triangle
Extends upwards deep to the
mandible up to the mylohyoid line
Has inferior , lateral and medial
surfaces

DEEP PART:
Small in size
Lies deep to mylohoid
Superficial to hyoglossus and the
styloglossus
Posteriorly , continuous with the
superficial part round the posterior border
of the mylohoid
Anteriorly , extends up to the posterior
end of the sublingual gland

SUBMANDIBULAR DUCT:
Thin walled
About 5cm long
Emerges at the anterior end of the deep
part of the gland and runs forward on the
hyoglossus , between the lingual and
hypoglossal nerves.
Opens on the floor of the mouth on the
summit of the sublingual papilla, at the
side of the frenulum of the tongue

 BLOOD SUPPLY : Facial artery

VEINS : Common Facial vein or
Lingual vein
LYMPH NODES: Submandibular
lymph nodes

 NERVE SUPPLY :
Branches from submandibular
ganglion
These branches convey:
a)secretomotar fibers
b)sensory fibers from lingual nerve
c)vasomotar sympathetic fibers
from the plexus on facial artery

SUBLINGUAL SALIVARY GLAND

Discovered by Bartholinus hence
duct named Bartholin duct
Smallest gland
Flattened almond shaped
Weighs: 2gm
Measures about 2.5cm

 Lies above the mylohyoid , below the

mucosa of the floor of the mouth, medial
to the sublingual fossa of the mandible
and lateral to the genioglossus.
About 15 ducts emerge ( also k/a Ducts of
Rivinus) from the gland.
Most of them opens directly into the floor
of the mouth on the summit of the
sublingual fold , a few of them join the
submandibular duct.

MINOR SALIVARY GLANDS

Lie within the submucosa of the oral
cavity, palate, paranasal sinuses,
pharynx, larynx, trachea and bronchi
Particularly concentrated in the buccal ,
labial , palatal and lingual regions
Gingiva , anterior hard palate and true
vocal cords have relatively sparse
concentration
Serous glands of von Ebner are small
glands whose ducts open into the sulci
of the circumvallate papillae.

DEVELOPMENT AND GROWTH OF THE

SALIVARY GLANDS

During fetal life each salivary gland is

formed at a specific location in the oral
cavity through the growth of a bud of oral
epithelium into the underlying
mesenchyme so it is ectodermal in origin
Primordia of parotid and submandibular
glands appear during the 6th week,
whereas the primordia of the sublingual
gland appears after 7-8 weeks of fetal life
Minor salivary glands begin their
development during the 3rd month

HISTOLOGY : GENERAL ASPECTS

Both the major and minor glands are
composed of parenchymal elements invested
in and supported by connective tissue
The parenchymal elements are derived from
the oral epithelium and consist of terminal
secretory units leading into ducts that
eventually opens into the oral cavity. The
connective tissue forms a capsule around the
gland and extends into it, dividing groups of
secretory units and ducts into lobes and
lobules

 STRUCTURE AND FUNCTION OF

SALIVARY GLAND CELLS :
The terminal secretory units are
composed of serous , mucous and
myoepithelial cells arranged into
the acini or secretory tubules.
The secretions of these units are
collected by the intercalated ducts
which empty into the striated ducts

 SEROUS CELLS :
Are specialized for the synthesis , storage and
secretion of proteins
Typical serous cell is pyramidal in shape, with its
broad base resting on a thin basal lamina and its
narrow apex bordering on the lumen

 MUCOUS CELLS:
Like serous cells , is specialized for the
synthesis , storage and secretion of a secretory
product.
Secretory products of most mucous cells differ
from those of serous cells in two respects :
1) Have little or no enzymatic activity and
probably serve for lubrication and protection of
the oral tissues
2) Ratio of carbohydrates to proteins is greater
and larger amounts of sialic acid and
occasionally sulfated sugar residues are
present

 MYOEPITHELIAL CELLS :
Are closely related to the secretory and
the intercalated duct cells, lying between
the basal lamina and the basal
membranes of the parenchymal cells
Appearance is reminiscent of a basket
cradling the secretory unit ; hence the
name BASKET CELL in the old literature
Are considered to have a contractile
function , helping to expel secretions
from the lumina of the secretory units
and ducts.

 DUCTS :
The duct system of salivary glands is
formed by the confluence of small
ducts into ones of progressively
larger caliber
3 types :
1) Intercalated ducts
2) Striated ducts
3) Excretory ducts

 The ducts of the salivary glands

form a treelike pattern
Finest branches are the
intercalated ducts; the larger
branches and the stem form the
excretory ducts ; striated ducts are
usually present between the
intercalated and excretory ducts

 INTERCALATED DUCTS :
The products manufatured by the acinar cells
are first transported through intercalated ducts
Length of these ducts largely depends upon the
nature of the acini
In predominantly serous glands such as
parotids these are fairly long , and they may
join with several other intercalated ducts
In glands with mucous acini , the acini are
moderately elongated and the intercalated
ducts are correspondingly shorterand often
inconspicous
Formed by a single layer of cuboidal cells
Source of reserve cells

 STRIATED DUCTS :
Cells are tall to low columnar , usually
arranged in a single layer
Under a light microscope , fine striations
are visible in the bases of these cells,
running parallel to the cells long axis
These striations are responsible for the
name striated duct
The transport of sodium cations,
chloride anions , water potassium
cations takes place mainly through the
cells of striated ducts

 EXCRETORY DUCTS:
Transport saliva from the striated
ducts to the oral cavity
Are located entirely within
connective tissue septa and
consist of several layers of
epithelial cells which may vary in
shape from cuboidal to squamous

 FUNCTIONS OF SALIVARY DUCTS :

Transport primary saliva secreted by the terminal
secretory units to the oral cavity
Actively modify primary saliva by secretion and
reabsorption of electrolytes and secretion of proteins:
a) the intercalated duct cells contain secretory
granules , and 2 of antibacterial proteins present in
the saliva, lyzozyme and lactoferrin have been
localized to these ducts by immunofluorescent
studies
b) striated ducts contain kallikrein , an enzyme found
in saliva and synthesize secretory glycoproteins

c) both intercalated and striated

duct cells are capable of
reabsorbing proteins from the
lumen by endocytic mechanisms
d) striated duct cells plays a role in
electrolyte secretion and
reabsorption

 CONTROL OF SECRETION :
The secretion of saliva is controlled by
sympathetic and parasympathetic neural
input
The stimulus for fluid secretion is primarily
via muscarinic cholinergic receptors and
the stimulus for protein release occurs
through beta- adrenergic receptors
Ligation of these receptors induces a
complex signaling pathway within the cells,
involving numerous transport systems

SALIVA
Saliva is the product of multiple salivary
glands lying beneath the oral mucosa.
Each day, the human salivary glands
produce almost 600ml of serous and
mucinous saliva containing minerals,
electrolytes, buffers, enzymes, mucins and
other glycoproteins.
Once saliva passes through the ducts and
enters the oral cavity, it mixes with blood
cells, microorganisms and their products,
oral epithelial cells and cell products, food
debris and upper-airway secretions.

MECHANISM OF SALIVARY SECRETION

Reflex secretion of saliva occurs as a result of stimulation of oral
mechanoreceptors present in periodontal ligament and taste
buds.
Afferent impulses traced along sensory fibres in the trigeminal,
facial and glossopharyngeal nerves, synapsing on 2nd order
neurous in the trigeminal and the nucleus of tractus solitarius.
This will constitute the afferent pathway.

The fibres from the trigeminal and solitary tract nuclei crisscross the median plane and synapse in the ventral posterior
medial nucleus of the thalamus. 3rd order neurons relay in the
post central gyrus of cerebral cortex.

Efferent activity to the salivary glands originate in the

parasympathetic salivatory (superior and inferior) nuclei and the
sympathetic nuclei in the spinal cord.

 Parasympathetic salivatory nuclei are

closely associated with the medial
border of the tractus solitarius and
have inter connections. The afferent
fibers from the trigeminal and the
solitary tract nuclei travel in the
intermediolateral column to reach
the sympathetic preganglionic
neurons in the spinal cord.

 Hence, both parasympathetic and sympathetic

systems are connected to brain stem nuclei and
relay sensory information from the oral cavity.
The nuclei also receive fibers from the
hypothalamus via the descending autonomic
pathways.
Efferent parasympathetic fibers originating in the
salivatory nuclei travel in the cranial nerves VII
and IX and distributed to all the salivary glands.
Fibers to sub-mandibular and sub-lingual glands
exit the brain stem in the nervus intermedius (VII
N) and join the chorda tympani, which then
merge with the lingual branch of trigeminal
nerve and relay in the submandibular ganglion.
Post ganglionic fibers supply the glands.

 Parasympathetic activity provides

the main drive for the secretion of
fluid by salivary glands rich in
water and electrolytes whereas
sympathetic stimulation leads to
secretion of protein.

SIGNAL TRANSDUCTION:
When a nerve to the salivary gland is stimulated, the
transduction of this signal to increase the formation of
saliva is first brought about by the release of neurotransmitters that is nor-adrenaline (Sympathetic) and
acetylcholine, substance P & VIP (Parasympathetic) .
This neuro-transmitter on reaching the secretory cell
membrane binds to the receptor present on the external
surface of the membrane and activates it. The receptor
can be excitatory / inhibitory.
This is turn activates an intermediate (Guanine
nucleotide dependent) membrane protein known as
G protein with in turn activates a regulatory enzyme
present on the inner cytoplasmic surface of the cell.
This enzyme can be phospholipase C / adenyl cyclase.

There are 2 pathways of functioning:

1)Phospholipase C pathway
2)Adenyl cyclase pathway

Phospholipase C Pathway:

This Phospholipase C is activated when acetylcholine binds

to muscarinic receptors, Substance P at peptidergic receptors
on the acinar cell membrane. This pathway leads to secretion
of water and electrolytes.
Phospholipase C hydrolyses phosphatidyl inositol biphosphate
(PIP2), a membrane phospholipid to form Diacylglycerol (DAG)
and Inositol triphosphate (IP3). IP3 stimulate endoplasmic
reticulum to release calcium ions. This increased cytoplasmic
calcium ion concentration causes opening of Ca2 activated
Potassium (K+) channels in the baso-lateral membranes of the
acinar cell and allow K+ to diffuse out of the cell down the
concentration gradient established by Na/K membrane pump
acinar cell and also causes chloride to the leave the cell
through chloride channels on the luminal membrane of the
acinar cell. This increases the lumen negativity, which allows
Na+ to move between the cells into the narrow intercellular
spaces and to the luminal ends through the leaking intercellular
junctions.

 The net result of these transport events is

the transcellular NaCl transport, followed
by water because of the osmotic gradient
created by the movement of NaCl.
Because of this loss of water, the acinar
cells shrink during stimulation and regain
their resting volume when stimulation
ceases. This is accompanied by increase in
the free intracellular Ca2+ concentration,
which returns to basal levels once the cell
volume returns to normal.

Adenyl Cyclase Pathway:

Adenyl cyclase is activated when nor-aderenaline binds to adrenergic acinar
receptors/vaso-active intestinal peptide to peptidergic receptors. This leads to
exocytosis of secretory proteins.

Adenylcylase causes the intra cellular formation of 3,5 cyclic AMP from ATP. This
cAMP activates and second enzyme called cAMP dependent protein kinase (CAPK). CA-PK exists in 4 sub units that is 2 receptor molecules (2R) and 2 catalytic
subunits (2C). 2R molecules bind with cAMP (2R cAMP) thereby liberates the 2C
molecules, which activate effector proteins (Pr) by phosphorylation (Pr-P). The
activated effector proteins then stimulate exocytosis.

Diacylglycerol (from the PLC pathway) also promotes exocytosis. This complex
sequence of intra cellular events thus leads to the formation of primary salivary
fluid.

Once the secretion is initiated, contractions of myoepithelial cells that are

innervated by both parasympathetic and sympathetic nerve fibres facilitate
expulsion of saliva from the gland.

 Since both the branches of autonomic nervous system

innervate myoepithelial cells, stimulation of either one of
them causes contraction of the cell increasing the ductal
pressure thus actively expelling saliva from the glands.
Hence, the primary saliva ejected into the lumen of
secretory end piece is an isotonic fluid having higher Na+
and Low K+ content.
As it passes through the striated duct, Na+ diffuses from
the lumen by the action of mitochondria and via the
folding of basal plasma membrane and is depleted into
the tissue fluid establishing a concentration gradient
between the cell and luminar fluid. In exchange, K+ is
actively transported into the lumen. But water is not
reabsorbed. Thus saliva while passing through the
striated ducts becomes hypotonic from isotonic. The main
excretory ducts modify the final saliva by altering the
electrolyte concentration and adding mucoid component.

UNCONDITIONAL SALIVARY REFLEXES:

The most important stimuli to salivation are:
Mastication
Gustation
Mastication:
This is a reflex response. Receptors in the muscle of mastication,
temporomandibular joint, periodontal ligament and mucosa detect
the presence of a bolus and its mastication and stimulate the
salivary nuclei to increase the parasympathetic secretomotor
discharge to increase in saliva flow of about 3 fold.
Gustation:
The reflex effects of taste stimuli give rise to 10-fold increase in
saliva flow. Sour stimuli are most effective, followed by sweet, salt
and bitter. Acids, particularly citric acid, initiate copious flow rates
of saliva. Sucrose promotes only a small increase in flow but rich
in salivary amylase. From this, it can be postulated that both
sympathetic (responsible for protein secretion) and
parasympathetic (responsible for high flow rate) systems are
stimulated and that there definitely exists connections between
sensory and autonomic nuclei.

Other stimuli:
There appears to be connections between
the salivary nuclei and vomiting center in
the medulla because reflex copious
salivation and nausea frequently occur
just before vomiting probably to
dilute/neutralize the irritant, which is
responsible for nausea.
Hypersalivation occurs in pregnancy and
stems from morning sickness or
esophageal irritation following reflux of
gastric contents due to raised abdominal
pressure in late pregnancy.

COMPOSITION OF SALIVA
Saliva is a very dilute fluid consisting of 99%
water and 1% of large and small molecules and
electrolytes. It is not considered as an ultra
filtrate of plasma, but is a hypotonic fluid.
Because of its hypotonicity, it allows taste buds
to perceive different tastes without being
masked by normal plasma sodium level and
allows for expansion and hydration of mucin
glycoprotein with protectively blankets tissues of
the mouth. Lower levels of glucose, bicarbonate
and urea in unstimulated saliva augment the
hypotonic environment to enhance taste.

SALIVARY CONSTITUENTS:
Proteins,Albumin,Kallikrein,Amylase,Lactoferr
in Glucuronidase,Mucin,Lipase,Parotid
aggregin,EsteraseProline rich proteins,
Peptidase,Serum proteins (Trace)Phosphatase,
Tyrosine rich proteins,Salivary
peroxidase,Vitamin binding
proteins,CarbohydrateEpidermal growth
factor,Lactic dehydrogenase.
LysozymeRibonuclease. Nerve growth
factor.CystatinIgA, IgG,
IgM.FibronectinSecretory IgA.GustinSecretory
component.Histatin

Electrolytes

Ammonia

Magnesium

Bicarbonate

Non specific buffers

Calcium

Phosphates

Chloride

Potassium

Fluoride

Sodium

Iodide

Sulphates

Small organic molecules

Creatinine

Sialic acid

. Glucose

Urea

Lipids

Uric acid

Nitrogen

 Albumin, IgG, IgA, IgM, vitamins, drugs,

hormones, water and ionic constituents of
saliva are derived from blood plasma. Most of
the organic molecules are produced by the
acinar cells such as major proteins like
histatins and cystatins and minor proteins like
epidermal growth factor and lactoferrin. Duct
cells produce lysozyme.
Components of saliva occur in small amounts
and vary with changes in flow. But saliva is a
unique biologic fluid and must be considered
as a whole that is greater than the sum of its
parts116.

ORGANIC COMPONENTS
Protein:
Salivary proteins comprise approximately
200mg/100 ml-only about 3% of the
protein concentration in plasma
Alpha Amylase:
Alpha- amylase is a major digestive
enzyme of saliva found in highest
concentrations that metabolizes starch
and other polysaccharides and is
produced by serous acinar cells of major
salivary glands.

Lipase:
Lipase is secreted by the lingual
(Von-Ebners) salivary glands and
is responsible for the first step in
fat digestion. It is active at
stomach pH and it particularly
important when pancreatic levels
of lipase are low as in new born
and diseases like cystic fibrosis.

Immunoglobulins:
Secretory IgA is the predominant
immunoglobulin at approximately
20mg/100ml with IgG (1.5mg /
100ml) and IgM (0.2 mg/100ml)
arising from the gingival crevice.
Secretory IgA aggregates oral
bacteria and make it difficult for the
cells to bind to oral epithelial / hard
tissue surfaces.

 Antibacterial Proteins:
Lysozyme, lactoferrin and sialoperoxidase are
antibacterial proteins.
Lyzozyme (Muramidase) cleaves the linkage between
N-acetyl muramic acid and N-acetyl glucosamine of the
peptidoglycan component of the bacterial cell wall. But
oral bacteria are resistant to this action. Lysozyme
increases its anti bacterial effects by synergising, with
IgA, H2O2, peroxidase and certain complement
components.
It degrades bacterial peptidoglycan, the main structural
component of bacterial cell walls and makes bacteria
susceptible to osmotic disruption and death.

Lactoferrin:
is a product of the serous cells. Lactoferrin can
directly interact with the bacterial surface through a
carboxy anion interaction thus causing antibacterial
effect. Iron saturated lactoferrin may generate OH
radicals thus showing its bactericidal activity.
Lactoferrin and secretory IgA may function together
to modify the metabolism of oral strepotococci.
Lactoferrin is an iron binding protein, which removes
free iron from saliva depleting iron supply needed for
bacterial growth. Lactoferrin with bound iron has the
ability to kill actinobacillus actinomycetemcomitans
and prevent its binding to host cells which is absent
in lactoferrin with reduced levels of bound irons.

 Salivary Peroxidase is derived from

2 principle sources: From the parotid
and submandibular gland and from
the leukocytes that enter the oral
cavity in the GCF. Sialoperoxidase
oxidizes salivary thiocyanate ion (SCN)
to hypothiocyanate (OSCN) a potent
antibacterial substance, using
hydrogen peroxide produced by oral
bacteria as an oxidant.

Mucin:
Mucin is a high molecular weight glycoprotein produced
by mucus secreting cells located primarily in the sub
mandibular, sublingual and minor salivary gland. It
lubricates oral surfaces and forms a barrier to
penetration of destructive materials.
It also prevents drying of the mucosa. Mucin complexes
with salivary IgA thus enhancing antibody binding
characteristics and also concentrates the antibody at
vulnerable mucosal surfaces.
Mucins also complex directly with many oral
bacteria/bacterial components. Such bacteria are less
likely to adsorb to oral surfaces and thus are more
readily cleared from the oral cavity. Bacterial toxins may
be cleared by first complexing with mucins.

Glycoproteins:
Two major groups of salivary
glycoproteins exist.
Mucous glycoproteins (MG1 &
MG2) found in submandibular and
sublingual saliva.
Proline rich glycoproteins (PRPs)
found in parotid saliva.

Other Polypeptides:
Statherin:
It is a small phosphoprotein (12000D)
relatively rich in tyrosine and proline. It
inhibits hydroxyapatite crystal growth. It
also prevents the precipitation of calcium
phosphates from supersaturated
solutions like saliva. It may be important
as an inhibitor of calculus formation both
in the glands and on the teeth33,103

Sialin:

A tetra peptide (glycine-glycinelysine-arginine) can be utilized by

several bacteria leading to the
formation of alkaline end products,
which are believed to help regulate
the pH of the plaque.

Histidine Rich Peptide:

May have a role in pellicle

formation and aggregation of
bacteria thus contributing to its oral
clearance. These phosphoproteins
inhibit crystal growth in case of
CaPO4 supersaturation. They inhibit
the growth and viability of mutans
streptococci and the viability and
germination of candida.

Other organic compounds:

Many free amino acids are present at

low concentrations (less than
0.1mg/100ml). This will not provide a
medium for bacterial growth.
Urea is present at about 12-20mg/100ml.
Many bacteria hydrolyse urea with the
release of ammonia leading to rise in pH.
Glucose concentrations (0.5 1 mg /
100ml) are too low for the growth of
bacteria but may be increased in diabetics.

Inorganic Constituents
Sodium ,Potassium,Calcium
,Phosphorus ,Chloride ,Thiocyanate
,Flouride , Bicarbonate.

 The major ions (Na, K, Cl and HCO-) are

the main contributors to the molarity of
saliva which is approximately half that of
plasma.
Bicarbonate is the principle buffer in
saliva.
Fluoride content is similar to that of
plasma but is slightly elevated in those
who drink fluoridated water/use fluoridated
toothpaste. These small increases are
important in the anticaries action of
fluoride.

Calcium and Phosphate:

Part of the calcium is bound to protein and part
is in soluble complexes with carbonate,
phosphate/lactate. 10% of the phosphate is in
the ester form in phospho-proteins and part as
traces of pyrophosphate .
These non-ionic forms of calcium and phosphate
makes saliva supersaturated with respect to
hydroxyapatite at normal intra oral pH.
If the pH falls (that is H+ concentration rise),
the PO43- ions are converted to HPO42-.
H2PO4- and the OH- ions are neutralized to form
water. The reaction shifts to right and the saliva
is no longer

 supersaturated causing dissolution of

hydroxyapatite crystals. But if pH rise,
reaction shifts to left with increase in
degree of supersaturation and
causing remineralisation of
hydroxyapatite crystals. The pH at
which these reactions are balanced
are called critical pH attachment and
may serve as potential metabolic
substances for plaque micro flora
because of their small size.

FUNCTIONS OF SALIVA
Functions of saliva can be organized into
5 major categories that serve to
maintain oral health:
Lubrication and protection
Buffering action and clearance.
Maintenance of tooth integrity
Antibacterial activity
Taste and digestion

Lubrication and Protection:

Saliva lubricates and protects oral mucosa (with
the help of these mucins) acting as a barrier
against irritants which may be proteolytic and/
hydrolytic enzymes produced in plaque, potential
carcinogens from smoking and exogenous
chemicals and desiccation from mouth breathing.
The lubricating effects of mucins aid mastication,
speech and swallowing all.
Fluid consistency provides a mechanical washing
action that flushes away non-adherent bacteria
and acellular debris and sugar. Hence limits their
availability to acidogenic plaque microorganisms.

Buffering action and Clearence:

Salivary buffering capacity protects in 2 ways:

Prevents potential pathogenic organism from colonizing
the mouth because many bacteria require specific pH.
Plaque microorganisms can produce acid from sugars,
which if not rapidly buffered and cleared by saliva is
able to demineralize enamel119.
Buffering action of saliva is through
Bicarbonate
Phosphates
Urea
Amphoteric proteins
Enzymes.
Bicarbonate and salivary nitrogenous compounds
diffuses into plaque and neutralizes the acids. It
generates ammonia to form amines, which also act as a
buffer by neutralizing acids.

Maintaining tooth integrity:

Saliva maintains tooth integrity by facilitating

demineralization and remineralization process. Along
with saliva, thickness of plaque and number of bacteria
present determines the demineralization process and
action of buffers.
Caries occurs when the chemical conditions at the tooth
surface favour demineralization over remineralisation
that is when the concentrations of Ca, PO4 and OH are
too low to prevent the apatite like crystals of the tooth
dissolving.
Therefore demineralization is determined by eating
behaviour and oral hygiene practices, while
remineralisation can be promoted by means of fluoride
and (low concentrations) which accelerates
remineralisation by salivary ions.

Antibacterial activity:

Saliva contains immunologic

(Secretory IgA, IgM and IgG) and nonimmunologic agents (Selected proteins,
mucins, peptides and enzymes) coming
from 2 different sources- plasma cells
and ductal cells Secretory IgA produced
by plasma cells in connective tissue and
translocated through the duct cells
neutralize viruses, serves as an antibody
to bacterial antigens and works to
aggregate bacteria thus inhibiting their
attachment to host tissue.

Taste and Digestion:

Saliva contains a protein Gusten that is
thought to be necessary for growth and
maturation of taste buds.
Saliva also serves to dissolve
substances to be tasted and carry them
to the taste buds.
Salivary enzymes initiate fat digestion.
Saliva lubricates food bolus, which aids
in swallowing.

SALIVARY FLOW RATE

Normal range of Unstimulated salivary flow
is 0.1ml / min and Stimulated salivary flow
is 0.2 ml/mm.
FACTORS AFFECTING FLOW RATE:
Duration of stimulus
Nature of stimulus
Dietary factors
Hormonal influence
Salivary flow rate and systemic
factors

Measurement Of Salivary Flow Rate:

The flow rate of saliva may readily be measured in the dental

office. All that is needed is a quiet area, paraffin wax, a
stopwatch, and a device to collect the saliva and measure the
amount secreted.
Of these, the most difficult is the quiet area. Since the flow
of saliva is affected by a hormonally regulated circadian
rhythm, the time of collection should be standardized for
each patient.

Dentists are advised to conduct these salivary tests at the

start of the day, after the patient has fasted overnight and
brushed the teeth in the morning with water only.
Alternatively, it may be performed about 2 hours after eating.

Saliva collection can be 1) whole saliva. 2) Individual saliva.

Whole Saliva:
Whole saliva is the mixed fluid contents of the mouth,
composed of saliva from the major and minor glands, in
addition to variable contributions of serum from the
gingival crevicular fluid or transmucosal exudates,
bacteria and bacterial products, epithelial and blood
cells and their products, debris, and bronchial fluid.
Due to the presence of large number of bacteria
continually loosed from tooth and soft tissue surfaces,
as well as shed epithelial cells, whole saliva usually
requires centrifugation to provide a clear sample. In
some situations, however, the bacteria or cells have
diagnostic value
Individual Saliva:
Individual saliva is the saliva collected from the
individual major salivary glands separately.

Methods of Saliva Collection

Both whole and individual saliva can be collected in either stimulated

or unstimulated form.
To collect resting saliva, the patient is seated comfortably in a chair
and told not to swallow or move the head, mouth, tongue etc. during
the performance of the test. She / he is then instructed to
Swallow before the actual test is initiated.
Allow the saliva to seep into the mouth for a period of two minutes.
Expectorate it into the collecting vessel.
There should be two additional two minute collections for a total
collection time of six minutes. Swallowing is permitted between each
collection.
To collect stimulated saliva, the patient is seated as above and
asked to:
Soften a piece of paraffin wax.
Swallow any saliva that may have been produced in the softening-up
process.
Chew the wax for three, 2-min periods as described above.

 Method of collecting whole saliva:

The main methods of whole
unstimulated saliva collection
include80:
Draining method
Spitting method
Suction method
Absorbent (swab) method

 Draining and spitting methods are used when volume

measurements are required because the concentration
of some saliva constituents is flow rate dependent.
When volume measurement is not required, the saliva
can be collected on cotton swabs, cotton rolls, gauze or
filter paper strips, then eluted or centrifuged, or
aspirated directly from the floor of the mouth with
plastic pipettes.
Draining method: Passive method and requires the
patient to allow saliva to flow from the mouth into a
preweighed test tube or graduated cylinder for a timed
period. It is more reliable and reproducible for
unstimulated whole saliva collection.
Spitting method: The patient allows the saliva to
accumulate in the mouth and then expectorates into a
preweighed graduated cylinder, usually every 60
seconds, for 2 to 5 minutes. It is more reliable and
reproducible for unstimulated whole saliva collection.

 Suction method: Uses an aspirator or saliva ejector to

draw saliva from the mouth into a test tube for a defined
time period. It is less reproducible.
Absorbent method: Uses a preweighed gauze sponge
that is placed in the patients mouth for a set amount of
time. After collection, the sponge is weighed again, and
the volume of saliva is determined gravimetrically. It gives
a variable degree of stimulation of secretion and therefore
less reproducible.

If a stimulated whole saliva collection is desired, a

standardized method of stimulation should be used.
Chewing unflavored gum base or an inert material such as
paraffin wax or a rubber band at a controlled rate is a
reliable and a reproducible means of inducing saliva
secretion. One can also apply 2% citric acid to the dorsum
of the tongue at regular intervals (every 15 seconds). The
flow rates are expressed as ml/min.

SALIVA IN DIAGNOSIS
Saliva provides an easily available, now increasing
diagnostic medium for a rapidly widening range of
diseases and clinical situations.
It is used in the diagnosis of oral and systemic viral
diseases such as measles, mumps, rubella, hepatitis A,
B and C and HIV-1 and 2.
Saliva also aids in the diagnosis of sarcoidosis,
tuberculosis, lymphoma and Sjogrens syndrome. In
addition saliva is used to monitor the level of
endogenous molecules in the body, including
polypeptides and steroid hormones and antibodies.
Saliva also is being used to monitor the level of selected
chemicals introduced into the body alcohol, drugs and
addictive substances among them.

 Advantages:

Saliva has clinical advantages over other body

fluids like blood, serum / urine in diagnosis.
It is easy to collect, (very young and very old) store and
ship. Patient can collect samples at home when clinically
relevant or in other places, including the workplace,
were collecting blood or urine may be difficult.
It can be obtained at low cost and in sufficient quantities
for analysis. Its non invasive collection technique
reduces anxiety in subject and is safer for health care
workers than serum analysis with its associated
exposure to needles and, possibly, AIDS or hepatitis
viruses.
Most molecules found in blood and urine are found in
saliva, although the concentrations one tenth to one
thousandth of those in blood

SALIVA IN ORAL DISEASES

Saliva can be used to assess susceptibility to dental caries and to

screen neoplasms; to detect oral fungal and periodontal
infections.

Salivary tests for caries susceptibility can be easily performed in

dental office, which measures the density of colonies of 2
bacterial species after 2-4 days incubation. It can be used on a
patient as risk potential and need for aggressive preventive
measure49. Dip stick technique monitor salivary mutans and
lactobacilli identify children at high risk for enamel caries and
older adults susceptible to root caries.

P.gingivalis can be detected by PCR using saliva, the pathogen

that is frequently identified in saliva of periodontitis patients. The
technique can be used to monitor and measure improvement also.

Salivary fungal CFU can be used for detection of oral candidiasis.

Quantization of candida from whole saliva can be used as an
indicator of oral candidiasis in patients on multiple drug regimen,
in HIV infection and people wearing complete denture

 SALIVA IN DENTAL CARIES

Saliva is important for the health of both oral soft and hard
tissue. It influences the tooth structure by affecting the caries
process. Individual components of saliva are related in some way
or the other to dental caries.

Saliva collected by expectoration contains a fair

representation of the bacterial and fungal species that coat the
teeth, tongue and mucous membranes. By culturing a known
volume of saliva (in various dilutions) on selective media a
quantitative determination can be made of specific organisms.
Counts of Streptococcus mutans and Lactobacilli are being
employed for identifying children at high risk for enamel caries
and older adults susceptible to root surface caries.

Caries activity refers to the increment of active lesions,

including new and recurrent lesions that occur over a stated
period of time. Saliva has been used in various caries activity tests
like:
Lactobacillus colony count:
Colorimetric Snyder Test:
Streptococcus mutans levels in saliva:

 SALIVA IN PERIODONTAL DISEASES

Saliva is a fluid that can be easily
collected, contain locally derived and
systemically derived markers of
periodontal disease and hence may
offer the basis for a patient specific
diagnostic test for periodontitis. Saliva
contains certain proteins of host origin
(i.e. enzymes, immunoglobulins);
phenotypic markers, (Epithelial
keratins), host cells, hormones
(cortisol), bacteria and bacterial
products, volatile compounds and ions

 ANTIOXIDANT CAPACITY OF SALIVA

Saliva may constitute a first line of defense against

free radical-mediated oxidative stress, since the process
of mastication promotes a variety of such reactions,
including lipid peroxidation.
Pro-oxidant and Antioxidant Features of saliva:
Saliva contains many biochemical systems known to be
involved in soft tissue repair, and many antibacterial
components including lysozyme, lactoferrin and salivary
peroxidase. One of the most important functions of
salivary peroxidase is the control of oral bacteria that
form dental plaque, to imbalances in the ecology and
which lead and to dental caries and to CIPD. Salivary
peroxidase catalyses the peroxidation of the thiocyanate
ion (SCN-) to generate oxidation products (O2SCN-,
O3SCN-, (SCN)2, HOSCN and the more stable OSCN-) that
inhibit the growth and metabolism of many micro
organisms.

SALIVA IN ORAL INFECTIONS

molecularly based determinants are used in saliva fluid diagnostics
A Detection of viruses using antibodies (immunoglobulins IgM, IgG
and IgA) specific for a viral antigen.
Hepatitis A & Hepatitis B
HIV 1 & HIV 2
Measles
Mumps
Rubella
B. Detection of microbe-specific antigenic determinants
Neuraminidase (enzyme associated with influenza A and B)
N-acetylglucosamine (molecule associated with streptococcus A)
Salivary estradiol hormone (Preterm labor indicator)
CA-15; epidermal growth factor, receptor; cathepsin-D; and Waf1 (proposed breast
cancer biomarkers).
Zinc-binding cystic fibrosis antigen (proposed cystic fibrosis biomarker)
Glutamic acid decarboxylase autoantibody (Proposed predictive biomarker for Type I
diabetes)
C. Detection of bacterial organisms in saliva
Lactobacillus acidophilus (associated with dental caries)
Streptococcus mutans (associated with dental caries)
Porphyromonas gingivalis (associated with periodontal disease)

Saliva In Viral Infections:

Monitoring HIV loads through saliva tests, as an adjunct to blood tests,

helps in identifying high levels of HIV in the oral cavity that might place
the patient at risk of transmitting the virus orally.

Secretory IgA and IgG classes to HIV-I are commonly found in saliva.

Saliva based tests for antibodies to HIV are the most popular and widely used
assay

Various kits are available for this purpose like:

Ora sure oral specimen collection system (Epitopic

inc.)
Omni sal, saliva diagnostic systems, Inc.
Ora screenTM HIV rapid test, Beacon diagnostics
They collect saliva by absorbant pads and
estimate salivary IgA levels. The salivary antibodies
reportedly remain stable for 1month at ambient
temperature. Using these devices, 100% specificity
and sensitivity in the results can be achieved
The tests are now finding its use in diagnostic and
epidemiological studies of herpes viruses, Hepatitis
B virus, EBvirus, Entemoeba histolytica infection.

Saliva In Bacterial Infections:

Saliva can help to measure the antibodies to bacterial

antigens for the basis of rapid diagnosis of whooping cough
and Helicobacter pylori infection.

Saliva In Fungal Infections:

Quantization of candida from whole saliva can be used as an indicator of oral

candidiasis in patients on multiple drug regimen, in HIV infection and people
wearing complete denture

SALIVA IN ORAL CANCER

High salivary levels of nitrate and nitrite may predict oral cancer
for epidemiological studies. Association is between ingested nitrate, its
conversion to nitrite and nitrosamines and the development of oral and
gastric cancer. Since the amount of nitrate secreted by the salivary
glands is directly related to the amount ingested, measurements of
salivary nitrate can provide a convenient index for epidemiologic studies

Cancer is caused by the accumulation of mutations that activate protooncogenes and inactivate tumor suppressor genes. The result is a clonal
expansion of genetically identical daughter cells that eventually become
clinical malignancies. The specific mutations acquired by the progenitor
cell are like a fingerprint carried by each cell of the tumor. These
mutations can serve as very specific markers for the presence of tumor
cells in a background of normal cells.

Head and neck tumors can be detected using microsatellite analysis of

DNA derived from exfoliated oral mucosal cell samples from saliva82.
Aberrant gene promoter methylation of DNA derived from exfoliated oral
mucosal cells sampled from whole saliva has also been reported
suggesting that this may form the basis of a screening test for occult
disease

SALIVA IN SYSTEMIC DISEASES

Because of interest in the link between oral and general
health, clinicians are increasingly using salivary
analyses to diagnose systemic disease and to monitor
general health.
The reason for this interest lies in the ability of new
diagnostic tools such as sensitive enzyme linked
immunosorbent assays, as well as other technologies, to
distinguish a range of salivary components that are
biomarkers for changes in the bodys health.

Respiratory Diseases:
Chronic respiratory infection, especially in
children, is often associated with specific
secretory IgA deficiency.
Secretory IgA is the major immunoglobulin of
exocrine gland secretions and determination of
complete or near complete IgA deficiency can
readily be made with a whole saliva sample,
aspirated from the floor of the mouth in young
children or expectorated in older children.
A measurement of IgA from whole saliva
aspirated from the floor of the mouth or preferably
from parotid saliva is diagnostic of the disease.

Diabetes:
patients with diabetes mellitus
have less control over the
pathogens in the oral cavity and
maintainence of oral biological
flora.
significantly decreased salivary
total protein concentration in all
diabetic groups

Chronic Heart Failure:

Salivary endothelin1 concentration
is elevated in patients with chronic
heart failure and can be used to
assess disease severity
Plasma concentrations of the
vasoconstrictor peptide Endothelin
I are raised 2-3 fold in patients
with chronic heart failure (CHF).

Cushings Syndrome and Addisons

disease:
Although many hormones influence the
composition of saliva, the most dramatic
changes have been noted in diseases of
the adrenal cortex.
The sodium and potassium concentration
is markedly affected by corticosteroids,
especially aldosterone, via their impact on
the NaK/ATPase in the striated duct cells.

Stress and Depressive Disorders:

Increased salivary cortisol levels can be used as an
indicator of stress.
Patients with affective disorders secrete significantly
less saliva than normal. Salivary flow rate is reduced in
patients with clinical depression more often because of
psychoactive drugs than the disease per se.
Salivary cortisol is a valid indicator of cortisol
concentration in the serum and is not dependent on
salivary flow rate. Increased levels of circulating and
salivary cortisol (the stress hormone) result from the
activation of the hypothalamic-pituitary adrenal axis
brought on by psychological stress and extensive
physical activity.

Sjogrens Syndrome:

Sjogrens syndrome is a chronic

autoimmune disorder that affects many
systems, including the salivary and
lacrimal glands . Attempts have been
made to use xerostomia (dry mouth) and
salivary gland hypofunction (reduce
saliva flow rate and /or altered
sialochemistry) for the clinical diagnosis
of this medical condition.
Sialochemistry provides helpful screening
procedures to determine whether the
biopsy indicated.

A number of studies have shown that if the disease is

developing in the salivary glands, the periductal infiltrate and
its products (cytokines) can have a profound effect on the
resorptive, transport and synthetic function of the striated duct
cells which result in
a) elevated sodium and chloride concentration and a
decreased phosphate concentration despite reduced flow rate.
b) Elevation in lactoferrin.
c) Elevation in 2-microglobulin and in
d) kallikrein.
Parotid lysozyme was found to be elevated in patients with
primary Sjogrens syndrome but not in secondary Sjogrens
syndrome.
The alteration in glandular structure produced by the disease
resulted in a marked impact on the lipid content of saliva with
a 20 fold elevation in the concentration of phospholipids.
Salivary gland chemistry in Sjogrens syndrome is not only
potentially useful for diagnostic purposes but also for following
disease development and monitoring therapy.

Cystic Fibrosis:
In cystic fibrosis, the most dramatic changes reported
have been an elevation in calcium and proteins,
especially apparent in the sub mandibular, sub-lingual
and minor salivary glands.
In the former, these elevations result in a very apparent
turbidity in the fluid secreted due to formation of a
calcium protein complex and possibly of hyroxyapatite
as well.
In the minor salivary glands, the precipitate physically
obstructs the narrow excretory duct and markedly
reduces the rate of secretion to virtually zero. This
phenomenon can be used as a diagnostic test by
measuring the flow from the readily accessible labial
glands on the lower lip with a capillary tube.

Celiac Disease:
Celiac disease is a congenital disorder
of the small intestine that involves
malabsorption of gluten.
Salivary IgA-AGA measurement has
been reported to be a sensitive and
specific test for the screening of this
disease and monitoring the patients
adherence to the required gluten free
diet.

Down Syndrome:

Saliva can be used as a model for studying

mucosal immuno competence in Down
syndrome patients by monitoring the level of
salivary total immunoglobulin Down syndrome
patients as a possible factor in the susceptibility
of mucosal surfaces to infections and they
found significantly decreased secretion rates of
IgA and IgG which suggested that Down
syndrome patients are immunodeficient in the
humoral mucosal immune response and hence
have a high incidence of recurrent infections in
target organs of the secretory immune systems.

XEROSTOMIA AND SALIVARY GLAND

HYPOFUNCTION
Salivary gland hypofunction may go
unnoticed by patients and practitioners,
because the subjective perception of dry
mouth is not always correlated with
objective evidence of salivary hypofunction
and vice versa.
Therefore, it is imperative to include
salivary gland assessment as part of every
practice.

 Xerostomia means Dry Mouth.

It is a SYMPTOM.
It is not synonymous with salivary gland disease and is not a
reliable indicator of salivary hypofunction. Hence, it SHOULD
NOT BE used as a DIAGNOSIS.
Distinction should be made between the symptom of oral
dryness, signs of salivary dysfunction and specific diagnosis of
salivary disorders and the term Xerostomia should be reserved
for the description of subjective impression of oral dryness. It
has been estimated that 50% reduction in salivary secretion
needs to occur before xerostomia becomes apparent
Definition:

Xerostomia is defined as a subjective complaint of dry

mouth that may result from a decrease in the production of
saliva. Causes of xerostomia:

Xerostomia or dry mouth in most, but not all instances is

related to reductions in salivary output. The most common
causes of salivary hypofunction are medications, medical
treatments and systemic diseases.

Medications:

There are more than 500 medications that

report xerostomia as a side effect. But only a
small number of drugs results in actual reduced
salivation. Though the cause in many instances
is not known, it is possible that medication
induced alterations in the protein content of the
saliva could influence the perception of dry
mouth.
Drugs that reduce salivary function directly
include tricyclic antidepressants,
antihistamines, antihypertensives and diuretics.
The risk of xerostomia increases with the
number of drugs being taken. Therefore
geriatric population is more likely to be affected.

Radiation therapy:
Radiation therapy of the head and neck
regions used as a treatment modality for
primary and recurrent tumours can injure
major and minor salivary glands leading to
atrophy of the secretory components resulting
in varying degrees of temporary / permanent
xerostomia.
Salivary dysfunction may also result from
internal sources of radiation like the treatment
of thyroid carcinoma with radioactive Iodine
(I131) causing both transient and chronic
salivary hypofunction.

Systemic Diseases:

Many systemic diseases cause salivary dysfunction

and xerostomia. Among the most prominent is Sjogrens

syndrome.
Xerostomia associated with primary and secondary
Sjogrens syndrome has been attributed to the
progressive lymphocytic infiltration that gradually
destroys the secretory acini of major and minor salivary
glands or due to an inhibition of nerve stimuli of the
glands leading to loss of glandular function.
Minor salivary glands are affected first.
Other systemic diseases with salivary involvement
include cystic fibrosis, sarcoidosis, poorly controlled
diabetes mellitus, hypertension, thyroid disorders and
depression.

 There are many other conditions that

may involve the salivary glands
occasionally as follows: Primary
biliary cirrhosis, Vasculitis, Chronic
active hepatitis, AIDS, Bone marrow
transplantation, Graft v/s host
disease, Renal dialysis, Dementia of
Alzeheimers type, Neurologic
diseases (Bells palsy, Cerebral palsy,
Parkinsonism).

 Xerostomia is reported in 45-60% of patients

who developed chronic graft v/s host disease
after undergoing allogenic bone narrow
transplantation; so also as a complication of
silicone breast implants. Patients undergoing
hemodialysis develop xerostomia because of
drugs used to treat renal disease. Acute
anxiety / depression / stress cause xerostomia
because of predominant sympathetic
stimulation during such periods leading to
sparse and more viscous salivary secretion.
Infection with HIV has been associated with
parotid enlargement and xerostomia.

Xerostomia and aging:

The data suggest that one out of every 7 adult
patients may suffer from some degree of salivary
hypofunction.
It is more frequently observed in older subjects
(40 per cent in those aged over 65 years). But it
is present in adults of all ages, e.g. about 15 per
cent of the 18-24 year old subjects complain of
xerostomia.
Xerostomia is not a result of normal aging and
salivary function is well preserved through out life
in healthy individuals. Parotid gland output and
composition are stable across the human life
span.

SALIVARY GLAND IMAGING:

Plain films
Sialography
Computed tomography
Magnetic resonance imaging
Ultrasonography
Scintigraphy
PET scan

 Plain films :
Rarely used
Best for grossly detecting radiopaque
sialolithiasis, dystrophic calcifications or
mandibular bone and dental disease
Can be obtained quickly and relatively
inexpensively but may miss a clinically
significant small sialolith

 If plain films are to be obtained for parotid

region, the survey examination should consist of
an extended chin, open-mouth lateral film with
both posteroanterior views ( with or without the
cheeks blown out for detection of stensons duct
stones or other calcifications) and oblique views

FRONTAL VIEW:

 For submandibular gland , an extended chin,

open mouth lateral view with patients finger
depressing the tongue, an intraoral occlusal film
and oblique views are routinely obtained

LATERAL VIEW:

OCCLUSAL VIEW:

 Fluoroscopy :may also help to detect a small

calculus by allowing visualisation of the stones
motion and/or by providing a means to optimize
the patients position in order to demonstrate the
calculus.

 SIALOGRAPHY:
Uses a positive contrast medium to demonstrate
radiographically the ductal anatomy of either the
parotid gland or the submandibular gland

 This examination remains the only imaging study

for examining the fine anatomy of the salivary
ductal system
Sublingual and minor salivary glands are not
studied by this technique

HISTORICAL BACKGROUND:
The term SIALOGRAPHIE was first used by
Jacobvici to characterize the radiographic
demonstration of salivary glands and their ductal
systems.

INDICATIONS:
Detection of a calculus or
calculi or foreign bodies,
whether these are
radiopaque or
radiolucent.
Determination of the
extent of destruction of
the gland secondary to
obstructing calculi or
foreign bodies.

 Detection and portrayal of a fistulae, diverticula

or strictures
Detection and diagnosis of recurrent swellings
and inflammatory processes
Demonstration of a tumor
Selection of site for biopsy

 Outline of the plane of facial nerve as a guide in

planning a biopsy or dissection
Has also been recognized as a therapeutic
procedure because the dilatation of the ductal
system produced during the study may aid in the
drainage of ductal debris

 CONTRAINDICATIONS:
Sensitivity to iodine compounds, and patients who have
experienced severe asthamatic attacks or anaphylaxis following
the use of iodine
Contraindicated in acute inflammation as the ductal epithelium
may be disrupted and escape of the contrast medium from the
ductal system into the parenchyma can produce severe foreign
body reaction accompanied by severe pain
Administration and retention of the iodinated contrast agent may
interfere with subsequent thyroid function tests so such function
studies be performed prior to the use of sialography

CONTRAST MEDIA:
Should have physiologic properties similar to
those of saliva
Miscibility with saliva
Absence of local or systemic toxicity
Pharmacologically inert
Satisfactory opacification
Low surface tension and low viscosity

 Easy elimination
Residual contrast media should be absorbed by
the salivary gland and detoxified by the liver or
excreted by the kidney
TWO TYPES OF CONTRAST MEDIA :
1) Water soluble
2) Oil based

WATER SOLUBLE:
Are principally iodinated benzene or pyridone
derivatives
Low viscosity and low surface tension
More miscible
Physical properties permit filling of the finer
ductal system under lower pressure and
facilitate prompt drainage

FAT SOLUBLE MEDIA :

Two types :1.Iodized oil
2.water insoluble organic compounds
Produces a satisfactory degree of opacification
Are excellent contrast agents if the ductal
systems are intact
Are more viscous and require a higher injection
pressure

PROCEDURE:
Can be divided into three phases:
1) Preliminary plain film evaluation
2) Injection or the filling phase
3) Parenchymal phase or evacuation phase

EQUIPMENT :
Polyethylene tubing with a special blunt-end
metallic tip with side holes for parotid gland
injection; similar for submandibular but has an
end terminal hole
5-10 cc. syringe
Lacrimal dilators
Contrast medium
Lemon slices or artificial lemon extracts

PREPARATION OF PATIENT AND

RADIOGRAPHIIC TECHNIQUE:

Filming procedure is always carried out in supine position

All dentures should be removed
Three to four sets are obtained during the entire procedure :
1) Preliminary films in the anteroposterior, lateral and oblique
positions
2) Filling phase films in the anteroposterior , lateral and oblique
positions
3) Postevacuation phase following stimulation of saliva flow
consists of films completed 5 minutes after the emptying phase in
the anteroposterior, lateral and oblique positions

LOCALIZATION AND CANNULATION OF THE

SALIVARY DUCTAL SYSTEM :
PAROTID GLAND:
Once the orifice is localized , the special parotid cannula
is inserted
Cannula is made from a Tenner lacrimal cannula with
specially bored exit holes to permit the injection of
contrast media, the blunt tip serves the purpose of
acting as a dilator and a probe as well as a cannula

 The larger tapered barrel segment of the

cannula will fit snugly into Stensons duct and act
as a plug to prevent the backflow and escape of
the contrast agent
Tenner lacrimal cannula is then connected to a
polyethylene tubing and syringe containing the
contrast medium

SUBMANDIBULAR GLAND:
Surgical exposure of the duct is done if
cannulation fails. The use of 2% novacaine with
epinephrine injected into the periductal tissues
aids in the cannulation when operative
techniques are used.

RADIOGRAPHIC INTERPRETATION:
PAROTID GLAND:
The overall appearance is that of a leafless tree, and no area
should be devoid of peripheral ducts
As the ducts arch behind ramus of the mandible, they may
appear slightly stretched on frontal films, this appearance should
not be confused with a mass lesion; on lateral films , no mass
effect will be seen.
Normally the ducts do not lie parallel to one another in any
plane , if this appearance is seen, it usually indicates that a mass
is present displacing some of the ducts away from their normal
arborization configuration and causing them to appear parallel to
one another

SUBMANDIBULAR GLAND :
The walls of the submandibular duct are much
thinner than those of the parotid duct and can be
more easily injured during manipulation, if a long
rigid metallic cannula is utilized.
Extravasation of contrast medium in such a case
should not be mistaken for pseudodiverticulation
or a neoplastic process with tissue destruction

SUBLINGUAL GLAND :
Cannulation of sublingual ducts in orifices is
virtually impossible , however where the major
sublingual ducts empty into the whartons duct,
concomitant sublingual sialography is obtained
on occasion during the visualization of the
submandibular gland.

ACINAR FILLING :
Seen occasionally, after the injection of contrast
media into a main duct
Filling or non-filling of the acinar parenchyma
does not constitute a pathologic finding by itself,
since this appearance will vary greatly upon the
pressure utilized in the injection, the contrast
medium used, and the condition of the gland
under examination.

COMPUTED TOMOGRAPHY:
Computed Tomography is one of the latest
imaging modality in which computer analysis of a
series of cross-sectional scans made along a
single axis of a bodily structure or tissue is used
to construct a three-dimensional image of that
structure. The technique is widely used in
diagnostic studies of internal body structures.

CT is the examination of choice in salivary gland

imaging :
For inflammatory salivary gland diseases.
Presence and number of sialoliths.
Differentiate between cellulitis and cellulitis with an
abscess
Differentiate between clinically confused parotid and
masticator space disease.
CT can also distinguish between submandibular gland
sialadenitis and adjacent reactive lymphadenitis.

can confirm the presence of a clinically

palpable mass or identify the presence of a
clinically silent mass either in the same gland
or in the opposite gland

Normal parotid gland : CT imaging

Usual CT attenuation of the gland is lower than
that of muscle but greater than that of fat. In
children and some adults, a clinically normal
parotid gland can have an attenuation similar to
that of muscle.
The fine anatomy of the intraglandular ducts is
not normally visualized on CT, and Stensen's
duct is seen only if abnormally dilated

 On axial CT scans, an area of high attenuation is

routinely visualized near the caudal root or the
attachment of the pinna of the ear. This
musculotendinous region may mimic a small mass in
the upper pole of the parotid gland

 Normal Submandibular Glands: CT Imaging

Compared to the parotid glands, the
submandibular glands are more homogeneous
and have a higher attenuation on CT.
After contrast administration, both
submandibular glands should enhance to the
same degree.
If not, one gland is functioning abnormally,
usually the gland that is more enhanced.

Normal Sublingual Glands: CT Imaging

The gland enhances with contrast and has either a
linear or slightly medial concave configuration.

CT Sialography:
A combination of a sialogram and a simultaneous CT
scan of the gland.
As a result of the development of high-resolution CT
scanners and MR imaging, this is no longer performed.

MAGNETIC RESONANCE IMAGING:

Normal Parotid Gland: MR Imaging
Fat content of the parotid gland accounts for its signal
intensities:an overall intermediate to high T1-weighted
and a low to intermediate T2-weighted signal intensity.
The T1-weighted signal intensity of the gland is non
homogeneous, with multiple irregular areas of lower
signal intensity that represent interstitial tissues, salivary
ducts, and possibly branches of the facial nerve.

 The parotid gland showed intermediate signal intensity

and the fat spaces showed high signal intensity.
T1-weighted images may be the best overall sequence
to localize a mass.
T2-weighted scans often best show the tumor margins,

Normal Submandibular Glands: MR Imaging

The submandibular glands have a less fatty
parenchyma than the parotid glands. As a result,
compared to the parotid glands, the submandibular
glands are more homogeneous and have a slightly
lower Tl-weighted and higher T2-weighted signal
intensities on MR imaging.

Normal Sublingual Glands: MR Imaging

T1-weighted signal intensity of the sublingual
gland is lower than that of the surrounding fat
but higher than that of muscle.
The T2-weighted signal intensity is high.

PET scan :
was invented in the 1950s by Brownell and Sweet
Positron emission tomography (PET) is a nuclear
medicine imaging technique which produces a threedimensional image or picture of functional processes in
the body.

 PET scanning :
Imaging using 2-(F-18) fluoro-2-deoxy-D-glucose (FDG)
,tumors with increased metabolic activity are seen as
areas of increased PET activity.
PET can identify the higher grade malignancies , there
is confusion with the common benign Warthins tumor ,
which also has high metabolic activity.
Limitation: the cost is high
Long procedure time

ULTRASONOGRAPHY :
Ultrasonography : non invasive and cost effective
imaging modality
Being paired superficial structures, the parotid and
submandibular glands are suitable for high resolution
ultrasound examination.
Can be used to visualize all of the submandibular and
sublingual salivary glands and the entire parotid gland

 Obstructive, inflammatory and tumourous lesions can be detected

and differentiated by ultrasound.
Assist diagnosis by guiding needle aspirations for all types of
superficial lesions in this region
In acute inflammation, salivary glands are enlarged and hypoechoic
with increased blood flow; they may contain multiple small, oval,
hypoechoic areas.
In chronic inflammation, salivary glands are normal sized or
smaller, hypoechoic, and inhomogeneous.
Sialolithiasis appears as markedly hyperechoic lines or points with
distal acoustic shadowing.
Sialosis appears as enlarged hyperechoic glands without focal
lesions or increased blood flow.

 The ultrasonography features of advanced Sjgren syndrome

include inhomogeneous salivary glands with scattered small, oval,
hypoechoic or anechoic areas, usually well defined, and increased
parenchymal blood flow.
Pleomorphic adenomas are usually hypoechoic, well-defined,
lobulated lesions with posterior acoustic enhancement that may
contain calcifications;
Warthin tumors are usually oval, hypoechoic, well-defined lesions
that often contain anechoic areas and are often hypervascularized.
Malignant neoplasms of the salivary glands may have irregular
shapes, irregular borders, blurred margins, and a hypoechoic
inhomogeneous structure or may have a benign appearance.
Salivary gland cysts have well-defined margins, anechoic contents,
posterior acoustic enhancement, and no internal blood flow.

SCINTIGRAPHY:
Using salivary gland scintigraphy with Tc-99m the functional
capabilities, structural integrity and location of the glands can be
assessed.
Advantages of salivary gland scintigraphgy using Tc-99m are:
Quantification of function
Quantification of obstruction
Reproducible
Well-tolerated
Easy to perform.
Indications of salivary gland scintigraphy are in Sjogrens
syndrome, after multiple high-dose radioiodine treatments, after
external irradiation, and assessment of salivary duct obstruction.

 Scintigraphy has successfully been used to study the

effect of radiation on salivary gland function
Detect subclinical salivary leakage after extensive neck
surgery as major cause of postoperative wound
infection
As a non invasive procedure scintigraphy is particularly
useful in the diagnosis of Sjogrens Syndrome and other
systemic diseases involving the salivary glands.
Salivary gland scintigraphy can be used as an
alternative procedure to submandibular salivary flow
test for early prognosis of Bells Palsy

SALIVARY GLAND
DISORDERS :

WHO classification :
A) Epithelial tumors:
a. Adenoma: Pleomorphic adenoma
Monomorphic adenoma
Adenolymphoma
Oxyphilic adenomas
Other types

b.Mucoepidermoid tumor
c.Acinic cell tumor
d.Carcinoma: Adenoid cystic carcinoma
Adenocarcinoma
Epidermoid carcinoma
Undifferentiated carcinoma
Carcinoma in Pleomorphic adenoma
B) Nonepithelial Tumors
C) Unclassified tumors
D) Allied conditions: Benign Lymphoepithelial lesion
Sialosis
Oncocytosis

DEVELOPMENTAL
ABNORMALITIES:
Salivary gland aplasia :
Absence of salivary gland
Rare condition
Clinical features:
Xerostomia and increased dental caries
Enamel hypoplasia
Congenital absence of teeth
Extensive occlusal wear

Parotid gland agenesis :

reported in conjunction with several congenital conditions like:
Hemifacial microstomia
Mandibulofacial dysostosis
Cleft palate
Lacrimoauriculodentodigital syndrome
Treacher collins syndrome
Anophthalmia
Hypoplasia of parotid gland has been associated with
MELKERSSON- ROSENTHAL SYNDROME

ABERRANT SALIVARY GLANDS:

Salivary tissues that develop at unusual anatomic sites
Including: middle ear cleft, external auditory canal, neck, post.
mandible, ant. mandible, pituitary and cerebellopontine angle
Do not require intervention
When the submandibular salivary gland sits wiithin a depression
on the lingual posterior surface of the mandible , it is referred to
as Staphnes cyst
Palpation is possible sometimes and sialography aids in
diagnosis
Surgical intervention is recommended only in atypical situations
in which the diagnosis is unclear and tumor is suspected

ACCESSORY SALIVARY DUCTS:

Are common , do not require treatment
Most frequent location was superior and anterior to the
normal location of Stensons duct

DIVERTICULI:
Is a pouch or sac protruding from the wall of a
duct
Diverticuli in the major salivary glands often lead
to pooling of saliva and recurrent sialoadenitis
Diagnosis is made by sialography

DARIERS DISEASE :
Salivary duct abnormalities have been reported
Sialography of parotid glands in this condition revealed
duct dilation, with periodic stricture affecting the main
ducts
Symptoms of obstructive sialadenitis have been
reported

Obstructive Salivary Gland Disorders:

Sialolithiasis
Mucous retention/extravasation

SIALOLITHIASIS :
Are calcified and organic matter that forms within the
secretory system of the major salivary glands
Etiology : unknown , but factors that contribute to stone
formation are:
Inflammation
Irregularities in the duct system
Local irritants
Anticholinergic medications

 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.
obstructive phenomemnon such as mucous plugs and
sialoliths are most commonly found in the SMG

 Obstructive phenomemnon such as mucous plugs and

sialoliths are most commonly found in the SMG; this
may be because:
Higher concentration of calcium and phosphate in the
saliva
Higher mucus content
Torturous course of duct
Anti-gravity flow

Gout is the only systemic disease known to

cause salivary calculi and these are
composed of uric acid.

 Stone Composition:
Organic:
Glycoproteins
Mucopolysaccarides
Bacteria
Cellular debris
Inorganic:
Calcium carbonates & calcium phosphates in the form of
hydroxyapatite
Trace amounts: magnesium, ammonium, potassium chloride

CLINICAL PRESENTATION:

Acute painful and intermittent swelling

Eating will initiate the swelling
Salivary pooling within the duct and gland body
Involved gland is enlarged and tender
In chronic cases: fistulae, sinus tract or ulceration

EVALUATION:
Bimanual palpation:
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

RADIOGRAPHIC EXAMINATION:
Occlusal view : submandibular gland
Anteroposterior view: parotid gland
Computed tomography : 10 times the sensitivity of plain
film
Ultrasound: operator dependent, can detect small
stones (>2mm), inexpensive, non-invasive
Sialography
MR Sialography
Sialendoscopy

TREATMENT:
Acute phase : primarily supportive
Standard care : analgesics , hydration, antibiotics and
antipyretics
Pronounced exacerbations : surgical interventions for
drainage
Lithotripsy

MUCOCELES:
Swelling caused by the accumulation of the saliva at the
site of a traumatized or obstructed minor salivary gland
duct.
Two types: 1) Extravasation
2) Retention
A large form of mucocele located in the floor of the
mouth is known as RANULA .

ETIOLOGY:
EXTRAVASATION : as a result of trauma to minor
salivary gland exceretory duct, laceration of duct results
in the pooling of the saliva in the adjacent submucosal
tissues and consequent swelling
RETENTION: caused by the obstruction of the minor
salivary gland duct by calculus or possibly by the
contraction of the scar tissue around an injured salivary
gland duct,causing blockage of salivary flow and dilation
of duct

CLINICAL
PRESENTATION:
Extravasation : most common on
lower lip followed by buccal mucosa ,
tongue, floor of the mouth and
retromolar region
Retention : palate or floor of the
mouth
Discrete , painless, smooth surfaced
swelling
Superficial lesions: bluish hue
Deeper lesions: more diffuse,
covered by normal appearing mucosa

TREATMENT:
Surgical excision
Removal of the associated salivary glands is essential
to prevent recurrence

RANULA:
Large mucocele located on the floor of the mouth
May be either : mucous extravasation or retention type
The term RANULA is used because it resembles
swollen abdomen of a frog
Commonly associated with sublingual salivary gland
duct

CLINICAL
PRESENTATION:
Painless
Slow growing, soft and movable
mass in the floor of the mouth
Usually present on one side of
the lingual frenum but may cross
midline
Bluish hue
A deep lesion that herniates
through the mylohyoid muscle
and extends along the fascial
planes is reffered to as
PLUNGING RANULA.

TREATMENT :
Surgical excision
Marsupialization procedure : initial treatment of choice
in smaller lesions

INFLAMMATORY AND REACTIVE

LESIONS
Necrotizing Sialometaplasia
Radiation- Induced Pathology
Allergic Sialadenitis

NECROTIZING SIALOMETAPLASIA:
Benign self-limiting reactive inflammatory disorder
ETIOLOGY:
Initiated by a local ischemic event
CLINICAL PRESENTATION:
Clinically the lesion mimics a malignancy
Rapid onset
Predominant site: palate; anywhere salivary gland exists
like lips, retromolar pad region

 Initial lesion :Tender erthymatous nodule

Breakdown of mucosa results in deep ulceration with a
yellow base
Dull pain
Occurs shortly after: oral surgical procedures,
restorative dentistry, or administration of local
anesthesia
In induced vomiting practice by patients suffering from
Bulimia

TREATMENT :
Self- limiting
Lasts for 6 weeks , heals by secondary intention
No specific treatment is required
Debridement and saline rinses may help the healing
process

RADIATION INDUCED
PATHOLOGY:
Two types :1) External beam radiation
2) Internal radiation therapy

EFFECTS OF EXTERNAL BEAM

RADIATION:
E-BR is the standard for head and neck tumors and
salivary glands are often within the field of radiation
Doses of > 50 Gy will result in permanent salivary gland
damage and symptoms of oral dryness
Exact mechanism of destruction of salivary gland tissue
is not understood

CLINICAL PRESENTATION:
Acute effects : within a week of beginning treatments at doses of 2
Gy daily
Oral dryness by second week
Mucositis
At doses > 50 Gy , diificulty in speaking
Dysphagia
Increased dental caries: radiation caries; occurs at cervical or
incisal aspect of the teeth and wrap around the teeth in an apple
core fashion
Candidiasis
Sailadenitis
Osteonecrosis

TREATMENT :
Radiation planning
Radioprotective agents : amifostine
Antifungal : sugar free agents; antifungal oral rinses are
preferred

EFFECTS OF INTERNAL
RADIATION THERAPY:
Etiology :
Radioactive iodine 131 is given after surgery to patients
of Disseminated Thyroid Cancer to ensure that all
remnants of thyroid cancer are destroyed.
Taken up by the oncocytes in salivary gland tissue
Cause salivary gland damage and fibrosis resulting in
salivary gland hypofunction

CLINICAL PRESENTATION:
Xerostomia
As the treatment is less caustic than external beam
TREATMENT :
Following administration of iodine 131, patients should
suck on lemon drops or chew gum to stimulate salivary
flow

ALLERGIC SIALADENITIS :
Enlargement of salivary glands : associated with
exposure to various pharmaceutical agents and
allergens
Characteristic feature : acute salivary gland
enlargement
accompanied by itching over the gland
Compounds associated :
Phenobarbitols , phenothiazines, ethambutol,
sulfisoxazole,iodine compounds, isoproterenol and
heavy metals

TREATMENT :

Self limiting
Avoiding the allergen
Maintaining hydration
Monitoring for secondary infection

SIALOADENOSIS:
Is an unusual non-inflammatory condition.
May be associated with underlying systemic
problem: endocrine,nutritional or neurogenic.
CLINICAL FEATURES:
Slowly evolving swelling
May or may not be painful
Usually bilateral
Decreased salivary secretion can occur

VIRAL DISEASES:
Mumps
Cytomegalovirus infection
HIV infection
Hepatitis C virus infection

MUMPS :
Etiology :
Caused by a ribonucleic acid ( RNA) Paramyxovirus
Transmitted by direct contact with salivary droplets

CLINICAL
PRESENTATION :
In children : age range is 4-6
years
Incubation period : 2-3 weeks
Salivary gland inflammation
and enlargement
Preauricular pain
Fever
Malaise
Headache
Myalgia

 Majority cases: in parotid , only 10% in submandibular

alone
Overlying skin : edematous
Enlargement is sudden , painful on palpation
Salivary ducts are inflamed but without purulent
discharge
Swelling is usually bilateral and lasts for 7 days
Complications : mild meningitis , encephalitis, deafness,
myocarditis , thyroiditis , pancreatitis

 Diagnosis is made by :
Demonstration of antibodies to mumps S and V
antigens and to hemagglutination antigen
Serum amylase levels may be elevated
TREATMENT :
Symptomatic
Vaccination is important for prevention

CYTOMEGALOVIRUS INFECTION:
Etiology :
Human CMV is a beta herpes virus that infects only
humans
May remain latent after initial exposure and infection
CMV can be cultured from blood , saliva , feces,
respiratory secretions, urine , and other body fliuds
Horizontal transmission can occur through blood
transfusion, allograft transplants and sexual contact

 Transmission from children to adults or between

childrens is more common through fomites, urine, and
respiratory secretions
Transplacental spread of CMV may result in cogenital
infections and malformations

CLINICAL PRESENTATION :

Occurs in young adults

Acute febrile illness that salivary enlargement
Diagnosis is based on elevated titer of antibody to CMV
Patients on immunosupressive agents , and with
hematologic disorders are susceptible
TREATMENT :
Immunocompetent patients are treated symptomatically
Intravenous gancyclovir, forscarnet or cidofovir

HIV INFECTION :
Etiology :
Is not understood , but reactivation of a latent virus has
been hypothesized
Neoplastic and non-neoplastic salivary gland disease
occurs with increased frequency in HIV
Sjogrens syndrome like phenomenon is seen: k/a HIV
salivary gland disease

CLINICAL PRESENTATION :
Swelling may or may not be accompanied by
xerostomia
Must be distinguished from Sjogrens syndrome by
appropriate evaluation including salivary flow rates,
ophthalmologic evaluation and autoimmune serologies
Anti SS-A and anti-SS-B autoantibodies are negative
in HIV SGD
CD8-positive cells are present in HIV-SGD, whereas in
Sjogrens CD4 positive cells predominates

TREATMENT :
Primarily asymptomatic
Xerostomia may be relieved by sipping water, chewing
sugar free gums, or sugar free candy
Topical fluoride for control of caries

BACTERIAL SIALADENITIS :
Etiology :
Commonly seen in patients with reduced salivary gland
function
Formerly referred to as surgical parotitis
Majority occur in patients with disease or medication
induced salivary gland hypofunction
More frequent in parotid gland

CLINICAL PRESENTATION :
Sudden onset of unilateral or bilateral salivary gland
enlargement
Painful gland
Indurated
Tender to palpation
Overlying skin erythematous
Purulent discharge from duct orifice

Treatment :
If purulent discharge is present : empiric IV
administration of anti-staphylococcal antibiotic
Milking of gland several times a day
Increased hydration
Improved oral hygiene
Incision and drainage

SYSTEMIC CONDITIONS WITH

SALIVARY GLAND INVOLVEMENT:

METABOLIC CONDITIONS:
Diabetes
Anorexia Nervosa/ Bulimia
Chronic Alcoholism
IMMUNE CONDITIONS :
Mikulikczs Disease
Sjogrens syndrome
GRANULOMATOUS CONDITIONS:
Tuberculosis
Sarcoidosis

DIABETES:
Common endocrine disease ; especially in geriatrics
Assoc with multiple metabolic abnormalities n long term
complications such as renal hypertension, neuropathies and
ophthalmic disease
Uncontrolled diabetes often present with dry mouth, believed to
be due to polyuria and poor hyration
Patients with uncontrolled diabetes had lower salivary flow rates
as compared to patients with controlled diabetes
Etiology of diabetic salivary gland dysfunction is unclear
howerver it has ben suggested that poor glycemic control directly
effects salivary gland metabolism
Autonomic nervous system dysfunction may also play a role

MIKULICZS DISEASE:
k/a Benign Lymphoepithelial lesion
Etiology : unknown, autoimmune , viral, or genetic factors are the
trigger
Predominantly affects middle aged women
Unilateral or bilateral swelling of salivary gland
Reduced salivary flow
Differential diagnosis includes: Sjogrens syndrome, lymphoma,
sarcoidosis
Diagnosis is based on findings of salivary gland biopsy
Treatment : palliative , possibility of neoplastic transformation is a
concern

SJOGRENS SYNDROME :
Chronic autoimmune disorder
Characterized by oral and ocular dryness and lymphocytic
infiltration and destruction of the exocrine glands
Etiology : unknown
Salivary and lacrimal glands are primarily affected
Thyroid , kidneys and lungs may also be involved
Arthralgias, myalgias ,peripheral neuropathies and rashes may
also occur
Autoimmune associated anemia, hypergammaglubinemia

 SS primarily affects postmenopausal women( female to

male ratio is 9: 1)
Classified as : Primary and Secondary
PRIMARY SS: includes both lacrimal and salivary gland
dysfunctions without autoimmune condition
SECONDARY SS: includes salivary / or lacrimal gland
dysfunction in the setting of other connective tissue
disorders

CLINICAL MANIFESTATIONS :

Dry mouth
Difficulty in chewing, swallowing, and speaking
Dry cracked lips
Angular cheilitis
Mucosa will be pale ,dry
Minimal salivary pooling
Thick ropy saliva
Mucocutaneous candidiasis
Increased dental caries
Erosion of enamel structure

DIAGNOSIS :
Objective measurement of decreased salivary and
lacrimal gland function
Positive autoimmune serologies
Minor salivary gland biopsy
Sialography
MRI in assessing enlarged glands

MRI OF PAROTID GLAND IN

SJOGRENS SYNDROME:

TREATMENT:

Symptomatic : artifical saliva

Oral rinses and gels
Water sipping
Chewing sugar free gums
Systemic cholinergic drugs

SALIVARY GLAND TUMORS :

BENIGN TUMORS :
Pleomorphic Adenoma
Monomorphic Adenoma
Papillary Cystadenoma Lymphomatosum
Oncocytoma
Basal Cell Adenomas
Canalicular Adenoma
Myoepithelioma
Sebaceous Adenoma
Ductal papilloma

MALIGNANT TUMORS :
Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Acinic cell carcinoma
Adenocarcinoma
Lymphoma

PLEOMORPHIC ADENOMA :
Most common ; accounts for 60% of salivary gland
tumors
Mixed tumor
85% found in Parotid gland ; 8% in submandibular gland
Remaining are found in sublingual and minor salivary
gland
Occur at any age ; more in 4th to 6th decade
Slight predilection for female

CLINICAL
PRESENTATION :
Painless , firm , mobile masses
Rarely ulcerate overlying skin or
mucosa
Slow growing
Difficult to distinguish them from
malignant neoplasms and
indurated lymph nodes
Intraorally occurs most often on
palate followed by upper lip and
buccal mucosa
Vary in size

MRI OF PLEOMORPHIC ADENOMA:

TREATMENT :
Surgical removal with adequate margin
Superficial parotidectomy

WARTHINS TUMOR :

k/a Papillary Cytadenoma lymphomatosum

Second most common benign tumor of parotid gland
Mostly in inferior pole of the gland
Slight predilection for males
5th and 8th decade of life

CLINICAL
PRESENTATION:
Well defined slow growing
mass
In the tail of the gland
Usually painless
Painful if gets secondarily
infected
TREATMENT :
Surgical removal with a
margin of normal tissue

MUCOEPIDERMOID
CARCINOMAS:

Most common malignant tumor of parotid gland

Second most common of submandibular gland
60% to 90% occur in parotid
Palate is the most common site
Men and women are equally affected
3rd to 5th decades of life
Classified as High grade and Low grade

 Low grade presents painless slow enlargement

High grade shows rapid growth and higher likelihood for
metastasis
Pain and ulceration of overlying tissue are occassionally
associated
If facial nerve is involved , patient exhibits facial palsy

WARTHINS TUMOR ON MRI:

Treatment :
Superficial parotidectomy
Neck dissections to remove lymoh node in high grade
Post operative radiation therapy

ADENOID CYSTIC CARCINOMA :

Most common tumor of submandibular and minor
salivary glands
50% occur in minor salivary glands
Affects men and women equally
5th decade

CLINICAL PRESENTATION:

Firm unilobular mass

Occasionally painful
Parotid tumors may cause facial paralysis in some patients
Perineural invasion
Slow growing
Intraoral tumor may exhibit mucosal ulceration
Radiographically , reveals extension into adjacent bone
Metastases into lung are common

TREATMENT :
Radical surgical excision
Neutron beam radiation therapy