Presented by

Dr. ASLAM TARIQ MOHAMMED

Ist Yr PG
Dept.Of Orthodontics
 Contents
 Introduction

 History

 Salivary gland structure (macroscopic and microscopic) and development

 Mechanism of secretion of saliva

 Nerve distribution in glands

 Composition and functions of saliva

 Increased salivation/sialorrhea

 Decreased salivation/xerostomia
• Applied aspects
• Saliva and friction
• Saliva and bonding
• Salivary clearance rate
• Experimental salivary pellicles and orthodontic
materials
• Salivary ph and elastomers
• Saliva and corrosion
•Conclusion
• References
Introduction:

 Neglected by dentists and ignored by physicians, saliva is the least known and
the least appreciated of all the body fluids. Yet, this lowly secretion plays a vital
role in the integrity of the oral tissues; in the selection, ingestion and preparation
of the food for digestion and in our ability to communicate with one another.

 Hence it is justified for us to know the physiology of the secretion namely saliva
in depth so that when circumstances encounter us regarding its undersecretion
or oversecretion can suitably alter our modality of treatment so that best possible
treatment is rendered to our patients
 History
 “Dwell on the past and you will lose an eye, forget the past and you will lose both eyes”

 Orabasius (325-403 AD)- described submandibular salivary glands on each side of the
tongue

 Thomas Wharton (1614-1673)- Whartons duct.

 Dane Neils Stenson- parotid gland duct stensons duct.

 Antonius Nuck (1650-1692)-injected coloured wax into the ducts and studied their pattern.

 Ivan Pavlov-under took a classical study on reflex salivary secretion in dogs. He concluded
that different stimulus to the mouth produced qualitative and quantitative differences in
reflex salivary secretion.
 Major salivary glands
 The salivary glands of humans are considered the cyto-

architectural replica of salivary glands of rats, hence we

find a number of literature where in experiments on rat

salivary glands are correlated to that of human beings.

 Salivary glands are defined as compound, tubuloacinar,

merocrine , exocrine glands whose ducts open into oral

cavity.
Salivary glands are classified :
According to size of the glands as :
 Major : ex – parotid, submandibular, sublingual
 Minor : lingual salivary glands (vonebner’s glands), labial glands, palatal glands in
postero lateral aspect, buccal glands in cheek.
 According to histochemical nature of secretion:
Serous - parotid gland, vonebner’s gland.
Mucous – palatine, glossopalatine and glands in post part of tongue.
Mixed – sub mandibular (predominently serous , mixed).
sub lingual (predominently mucous, mixed).
 According to position:

 Extra oral : ex – parotid, submandibular, sublingual

 Intral oral : vonebners gland, labial, palatine, buccal glands

 In humans saliva secretion from parotid, submandibular, sublingual

glands contribute abut 90% of saliva volume and minor salivary
glands contribute – 10%

 Submandibular gland contributes : 65% of total saliva secretion.

 Parotid– 25%,Sublingual – 10% .

 MAJOR SALIVARY GLANDS (macroscopic view)

 Parotid salivary gland: – are enclosed within a well

formed connective tissue capsule with its superficial

portion lying in front of the external ear and its

deeper portion lying in the retromandibular fossa.

 On the surface of the masseter, small detached part

lies b/w zygomatic arch and parotid duct-accessory

parotid gland or ‘socia parotidis’

External Features
 Resembles an inverted 3 sided pyramid

 Four surfaces
 Superior(Base of the Pyramid)
 Superficial
 Anteromedial
 Posteromedial

 Separated by three borders

 Anterior
 Posterior
 Medial
Relations
 Superior Surface
 Concave
 Related to
 Cartilaginous part of ext acoustic meatus

 Post. Aspect of temperomandibular joint

 Auriculotemporal Nerve

 Sup. Temporal vessels

 Apex
 Overlaps posterior belly of digastric and adjoining part
of carotid triangle
 Superficial Surface
 Covered by
 Skin
 Superficial fascia containing facial branches of
great auricular N
 Superficial parotid lymph nodes and post fibers
of platysma

 Anteromedial Surface
 Grooved by posterior border of ramus of mandible

 Related to
 Masseter
 Lateral Surface of temperomandibular joint
 Medial pterygoid muscles
 Emerging branches of Facial N
Posteromedial Surface

Related
 to mastoid process with sternomastoid and posterior belly of digastric.

 Styloid process with structures attached to it.

 External Carotid A. which enters the gland through

the surface

 Internal Carotid A. which lies deep to styloid process

BORDERS:
 Anterior border:

 Separates superficial surface from anteromedial

surface.

 Structures which emerge at this border

 Parotid Duct

 Terminal Branches of facial nerve

 Transverse facial vessels

 Posterior Border:

 Separates superficial surface from posteromedial

surface.
 Overlaps sternomastoid.

 Medial Border:

 Separates anteromedial surface from posteromedial surface

 Related to lateral wall of pharynx
 Parotid Duct:

 Ductus parotideus; Stensen’s duct

 5 cm in length

 Appears in the anterior border of the gland

 Runs anteriorly and downwards on the masseter b/w the upper and lower
buccal branches of facial N.
 At the anterior border of masseter it pierces
 Buccal pad of fat
 Buccopharyngeal fascia
 Buccinator Muscle

 It opens into the vestibule of mouth opposite to the

2nd upper molar
Surface anatomy of parotid duct Corresponds to middle
third of a line drawn from lower border of tragus to a
point midway b/w nasal ala and upper labial margin.
 Submandibular salivary glands :
 Are enveloped by a well defined capsule and is located in submandibular
triangle below floor of mouth and mylohyoid.
 The main excretory duct, Whartons duct opens on either side of lingual
frenum in the floor of the mouth.
 Consists of both mucous and serous acini.
 Blood supply Artery : facial artery
 Vein : common facial vein
 Lymphnodes : submandibular group of lymphnodes
 Nerve supply : branches from submandibular ganglion, Secretomotor
pathway begins in superior salivatory nucleus ,
 preganglionic fibres pass through the sensory root of facial nerve,
geniculate ganglion, facial nerve, chorda tympani and lingual nerve.
 Sublingual Salivary glands :
 lies above mylohyoid but below floor of the mouth.
 Contains both serous and mucous acini but predominantly – mucous
acini.
 Blood supply Artery : lingual and submental arteries
 Nerve supply : from submandibular ganglion the main duct (Bartholins
duct) opens with the submandibular duct and several smaller ducts (ducts
of Rivinous) open independently along sublingual fold.
Development of salivary glands
 Three major pairs of salivary glands originate uniformly as oral epithelial
buds involving the underlying mesenchyme.

 All parenchymal (secretory) tissue of the glands arises from the proliferation
of oral epithelium, which is either ectodermal or endodermal in origin.

 The stroma (Capsule and septa) of the gland originates from the
mesenchyme that may be of either mesodermal or neural crest origin.

 Failure of the bud to canalize to form ducts before acinar cells starts
secretion cammernces results in retention type of cysts.
 We find initiation of salivary gland formation during the following
mentioned period of intra-uterine life of the developing fetus.
 Parotid – 6 week intra-uterine
 Submandibular -6 weeks intra-uterine
 Sublingual – 8 weeks intra-uterine
Mechanism of secretion of saliva
 Saliva is first secreted in the acinar cells. They determine the type of
secretion.
 Serous cells produce a watery seromucous secretion and mucous cells
produce a viscous mucin rich secretion.
 Saliva is formed in two stages:
a primary secretion occurs in the acini, then modified as it passes through
the ducts.
 The primary secretion is formed actively by the movement of sodium and
chloride ions into the lumen, creating an osmotic gradient which leads to
passive movement of water
 Other acinar components are added here, before the

fluid enters the duct, where sodium ions are actively

reabsorbed (chloride ions follow passively to

maintain electrical equilibrium) and potassium and

bicarbonate ions secreted.

 The macromolecular components (amylase, mucous

glycoproteins etc) are formed in the usual way in the

acinar cell endoplasmic reticulum, processed into secretory vesicles in

the golgi apparatus and are exported from the cell by exocytosis.
 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 a neurotransmitter substance.

 These include noradrenalin (sympathetics) and acetyl choline, substance P

and vasointestinal polypeptide (parasympathetics).

 When the neurotransmitter arrives at a secretory cell membrane it binds to

and activates a receptor (which may be stimulatory or inhibitory) on the
external surface of the membrane.
 This activates an intermediate guanine nucleotide-dependent membrane
protein known as a ‘G’ protein, which in turn activates a regulatory enzyme
on the inner, cytoplasmic surface of the cell.

 The regulatory enzyme may be either phospholipase C or adenyl cyclase.

 PHOSPHOLIPASE C PATHWAY:

 Phospholipase C enzyme (PLC) is activated on binding of acetyl choline at

muscarinic receptors, substance P at peptidergic receptors, or noradrenaline
at adrenergic receptors on the acinar cell membrane.

 It controls the intracellular pathway leading to the secretion of water and

electrolytes. The pathway is rather complex.
 PLC is responsible for hydrolyzing a membrane phospholipid (phosphatidyl inositol
biphosphate, PIP2) to form diacylglycerol (DAG) and inositol triphosphate (IP3).
 The latter stimulates the release of calcium ions from the endoplasmic reticulum.
This increased cytoplasmic calcium ion concentration causes the opening of
potassium channels in the acinar cell membrane, which allow potassium ions to
diffuse out of the cell down a concentration gradient established by a Na/K
membrane pump.
 The second is a sodium/potassium exchange pump in the membranes of the
intercellular canaliculi. Thus, the extrusion of potassium triggers the entry of
sodium and chloride ions into the intercellular canaliculi.
 The chloride ions which entered the cell with the sodium then diffuse across the
luminal membrane via a calcium - sensitive channel.
 The arrival of chloride ions in the lumen triggers the movement of sodium ions
from the intercellular canaliculi across the tight junction between the cells, thus
establishing the osmotic gradient for the movement of water into the lumen.

 ADENYL CYCLASE PATHWAY:

 Adenyl cyclase (AC) is activated when noradrenaline binds to beta adrenergic acinar
receptors, or vasoactive intestinal peptide (VIP) binds to peptidergic receptors.
Activation leads to exocytosis of secretory proteins.

 AC causes the intracellular formation of 3, 5- cyclic AMP from ATP. Cyclic AMP
(cAMP) activates a second enzyme, cAMP dependent protein kinase (cA-PK) which
exists in four subunits.
 Two subunits are receptor molecules which bind with cAMP (2R cAMP),
thereby liberating the other two catalytic subunits (2C) to activate effector
proteins (Pr) by phophorylation (Pr-P).

 The activated effector proteins then stimulate exocytosis. Diacylglycerol

(from the phospholipase C pathway) also promotes exocytosis.
 Composition
 Volume – 1/5th the plasma volume
 Specific gravity – 1.002 -- 1.012
 Osmolality – saliva is hypotonic to plasma
 Salivary flow rates, differ at different times of the day lowest rate of
saliva flow is observed in the early hours of the morning (4-6 o’ clock) and
peak flow rates are seen in the evening (16:00-20:00hrs).
 Inorganic components :
 Most important cations are Na+ and K+
 The major osmotically active anions are Cl- and HCO3-
 Water and ionic constituents of saliva are derived by translocation from
blood plasma.
 Although salivary electrolytes are derived from the blood supply, their
ionic concentrations are not identical to plasma .
So that saliva is not merely on ultra filtrate of plasma.

Organic components :
 They have different function such as enzymatic action, coating of tissue
surfaces, protection of dental tissues, control of tissue growth.
 The digestive enzyme salivary amylase or ptyalin is the organic component
found in highest concentration in saliva.
 Amylase consists of two families of isoenzymes – glycosylated
- non glycosylated
 Doubt has always existed concerning the function of salivary amylase,
since there is little time for the enzyme to be active before the food bolus
is swallowed and exposed to stomach pH that would inactivate the
enzyme.
 Lipase from van ebner’s gland has significant role in digestion of fat and is
active in stomach pH also.
 Mucous glycoproteins secreted in saliva have a high molecular weight and
consist of multiple oligosaccharide chains attachment to a peptide core.
 All oral soft tissues are coated with mucous glycoproteins which are
thought to act as trap for bacteria and a regulator of interaction and
interchange between surface epithelial cells and oral environment.
 Some of these glycoproteins bind strongly to the tooth surface and are
therefore an important constituent of enamel pellicle.
 There are 2 types of proline rich glycoproteins
 Basic glycoprotein – binds lipids and may preferentially adsorb to
membranes.
 Acidic glycoproteins – comprises of calcium binding proteins and attaches
to the tooth surface. These factors have role in stabilizing the tooth
surface and promote remineralization.
 Tyrosine rich peptide called statherin may play a role in stabilizing
supersaturated solution of Ca and phosphate and prevent calcium
precipitation from saliva thus prevents demineralization.
 Secretory IgA is synthesized by plasma cells,
 Functions of secretory IgA
 It has 2 functions - mucosal defense
- dental defense
 Perhaps compliment activating IgG antibodies are more potent with
regard to elimination of noncolonized bacteria than IgA antibodies that
do not engage this lytic system efficiently.
 Periodontal disease – secretory IgA is responsible for host resistance to
periodontal disease.
 hence secretory IgA antibodies have little or no effect in an established
dental plaque.
Functions:
 PROTECTION :
 The glycoprotein content, which makes saliva mucinous protects the
lining mucosa by forming is barrier against noxius stimulus, microbial
toxins and minor trauma.
 Its fluid consistency also provides a mechnical washing action which
flushes away nonadherent bacterial and cellular debris from mouth.
 In particular, the clearance of sugars from mouth by salivary washing
action limits their availability to acidogenic plaque microorganisms.
 The calcium binding proteins in saliva helps in formation of salivary
pellicle, which behaves as a protein membrane.
 BUFFERING ACTION :
 protects oral cavity in 2 ways :
 It prevents potential pathogens from colonizing in the mouth by denying
then optimal environmental conditions.
 Plaque microorganisms can produce acid from sugar, which if not rapidly
buffered and cleared by saliva, can demineralize enamel.
 Much of buffering capacity of saliva lies in –HCO3 and phosphate ions .
 Negatively charged residues on salivary proteins are also thought to serve
as buffers, a salivary peptide, sialin, plays a significant role in raising the
pH of dental plaque after exposure to fermentable carbohydrate.
 If access of saliva to the plaque is prevented there is a dramatic fall in
plaque pH, whereas unrestricted salivary flow to plaque results in little
alteration of plaque pH.
 Saliva is therefore able to prevent acidification of plaque.
 Resting parotid saliva has a pH of 5.82 and bicarbonate conc. of 0.6m
Eq/L.
 Whereas at high flow rates the pH rises to 7.67 and bicarbonate conc
increases to almost 30 mEq/L.
 It can be hypothesized that to increase the buffering power of saliva it is
necessary to increase the saliva flow.
 DIGESTION :
 Saliva provides taste acuity, neutralizes esophageal contents, dilutes
gastric chyme, forms the food bolus.
 Amylase content in saliva breaks down starch into oligosaccharides such
as maltose, maltotriose, thus occurs best at a pH of 6.7.
 Further digestion of oligosaccharides takes place in small intestine by
pancreatic amylases.
 TASTE :
 Although it enables the pleasurable sensations of food to be experienced,
its primary role is protection in that it permits the recognition of noxious
substances.
 Saliva is required to dissolve substances to be tasted and to carry them to
the taste buds.
 It also contains a protein called Gustin that is thought to be necessary for
growth and maturation of taste buds.
 ANTIMICROBIAL ACTION :
 Saliva has a major ecologic influence on the microorganisms that attempt
to colonize in oral tissues.
 In addition to the barrier effect of its mucus content, it contains a
spectrum of proteins with antimicrobial properties such as Histatin.
 Lysozyme is an enzyme that can hydrolyze the cell walls of some bacteria.
 The essential element secretory IgA has the capacity to clump or
agglutamate microorganisms.
 MAINTENANCE OF TOOTH INTEGRITY :
 Saliva is saturated with Calcium and phosphate ions. The high
concentration of these ions ensures that ionic exchange with the tooth
surface is directed to the tooth.
 This exchange begins as soon as the tooth erupts because, although the
crown is fully formed morphologically when it erupts it is
crystalographically incomplete.
 Interaction with saliva results in post eruptive maturation through
diffusion of ions such as Cal, phosphorus, magnesium, chloride into the
surface apatite enamel crystals.
 This maturation increases surface hardness, decreases permeability,
heightens the resistance of enamel to caries.
 Remineralization is achieved, largely through the availability of
phosphate and calcium ions in the saliva.
 If fluoride is also present remineralization occurs, the repaired lesion
thus is less susceptible to future decay.
 TISSUE REPAIR :
 Presence of epidermal growth factor in the saliva produced by the
submandibular glands helps in wound healing.
 SALIVA AS A DIAGNOSTIC TOOL :
 Flow rates of minor salivary gland as well as the calcium levels in saliva
have diagnostic importance in Cystic Fibrosis.
 Status of Bells Palsy can be measured by monitoring flow rate of
submandibular gland.
 Salivary eletrolyte levels have been used as adjuncts in diagnosing and
monitoring Hyperaldosteronism and in diagnosis Digitalis toxicity.
 Analysis of Hexosaminidase A in saliva has been reported to be useful in
identifying individuals with Tay-Sachs disease as well as carriers.
 Heavy metal toxicity such as mercurism (acrodynia, Pinks disease} can
also be monitored.
 In Pinks disease there will be drooling of saliva, loss of hair in patches,
mucosal erythema and ulcerations.
 LINGUAL LIPASE :
 Secreted by Van Ebner’s gland splits fats into fatty acids.
 Helps in articulation of words thus enhancing proficiency of speech.
 Exerts thirst mechanism thereby controlling body’s hydration
requirements.
 ANTIFUNGUAL ACTIVITY :
 Saliva has antifungal factors which prevent a healthy person with good
immunity from developing candidiasis.
Increased salivation/sialorrhea
 Causes of PTYALISM (Sialorrhoea) –
 Local reflexes.
 Oral infections (acute necrotizing ulcerative gingivitis)
 Oral wounds
 Dental procedures
 New dentures, appliances.
Systemic :
 Nausea
 Acid regurgitation (GERD)
Toxic :
 Heavy metal poisoning – mercury - Pinks disease (Acrodynia}.
 False ptyalism : (drooling)
 Pychogenic
 Bell’s palsy
 Parkinsons diseases
 Stroke
 Management :
 Adrenergic drugs such as atropine are used. Newer drugs like Banthine,
Probanthine, Scopalamine can also be used.
 Patient is instructed not to wear contact lens during the period while
on treatment with adrenergic drugs.
Decreased salivation/xerostomia
 Xerostomia or dryness of the mouth is a clinical manifestation of salivary
gland. But does not itself represent a disease entity.
 Xerostomia – decrease in salivation, Sialorrhea – increased salvation,
Aptyalism – absence of salivation.
 However the subjective complaint of dry mouth does not correlate reliably
with the objective finding of decreased
salivary flow rates.

Clinical evaluation of xerostomia. If tongue blade

sticks to buccal mucosa – xerostomia
 Chief compliant : does pt complian of dry mouth?

YES NO

DRY MOUTH QUESTIONAIRE: 1.)Does the amount of saliva in your mouth seem too
little or too much or you don’t notice it?
2.)Do you have any difficulty in swallowing ?
3.)Does your mouth feel dry when eating a meal?
4.)Do you sip liquids to aid in swallowing dry food?

YES NO

MEDICAL HISTORY AND REVIEW OF SYSTEMS: Does patient have any known risk factors??

CLINICAL EVALUATION: Does patient manifest any of the following symptoms??

Major salivary DENTITION:

LIPS: MUCOSA: Extensive?
gland : Enlarged? Dry? Dry?
Tender? Restorative?
Chapped? Erythematous? Rampant Caries?
No saliva pool? Lobulated?
Fissured? Caries Involving
Saliva contaminated Fissured?
Erythematous Incisal Edge,root ?
with pus and blood?

CONSIDER FURTHER DIAGNOSTIC WORKUP:

Sialometric evaluation,Serologic evaluation,Microbial analysis,Imaging, histological
examination,medical consultation,psychological evaluation.
 Xerostomia can be due to:
Non salivary circumstances
Salivary gland hypofunction / dysfunction

 Non-salivary circumstances including changes in patient, during

psychological distress, mouth breathing, sensory alterations in the oral cavity
that may lead to perception of dry mouth.
 Therefore it is important to determine if salivary function is actually
decreased using objective measurement techniques in patient complaining
of xerostomia .
 CAUSES OF XEROSTOMIA DUE TO SALIVARY GLAND
HYPOFUNCTION
Clinical features :
 Patient usually complains of dry or burning sensation in mouth.

 In partial xerostomia mucosa appears normal. In severe cases mucosa

will appear dry and atrophic sometimes inflammed, pale and translucent.

 Tongue has atrophy of papillae. Fissuring, inflammation, cracking of lips

may be seen.
 CAUSES OF SALIVARY GLAND HYPOFUNCTION
 Drugs
 External beam irradiation to the head and neck
 Oncologic chemotherapy
 Systemic diseases
sjogren’s syndrome primary and secondary
Granulomatous diseases(sarcodiasis , tuberculosis)
graft versus host disease
cystic fibrosis
bell’s palsy
diabetes
amyliodosis
 HIV infection
 Late stage liver disease
 Thyroid disease (both hypo and hyperthyroidism)
 Psychological factors
 Idiopathic
 1) Medication or pharmaceutical usage:
 ex : Antisialogogues.
 It is the most common cause of decreased salivary gland function.
 Several antisialogogues are used in dentistry, such as atropine, banthine,
Bellafoline, probanthine, scopolamine.
 Cholinergic agents are potent stimulants for salivary secretion. Therefore
anticholinergic medications, such as antihistamines are most likely to
cause hypofunction.
 Anti cholinergic drug – Atropine.
 Indications – as pre anesthetic mediation to decrease secretions
 - in bronchial asthma to relieve congestion.
 -causes mydriasis, used to check refraction in ophthalmologic
examination.
 - An article of relavence
 Brandt S, Servoss JM, Perslly KB, in 1981 conducted a study
 to evaluate antisialogogue effects of atropine sulphate injected
submucosally to the base of the tongue.
 1cc of atropine sulfate (0.4 mg / cc) was injected submucosally at the base
of the tongue adjacent to lingual frenum with help of a tuberculin syringe.
 After 5 minutes collection period of saliva began, usually in first 5-15
minute interval there was increase in salivation due to anxiety but after 20
minutes salivation reduced drastically and the effect was noticed upto 2
hours.
 Although recommended dose for teenagers was 0.75 – 1.7 mg a 0.4mg dose
was considered effective.
 With the injection the operator need not rely on the patient about
ingesting the drug orally 2 hours before the procedure.
 Sedatives, antipsychotics, anti depressants and diuretics are common
drugs which induce xerostomia.
 Fortunately medication induced xerostomia is usually reversible if
medication is discontinued.
 Irradiation therapy :
 Salivary glands are often in field of the external beam of radiation.
 Loss of salivary gland function is dependent on dose. Exposure to
radiation greater than 50 Gy usually results in permanent salivary gland
destruction.
 Usually after irradiation, in a couple of months normal saliva flow rate is
regained.
Radiation isotope 131I: used as internal radiation for thyroid malignancy
also causes reduced salivation.
 4) Bone marrow transplant : May lead to Graft V/s host reaction
(GVHD) and cause salivary gland hypofunction.
 5) SIALOLITHIASIS : is the occurrence of calcareous concentrations in
salivary glands or ducts. They from by deposition of calcium salts around a
central nidus which may consist of desquamated epithelial cells, bacteria,
foreign bodies.
 They cause xerostomia due to obstruction to flow of saliva. But normal
production rate is maintained.
 Clinical features :
 Moderate to severe pain just before, during and after meals associated
with swelling of salivary gland.
 Occasionally there may be firm mass palpable near the orifice.
 Occurrence : commonly in middle aged adults.
 Chemical feature of sialolith : may contain a solitary mass or may occur as
stones.
Composition – Calcium phosphate 75%
- Cal carbonate 11%
- Organic mater
- Water.
 Investigations : - Occlusal radiographs for submandibular duct stenosis
in terminal 2/3rd region of duct.


IOPA film radiograph of Stenson’s duct is taken if stone is located in
terminal 1/3rd region of duct.
 Increased plasma salivary amylase due to its escape from leaky junctions.
 Sialography.
 Treatment :
 Surgical extirpation of the gland if stone is present in the gland.
 Surgical manipulation of the duct to remove the stone if seen superficially.
 Lithotripsy.
SYSTEMIC DISEASES CAUSING XEROSTOMIA :
 1) Sjogren’s syndrome : It is a chronic autoimmune disease with
lymphocyte – mediated destruction of the exocrine gland.
 Sjogren syndrome patients manifest a full gamut of oral problems
secondary to salivary dysfunction, often experiencing a dry mouth and
needing to sip liquids frequently, difficulty in chewing, swallowing.

They usually present with : xerophthalmia, dysphagia, sinusitis, arthritis, renal
tubular defects, neuropathies.

Investigations : Include –ophthalmologic tests : Schirmers test

Rose Bengal dye test.

 Salivary collection rate to determine flow rate

 Serological examination for detection of auto antibodies.

 Histopathology of minor labial glands of lower lip.

 Treatment includes : to alleviate dry mouth with help of – saliva
substitutes -Frequent slips of water
 Maintain good oral hygiene.
 Suggest sugar free chewing gum.
 Chlorhexidine (0.2%) rinses
 Topical fluoride application.
 Antifungal mixtures for candidiasis.
 Ophthalmologic and connective tissue disorders to be investigated by a
specialist.
 Cystic fibrosis : Is a hereditary disease affecting lungs, pancreas and
salivary glands. It results from a defective chloride transport protein.
 Elevated calcium, phosphorous and proteins are detected in the saliva of
Cystic fibrosis patients.
 Bell’s palsy : It’s the idiopathic disruption of seventh cranial nerve
resulting in transient or permanent facial paralysis, paralysis often has
abrupt onset and is almost always unilateral.
 The affected side may have a decreased salivary flow rate.
 Decreased salivary flow is not due to gland pathology, but is a result of
altered neural innervations.
 Diabetes mellitus (uncontrolled) : decreased saliva flow due to
 Dehydration from polyuria
 Neuropathy.
 Vascular endothelial causes (microangiopathy).
 Amyloidosis : It’s the extracellular deposition of the fibrous protein
amyloid in one or more organs of the body.
 The etiology and pathogenesis of amyloidosis is unknown, orally it occurs
in tongue.
 The salivary glands maybe effected and cause salivary gland
hypofunction.
 HIV infection : affects salivary glands, influencing its flow rate and
saliva composition.
 They are prone to have an incidence of oral and esophageal candidiasis.
 Granulomatous disease : TB caused by mycobacterium tuberculosis,
cause granuloma formation and also decreased salivary gland function.
 Sarcoidosis : It also causes granuloma formation and these granulomas
cause destruction of normal tissues and lead to salivary gland
hypofunction.
 Hyperaldosteronism : Sodium potassium ratios in saliva are in excess
because due to increased reabsorption of sodium and potassium.
 Malnutrition : (anorexia, bulimia, dehydration) cause decrease in
salivary flow rates.
 Salivary gland dysfunction and xerostomia in geriatric population :
 Contrary to early belief, salivary gland function is generally well preserved
with age in healthy elderly people.
 There is general agreement that parotid gland function remains
unchanged across the human life span in healthy, non medicated adults.
 Xerostomia is a common complaint and may be found in upto 25% of
institutionalized adults.
 This is often caused by systemic disease or its treatments.
 Management of Xerostomia :
 It includes use of – saliva substitutes - Drugs / pharmaceuticals
 - Autologous saliva
 SALIVA SUBSTITUTES : These agents alleviate the patients discomfort
mainly by alleviating dryness of mouth, increases articulation of speech,
ease in swallowing, decreases burning sensation, prevents atrophy of
papilla.
 hence preserves taste acuity, prevents candidal infections and ulcer
formation.
 However use of water in regular quantity is mandatory to prevent the
person from dehydrating.
 Artificial saliva currently available are –
 DRUGS : Cholinergic drugs like pilocarpine is used to stimulate the gland in
production of saliva.
 Cevimeline hydrochloride (evoxac) can also be used. Which has lower
side effects.
 Indications of pilocarpine -to Increase secretions,- myasthenia gravis
 - open angle glaucoma.
 - to cause miosis, -Alzhimer’s disease.
 Contraindications of pilocarpine– causes fall in blood pressure.
 – Tachycardia.
 Dosage – 5 mg tablet, thrice a day.
 AUTOLOGOUS SALIVA :

 Before patient undergoes radiotherapy saliva is collected from the patient and
subjected to  radiation + lyophilisation + chlorhexidin (0.03%) and stored.

 During radiation therapy the stored saliva was sprayed.

 Since oral clearance rate in irradiated mouth is less, about 120 ml of saliva
would last for 40 days at the rate of spraying 0.3 ml / hour for 10 hours / day.

 The reason for not using artificial saliva was that it does not pocess protective
protein that are present in salivary secretions.

 Apart from these measures, chlorhexdin 0.12% oral rinse and application
of fluoride is essential to prevent dental caries and candidiasis.
 SALIVARY GLAND RADIOLOGY
 Diagnostic imaging of salivary gland disease is undertaken to
differentiate between inflammatory and neoplastic disease, distinguish
between diffuse and focal suppurative disease, identify and locate stone,
demonstrate ductal morphology.
Sialogram of parotid gland in
Sjogren’s Syndrome
• Applied aspects of saliva
• Saliva and friction

• Saliva and bonding

• Salivary clearance rate

• Experimental salivary pellicles and orthodontic materials

• Salivary ph and elastomers

• Saliva and corrosion

• Conclusion

• References
 APPLIED ASPECT OF SALIVA IN RELATION TO
ORTHODONTICS :
 I) FRICTION :

It has been suggested that saliva or a saliva substitute services

as an excellent lubricant in the sliding of the bracket along the wire.

Here are a few studies relating friction and saliva:

1) Frictional changes in force values caused by saliva substitution:

 Objective of the study was to determine the magnitude of frictional force changes between several

sizes of stainless steel orthodontic arch wires i.e. 018, 020, 018 x 025 and edgewise 022 x 028 slot

when an artificial saliva medium was introduced.

Yu-Jin Seo et al, European Journal of Orthodontics, 2015, 158–163 doi:10.1093/ejo/cju027.
 After tabulating results they concluded that :

 Xero lube, saliva substitute as a lubricant

 provided a 15% to 19% reduction in force value.

 They also concluded that saliva medium used has a viscosity of 14.0 centipoise at 370C.

 They conducted a similar research using glycerine which has viscosity of 325.0 centipose
but results obtained did not match to that obtained with xerolube artificial saliva.

2) Frictional resistance of ceramic and stainless steel orthodontic brackets:

a similar type of research and found that saliva substitutes increased static friction for all
combination tested.
Baker KL,Nieberg LG,Weimer AD,,Hanna M. Am J Orthod Dentofacial Orthop. 2013, 133187.e15–
187.e24.
 Saliva played an insignificant role in lubricating the surface of the wire or
bracket slot.

 The explanation for discrepancy may lie in the significance of loading forces
used between the arch wire and the brackets.

 At low load levels saliva acts as a lubricant, but at high loads saliva may increase
friction if its forced out from the contacts between the brackets and the arch
wire.
 3)The effect of artificial saliva on the frictional forces between
orthodontic brackets and archwires:
 Here the effect of artificial saliva on the static and kinetic frictional forces of stainless
steel and polycrystalline ceramic brackets in combination with round end edgewise
arch wire and stainless steel, nickel titanium and -titanium arch wire materials under
a constant ligature force were investigated.
 In all the cases artificial saliva had the effect of increasing the frictional force when
compared with the dry state.
 They concluded that artificial saliva played an insignificant role in lubricating the
surface of the arch wire in the bracket slot.
 The explanation they gave for this study was that arch wire touches the
bracket at only 2 points where the pressure is relatively great.

 The lubricant could be expelled from the areas of contact allowing no

lubrication between the arch wire and bracket to exist, hence increasing
friction.

 Use of  titanium arch wire produced smallest

percentage increase in frictional forces due to;

stick and slip phenomenon.

Downing A, McCabe JF, Gordon PH. Br J Orthod.2005 Feb;22(1):41-6

 STICK-SLIP PHENOMENON
There are two coefficients of force : 1)static friction
2)kinetic friction
 Stick-slip can arise when the coefficient of static friction is markedly greater than
the coefficient of kinetic friction.
 During stick phase, the friction force builds up to a certain value, and once a large
enough force has been applied to overcome the static
friction force, slip occurs at the interface.
 Usually, a saw tooth pattern in friction force-time
curve
Friction force as a function of time or distance
showing stick-slip phenomenon
 II) BONDING AND SALIVA:

 A few studies are hereby mentioned to see the ever

changing influence of saliva in bonding procedure with

advent of new generation of bonding agents, primers.

 1) Effect on a New Bonding agent in bond strength to saliva contaminated enamel:

The purpose of the study in vitro was to compare bond strengths of brackets applied to
contaminated and uncontaminated enamel following pretreatment of contaminated
enamel with Scotch MP bonding system.

Sonis AL .J Clin Orthod.2014 Feb;28(2):03-4.

 They concluded that bond strength were found to be

equal in brackets bonded to saliva contaminated etched enamel

treated with Scotch Bond MP primer and bonding

agent applied to uncontaminated enamel.

 Scotch band MP works slightly differently.

 The primer composed of HEMA and polyalkeonic copolymer

behaves similar to the liquid of glass ionomer in that it

forms stronger bonds to a moistened enamel or dentin surface.

2) A technique to prevent surface contamination of etched enamel:

 It has been recommended that a thin layer of primer be

applied to the entire etched enamel surface before bonding

to seal the enamel, protect it from decay, provide maximal

bond strength.

 If etched surface becomes contaminated by oral fluids before

bonding the bond is likely to fail at resin enamel interface.

Greer KS, Lindauer SJ, Darling SG, Browning H, Moon PCJ Clin Orthod. 2006 Mar;30(3):145-6
 This is most likely to occur when bonding to surgically exposed palatally
placed canines or to teeth with short clinical crowns.

 In such cases its more effective to apply the

primer directly to the adhesive resin on the back

of orthodontic attachment.

 Bond strength in this technique was considered best in

cases where there is poor visibility or limited exposure.

3) SALIVARY CLEARANCE AND FIXED ORTHODONTIC APPLIANCES :

 Since fixed ortho appliances have numerous recesses, pits, which entraps the food
particles, oral clearance rate is slowed.

 Here is a study to demonstrate the same.

 1) Care- Magnus forsberg, olively A, Jagerlof F in 2012.

The study was conducted for the purpose of establishing the possible
influence of orthodontic therapy with fixed appliances on salivary clearance of
sugar.
 Aim – to study 1) whether fixed orthodontic appliances increase the residual

volume of saliva in mouth.

2) Salivary clearance of sugar.

 Unstimulated salivary flow rate, RESID, and salivary clearance of sugar was
determined on two occasions i.e. before start of treatment and 21 days after fixed
appliance was placed in the mouth.

 In the results, the salivary flow rate before the start of orthodontic treatment was

Care- Magnus forsberg, olively A, Jagerlof F. Am J Orthod Dentofacial Orthop. 2012.

 0.46 ml/min, after a wear of appliance for 21 days mean value increased to .57 ml min.
Orthodontic appliance had a similar effect on the residual

volume of saliva in the mouth after swallowing.

 It is a well known fact that a foreign body put in the mouth

will initially increase the flow of saliva.

 The present study indicates that fixed appliances does not

prolong the salivary clearance of sugar during the first month

of treatment.
 Further studies with longer duration claimed to have decreased or normal
levels of salivary flow and RESID.

 Since appliance consists of many retentive components that provide

numerous recesses and minor pits where food particle may be trapped
accounting for delayed clearance of sugars on long term treatment schedules

 Because of this factor caries and demineralization will continue to be matters

of concern during orthodontic treatment.
2) The use of low tack chewing gums for individuals wearing orthodontic
appliances –

 A clinical study was carried out to determine the acceptability of a sugar free, low tack
chewing gum by orthodontic patients.

 It was concluded that low tack sugar free chewing gums can be used by orthodontic
patients to increase saliva flow with the potential to remineralise and help reduce
white spot lesion formation.

Gray A, Ferguson MM Aust Dent J. 2006 Dec;41(6):373-6

 EXPERIMENTAL SALIVARY PELLICLES ON THE SURFACE OF
ORTHODONTIC MATERIALS:
 Conducted a study with a purpose to find out whether composition of salivary
pellicles that form on surface of orthodontic materials vary qualitatively in respect
to stainless steel, elastomeric ligature ring, bracket
bonding resin.
 They concluded that least amount of salivary pellicle
which was cariogenic was found on stainless resin,
followed by adhesive resin, highest amount of cariogenic pellicle was found on
elastomers.
Lee SJ, Kho HS, Lee SW, Yang WS. Am J Orthod Dentofacial Orthop. 2011 Jan;119(1):59-66.
5) EFFECT OF SALIVARY PH ON ORTHODONTIC POLYURETHANE
CHAIN ELASTICS:
 1) The effect of hydrogen ion concentration on
forces degradation rate of orthodontic
polyurethane chain elastics :
 The effect of pH on force degradation rates of
seven commercial orthodontic polyurethane
Chain elastics was evaluated in an in vitro study.
 The pH values of 4.85 to 7.26 were selected for testing because they represent values
closes to the reported extremes of plaque and saliva pH.
Ferriter JP, Meyers CE Jr, Lorton L. Am J Orthod Dentofacial Orthop. 2009 Nov;198(5):404-10.
 All specimens were equally stretched which delivered equal initial force levels. Force
degradation rates were recorded after 4 weeks.

 They concluded that force decay rate of polyurethane orthodontic chain elastics is
inversely proportional to the pH of oral environment with a corollary that pH levels above
mentioned are more hostile to the polyurethane chain elastics thus increasing their force
decay rates.
 6) SALIVA AND CORROSION :

 Saliva acts as an electrolyte and hence aids in causing corrosion of

metal components of fixed orthodontic appliances.

 When metal components of orthodontic appliances are in contact with

an electrolyte such as saliva, metals corrode by a complex
electrochemical process of oxidation and dissolution known as galvanic
corrosion.

 The generation of an electric cell is simple when different metals are

involved, but it can also occur within a single metal.
 Atoms at the grain boundary dissolve faster

than those within the grain . Impurities, rough

surfaces or irregularities can also alter the corrosion resistance of a metal.

 Corrosion resistant metals are known

as noble metals or cathodic metals.

 Types of corrosion :

 Uniform corrosion : metal is attacked evenly and

throughout, and its mechanical property diminishes proportionately.

 This type is rarely seen in orthodontics since all the parts of the appliance are not evenly
exposed to corrosion agents.
 2)Localized or pitting corrosion : most common form seen in orthodontic
attachments. Affects the mechanical property of the metal.
This type is seen when several different metals are used.
3)Galvanic corrosion : the oral cavity because of saliva, with
its salts provides a weak electrolyte. Galvanic corrosion is an important type of
electrolyte corrosion which occurs when combination of dissimilar metals lie in
direct physical contact with each other.
4)Stress corrosion : if a stressed metal comes in contact with unstressed
metals, stressed metal will become the anode of the galvanic cells and will
corrode.
 Here is a study to indicate corrosion of orthodontic appliance:

 Nickel ion concentrations in the saliva of patients treated with self-

ligating fixed appliances:
 The aim of the study was to determine salivary Ni2+ concentrations in patients
undergoing orthodontic treatment with self-ligating fixed appliances.

 A group of 30 patients between 10 and 13 years of age were treated with self-
ligating brackets (Smart Clip™), molar bands, and nickel–titanium (NiTi)
archwires.
Gölz L, Knickenberg AC, Keilig L, Reimann S, Papageorgiou SN, Jäger A, Bourauel C Nickel ion
concentrations in the saliva of patients treated with self-ligating fixed appliances:J Orofac
Orthop. 2016 Feb 24.
 Unstimulated saliva samples were collected after different time points
(before treatment, after self-ligating bracket and band placement, before
archwire insertion, after archwire insertion, and finally 4 and 8 weeks
afterwards) and analyzed with an ICP mass spectrometer.

 And the results stated that Self-ligating orthodontic appliances may affect
salivary Ni2+ concentrations in vivo over the short term.

 However, levels resembled those documented in conjunction with

conventional bracket use and remained below the daily dietary Ni intake.
 Nickel and chromium levels in the saliva and serum of patients with
fixed orthodontic appliances:

 The aim of the study was to evaluate the concentrations of nickel and
chromium ions in salivary and serum samples from patients treated with
fixed orthodontic appliances.

 The second aim of the study was to determine any significant changes in
these concentrations during any period of the treatment time.

 Saliva and blood samples were collected.

Ağaoğlu G1, Arun T, Izgi B, Yarat A. Nickel and chromium levels in the saliva and serum of
patients with fixed orthodontic appliances. Angle Orthod . 2014 Oct;71(5):375-9.
 The results indicate certain differences in the amount of nickel and chromium
released from fixed orthodontic appliances during different periods of treatment.

 In saliva samples, nickel and chromium reached their highest levels in the first
month and decreased to their initial level in the rest of the groups.

 It can be concluded that fixed orthodontic appliance releases measurable amount

of nickel and chromium when placed in the mouth.

 Most metals used in oral cavity can be expected to undergo this type of corossion.

 Saliva has a dynamic composition that may be affected by many physiologic

variables such as diet, salivary pH, health conditions and salivary flow rate.
7) SALIVA AND DEMINERALIZATION (CARIES) :
The pH of saliva acts as a deciding factor, be it
demineralization and induction of caries or remineralization.
At pH value of 6.8 to 6.0 hydrogen ions reacts with phosphate ions in saliva
and plaque.
At pH value of 5.5 to 5.0 demineralization occurs wherein hydroxyapatite
dissolves but flurapatite forms in the presence of fluoride. At pH of 4.5 to 3.5
(critical pH) both fluropatite and hydroxyapatite dissolves.
On the contrary if pH rises to 5.5 from the critical pH and if H+ ion are not
exhausted remineralization occurs and fluorapatite forms.
 DEMINERALIZATION - REMINERALIZATION CYCLE
Critical PH
6.8 to 6.0 5.5 to 5.0 4.5 to 4.0 to 3.5

Hydrogen ions reacts with phosphate Demineralization: HA dissolves, FA FA and HA dissolve

ions in saliva and plaque forms in presence of fluoride
Remineralization FA reforms If H+ ions exhausted or neutralized and
all ions retained.
6.8 to 6.0 5.5 to 5.0 4.5 to 4.0 to 3.5

HA-HYDROXYAPATITE FA- FLOURAPATITE

CONCLUSION:
 With the innumerous number of functions of salivary glands and its secretion
namely saliva that we have come across, we can arguably call this secretion
namely saliva the champion among the factors that are involved in homeostasis
of our body.

 Since dentistry is basically a material science thorough knowledge is important

for us to come out with new innovations so that products we use render maximal
service to the patient.
 REFERENCES:
1) William G. Shafer., Maynard K. Hine, Barnet M. Levy. A Text Book of Oral
Pathology. 4th edition, W.B. Saunder’s Company.
2) Stuart C. White, Michael J. Paroah. “Oral Radiology Principles and
Interpretation”. 5th Edition. Mosby
3) Yu-Jin Seo et al, European Journal of Orthodontics, 2015, 158–163
doi:10.1093/ejo/cju027.
4) Lee SJ, Kho HS, Lee SW, Yang WS. Experimental salivary pellicles on the
surface of orthodontic materials. Am J Orthod Dentofacial Orthop. 2011
Jan;119(1):59-66.
5) Ağaoğlu G1, Arun T, Izgi B, Yarat A. Nickel and chromium levels in the saliva
and serum of patients with fixed orthodontic appliances.Angle Orthod . 2014
Oct;71(5):375-9.
6) Ferriter JP, Meyers CE Jr, Lorton L. Am J Orthod Dentofacial Orthop. 2009
Nov;98(5):404-10.

7) Care- Magnus forsberg, olively A, Jagerlof F. Am J Orthod Dentofacial Orthop. 2012.

8) Greer KS, Lindauer SJ, Darling SG, Browning H, Moon PCJ Clin Orthod. 2006
Mar;30(3):145-6

9) Sonis AL .J Clin Orthod.2014 Feb;28(2):03-4.

11) Downing A,McCabe JF,Gordon PH. Br J Orthod.2005 Feb;22(1):41-6

12) Baker KL,Nieberg LG,Weimer AD,,Hanna M. Am J Orthod Dentofacial Orthop. 2013

Apr;91(4):316-20.

13) Gray A, Ferguson MM Aust Dent J. 2006 Dec;41(6):373-6