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International Journal of Contemporary Dental and Medical Reviews (2017), Article ID 011217, 6 Pages
REVIEW ARTICLE
The composition, function and role of saliva in maintaining
oral health: A review
Brij Kumar1, Nilotpol Kashyap1, Alok Avinash1, Ramakrishna Chevvuri2, Mylavarapu Krishna Sagar3, Kumar Shrikant3
¹Department of Pedodontics and Preventive Dentistry, Rungta College of Dental Sciences and Research, Bhilai, Chhattisgarh, India, ²Department of Public
Health Dentistry, Rungta College of Dental Sciences and Research, Bhilai, Chhattisgarh, India, ³Department of Pedodontics and Preventive Dentistry, People’s
Dental Academy, Bhopal, Madhya Pradesh, India
Abstract
Saliva is certainly one of the most important components in the oral environment and an
integral component to oral health. The components of saliva, its functions in maintaining
oral health and the main factors that cause alterations in salivary secretion will be
reviewed, the importance of saliva in caries development and bacterial plaque formation
will be discussed, and its role as an aid to diagnosing certain pathologies will also be
discussed here. Saliva aids in maintaining mucosal integrity and in digestion through
salivary enzymes. Saliva is essential information of the pellicle, which protects the tooth
after eruption. Saliva has several oral benets including buering, remineralization, and
lubrication. Consider the acid attack on the teeth after a cariogenic episode, saliva aids in
mechanically removing food debris and bacteria from the oral cavity and teeth, reduced
salivary ow causes ill eects to the oral tissues.
Keywords: Caries, dental plaque, saliva, salivary ow rate, salivary proteins, xerostomia
Introduction
A critical component of the oral environment is saliva, a dilute
aqueous solution containing both inorganic and organic
constituents. Saliva plays an essential role during mastication,
in swallowing and in speech. The substances dissolved in saliva
during mastication are transported to stimulate taste receptors
for taste perception.
The salivary amylase is a digestive enzyme responsible for
the initial stage in starch and glycogen breakdown, and salivary
lipase secreted by lingual salivary glands (Von Ebner’s glands)
may play a signicant role in fat digestion. In many animals
evaporation of saliva spread on fur or while panting is important
in temperature regulation during heat stress.[1]
The functions of saliva are to protect the oral tissues by
keeping them moist and by providing a lubricating mucoid
secretion, by maintaining a uid environment with high calcium
and phosphate concentrations and the power of buering acids
and to initiate the digestion of starch. Impaired salivary secretion
(hyposalivation) increases the risk of oral diseases such as dental
caries and oral candidal infection.[2]
Recently, additional functions of salivary glands have been
uncovered. Salivary glands have been shown to contain, and possibly
secrete, a large number of physiologically active substances, such as
nerve growth factor, vasoactive peptides, and regulatory peptides.
Thus salivary glands may have a role in functions not normally
associated with that traditional alimentary function.[3,4]
Composition of Saliva [Table1][5]
Functions of saliva in humans
Digestive functions
Although amylase is a major component of the parotid secretion
and is present at an appreciable level in the submandibular uid
as well, its salivary role in the digestion of carbohydrates is really
minimal. The only eective conversion of starch to maltose that
occurs in the oral cavity is in food-retentive sites, and this benets
primarily the plaque bacteria. Most of the food is swallowed
rather quickly, and in the stomach salivary amylase would be
minimally eective, given the low pH and high proteolytic
activity of the gastric juice.[6]
Correspondence
Dr.Brij Kumar, Department of Pedodontics
and Preventive Dentistry, Rungta College
of Dental Sciences and Research, Bhilai,
Chhattisgarh, India. Phone: +91-8827800994.
E-mail: brij220787@gmail.com
Received: 30October 17
Accepted: 15 December 17
doi: 10.15713/ins.ijcdmr.121
How to cite this article:
Brij Kumar, Nilotpol Kashyap, Alok Avinash,
Ramakrishna Chevvuri, Mylavarapu Krishna
Sagar, Kumar Shrikant, “The composition,
function and role of saliva in maintaining oral
health: Areview,” Int J Contemp Dent Med
Rev, vol.2017, Article ID: 011217, 2017.
doi: 10.15713/ins.ijcdmr.121
Kumar, et al. e composition, function, and role of saliva in maintaining oral health
2
The high water content of the parotid secretions
moistening the food and the mucins generated by the
submandibular, sublingual, and minor salivary glands coating
the food combine eectively to facilitate ingestion. Other
lubrication molecules, such as the parotid proline-rich
glycoprotein albumin complex, may also participate in the rate
of food passage by becoming incorporated into pellicle, thus
providing a lubricating interface between teeth and facilitating
mastication.
Saliva also plays a gastronomic role by solubilizing many of
the food components and acting as a medium for interaction
with the receptors on the taste cell. It has been proposed that
a specic zinc-binding salivary protein, gustin, and mediates
taste sensation. Saliva also enhances taste perception by its
relatively low level of salts and its very low concentration of
sugar; thus, in a sense, it does not compete with exogenous
taste modalities.[7]
Protective Functions
Lubrication and demulcent properties
From an evolutionary point of view, the oldest function of
salivary glands is to supply lubrication molecules, to coat not
only the food but the oral soft tissue as well. The lubrication lm
allows for ready phonation as well as food passage and provides
for smooth tissue surfaces that exhibit minimal friction and are
comfortable as well as functional. The lubricating properties
of saliva have always been ascribed to the mucin glycoproteins
because they can provide uid layers with high lm strength,
and there are several experimental models to show that salivary
mucin and similar molecules do indeed have eective lubricating
properties. Very recently, Hatton et al. (1985) showed that the
proline-rich glycoprotein of parotid saliva, when complexed
with albumin, was also an extremely eective lubricant. The
distribution of this complex in the oral cavity remains to be
established, but it should be functional on teeth as part of
pellicle, and on mucous membranes as well. It could also be part
of the food coating but is probably overshadowed by the much
more adhesive mucin.
Maintenance of Mucous Membrane Integrity
The salivary mucins possess rheological properties which include
low solubility, high viscosity, elasticity, and adhesiveness, which
enable them to concentrate on the oral mucosal surface, where they
provide an eective barrier against desiccation and environmental
insults. The molecular structure of salivary mucins enables them
to bind water eectively, and hence their presence on the mucous
membrane surfaces serves as natural “waterproong” and helps to
maintain these tissues in a hydrated state.
Mucins have been shown to be important in the control of
permeability of mucosal surface, and the presence of a salivary
lm is important in limiting penetration of a variety of potential
irritants and toxins in foods and beverages as well as of potentially
hazardous agents from tobacco smoke and other sources.[8]
A variety of proteolytic enzymes is generated in the bacterial
plaque around the teeth and in the crevicular area, especially
in people with periodontitis. Proteases are also generated by
polymorphonuclear leukocytes, the numbers being related to the
level of inammatory disease. The bacterial and PMN proteases
(e.g., elastase, collagenase, and cathepsin) have the potential of
aecting the integrity of the mucous membranes and causing
ulceration. Mucins are protective in this regard since their
glycosylated regions are very resistant to proteolysis.
There is also a second line of defense against protease
activity, cysteine-containing phosphoproteins, in particularly
high concentration in submandibular saliva, which are identical
to Cystatin S. Cystatins S is an inhibitor of cysteine proteinases,
especially Cathepsin C. This antiprotease activity is augmented
by antileukoprotease, an eective inhibitor of granulocyte elastase
and Cathepsin G, present in both parotid and submandibular
glands, but to a much greater extent in the former.[9]
Table1: Composition of saliva:(mg/100 ml)
Whole(mixed) Resting Stimulated
Mean Range Mean Range
Total solids 500 300–800 530 400–900
Organic constituents
Proteins 220 140–640 280 170–420
Amino acids 4
Amylase 38
Lysozyme 22 11 0.4–62
IgA 19
IgG 1.4
Glucose 0.2
Citrate 1.0 1.0 0.5–3
Lactate Trace
Ammonia 3 1–12
Urea 20 12–70 13 0.6–30
Uric acid 1.5 0.5–3 3 1–21
Creatinine 0.1 0.05–0.2
Cholesterol 8 2.5–50
CAMP 7 50
Inorganic constituents
Sodium 15 0–20 60
Potassium 80 60–100 80
iocyanate‑smoker 9 6–12
Non‑smokers 2 1–3
Calcium 5.8 2.2–11.3 6
Phosphate(P) 16.8 6.1–71 12
Chloride 50 100
Fluoride(ppm) 0.028 0.015–0.045
e composition, function, and role of saliva in maintaining oral health Kumar, et al.
3
Soft Tissue Repair
Licking one’s wounds may be more than metaphor. The
presence of nerve growth factor and epidermal growth factor
in the submandibular saliva may accelerate wound-healing.
Epidermal growth factor is present in human saliva but at much
lower levels. The eect of saliva in oral wound-healing in humans
remains to be established.
An alternate role for saliva in wound-healing is suggested by
a paper of Volker (1942), in which he showed that saliva speeds
blood coagulation, both by aecting the anticoagulant valuable
property in an area where rough food or traumatic injury can
induce bleeding and bleed readily due to inammatory disease.[10]
Maintenance of Ecological Balance
Colonization of tissue surfaces, adherence is a critical event
for the survival of many bacteria, and interference with this
process, bacterial clearance, by mechanical, immunological, and
non-immunological means is one of the major functions of the
salivary defense mechanism. The ability of saliva to maintain an
appropriate ecological balance in the oral cavity is an important
evolutionary force in the long period of human existence before
plaque control.
Debridement and Lavage
The physical ow of saliva augmented by the muscular activity of
the lips and tongue eectively removes a large number of potentially
harmful bacteria from teeth and mucosal surfaces. This clearance
mechanism is similar to tearing and blinking in the eye, blowing the
nose, and coughing and expectorating to clear the lungs.[11]
Aggregation
In addition to physical eects, saliva can interfere with bacterial
adherence by more direct means that depend on molecular
interactions. The ability to inhibit bacterial attachment is a
major characteristic of the secretory IgA system and is the
rationale for the interest in an oral vaccine against caries. In
addition to these made to order antibodies, there is a variety of
ready-to- wear macromolecules, some very specic in action,
which mask bacterial adhesins or compete with them for
attachment sites on tissue. They may also function by clumping
or aggregating bacteria to the point where they can no longer
eectively adhere to hard or soft tissue and are expectorated
or swallowed. Most attention in experimental studies of
aggregation has been given to the high molecular weight
mucins. The presence of multiple complex oligosaccharide side
chains and a characteristic micro heterogeneity provide a wide
range of possibilities for interactions with many bacteria. The
amount of covalently bound lipid can also aect the properties
of mucins and can inuence their propensity for bacterial
interaction.[12,13]
Direct Antibacterial Properties
A group of salivary proteins lysozyme, lactoferrin, and
lactoperoxidase working in conjunction with other components
of saliva can have an immediate eect on oral bacteria, interfering
with their ability to multiply or killing them directly. Lysozyme
can cause lysis of bacterial cells, especially Streptococcus mutans
by interacting with anions of low charge density chaotropic ions
(thiocyanate, perchlorate, iodide, bromide, nitrate, chloride, and
uoride), and with bicarbonate. It has recently been shown that
another cationic peptide in saliva the histidine-rich peptide of
parotid saliva has growth-inhibitory and bactericidal eects on
oral bacteria. The histidine-rich peptides appear to be eective
antifungal agent as well, able to inhibit growth and kill Candida
albicans at very low concentration.[14]
Lactoferrin, the exocrine gland equivalent of transferrin, is
eective against bacteria that require iron for their metabolic
processes. It can compete with the bacterial iron-chelating
molecules, and deprive the bacteria of this essential element.
Lactoferrin is also capable of a bactericidal eect that is distinct
from simple iron deprivation.
Salivary peroxidase is part of an antibacterial system which
involves the oxidation of salivary thiocyanate by hydrogen
peroxide (generated by oral bacteria) to hypothiocyanite and
hypothiocyanous acid. These products, in turn, aect bacterial
metabolism (especially acid production) by oxidizing the
sulfhydryl groups of the enzymes involved in glycolysis and sugar
transport. The antimicrobial eect of salivary peroxidase against
S. mutans is signicantly enhanced by interaction with secretory
IgA. The protective potential of all the antibacterial proteins
can be extended by interaction with mucin which can serve to
concentrate this defense force at the interface of the mucosa and
the inhospitable external environment.
When teeth are present, especially if some gingivitis exists,
the oral uids will be augmented by a contribution from the
gingival crevice area, the gingival crevicular uid. This uid can
contribute to the oral defense system by providing: (a) Serum
antibodies against oral bacteria, especially IgG antibodies,
(b) phagocytic cells (PMN’s), and (c) antibacterial products
liberated from the phagocytic cells (e.g. lysozyme, lactoferrin,
and myeloperoxidase).[15]
Maintenance of pH
Saliva is eective in helping to maintain a relatively neutral pH
in the oral cavity, in the bacterial plaque, and on swallowing, in
the esophagus as well. In the oral cavity and the esophagus, the
major regulation of pH, especially during eating or drinking, is
the salivary bicarbonate, the level of which varies directly with
ow rate.
In the bacterial plaque, where acid production is the natural
sequela to bacterial metabolism of carbohydrates, saliva helps
regulate pH in several ways. Bicarbonate, phosphate, and
histidine-rich peptides act directly as buers once they have
Kumar, et al. e composition, function, and role of saliva in maintaining oral health
4
diused into the plaque. Urea from saliva is converted by bacterial
urease to ammonia, which can neutralize the acid. Amino acids
and peptides can be decarboxylated to form monoamines
and polyamines, a process which consumes hydrogen ions.
Arginine and arginine peptides can form ammonia as well as the
polyamine, putrescine, and thus can be particularly eective in
elevating plaque pH.
Maintenance of Tooth Integrity
In addition to helping to counter plaque acidity, saliva helps
protect the teeth in a number of other ways. This protective
function begins immediately after tooth eruption into the
oral cavity. Although the crown of the tooth is fully formed
morphologically when it erupts, it is crystallographically
incomplete. Interaction with saliva provides a post-eruptive
maturation through diusion of ions such as calcium, phosphorus,
magnesium, and uoride, as well as other trace components, into
the surface enamel. This maturation increases surface hardness,
decreases permeability, and has been experimentally shown to
increase resistance to caries.[16]
Once tooth begins to function in the mouth, its developmental
cuticle or pellicle is rapidly worn away and is replaced by a
constantly replenished salivary lm, the acquired pellicle. This
selectively adsorbed coating of proteins and lipids provides a
protective barrier and a lubricating lm against excessive wear,
a diusion barrier against acid penetration, and a limitation
against mineral egress.[17]
One of the major contributions of salivary research during
the past decade has been the characterization of the system
that regulate the ionic environment in the plaque and oral
cavity. A group of phosphoproteins acidic proline-rich proteins,
statherin, and cysteine-containing phosphoproteins provide
this protection by eectively binding calcium and helping to
maintain saliva in a state of supersaturation with respect to
calcium phosphate salts. They bind to the surfaces of early crystal
nuclei and retard crystal growth.[18]
Excretory Functions
Many drugs, as well as alcohol, are excreted into the saliva, which
could theoretically serve as a route of elimination. However,
since most of the saliva generated is swallowed rather than
expectorated, it is a very inecient disposal system, since the
substances would be absorbed and recycled. Clearly this is a
minor function.
Water Balance
Salivary glands are part of a control system for maintaining an
appropriate level of hydration. Thirst and need for uid intake
are usually signaled by dry mouth. This sensation results from
a diminution in resting secretion and activation of receptors
in the oral cavity. The signals to salivary glands result from
osmotic changes detected in hypothalamus or volemic changes
operating through the renin-angiotensin system of the kidney.
Thirst satiation and cessation of drinking are initiated by sensory
messages passing into the brain from taste receptors in the mouth.
Hormonal Function
Several studies have shown that the polypeptide hormone
known as an epidermal growth factor, is identical with human
urogastrone. Nerve growth factor and transforming growth
factor may be closely related as well. Human urogastrone, found
in very high concentrations in urine, is readily measurable in
the submandibular saliva. The major properties of urogastrone
include gastric cytoprotection and inhibition of gastric acid
secretion.[19]
Saliva and Periodontal Health
Role of saliva in oral diseases is most apparent when salivary ow
is markedly reduced. With respect to periodontal health, saliva
plays a role in two ways.
Pellicle and plaque formation
Saliva inuences supragingival plaque deposition and activity in
a variety of ways. It is predominantly involved in the rst step of
plaque formation, i.e., deposition of a pellicle (or cuticle) which
is a four stage process.
a. Bathing of the tooth surfaces by salivary uids which contain
abundant proteins.
b. Selective adsorption of certain negatively and positively
charged glycoproteins which act as an agglutinating base.
c. Loss of solubility of the adsorbed proteins by surface
denaturation and acid precipitation.
d. Alteration of the glycoproteins by enzymes from bacteria and
the oral secretions.
Now, this pellicle which is formed is actively involved
in the second stage of plaque formation which is “bacterial
colonization.”
1. The initial step in dental plaque formation involves the
adherence of bacteria to the salivary-coated tooth surface.
2. The bacteria that adhere to the pellicle initially are called the
“primary” colonizers which are usually Streptococcus sanguis
species followed by S. mutans.
3. Once an initial layer of bacteria attaches to the pellicle surface,
plaque can progress at a rapid pace, as many “secondary
colonizers” adhere to the primary bacteria and carve an
“ecological niche” for themselves. When we ask patients to
maintain a good oral hygiene, we are actually targeting to
counter this step.
4. In the third or maturation stage, saliva continues to
provide agglutinating substances and other proteins to
the intercellular matrix, and bacterial adhesion continues
unabated.
e composition, function, and role of saliva in maintaining oral health Kumar, et al.
5
5. Salivary proteins and carbohydrates serve as a substrate
for metabolic activity of the bacteria. Salivary calcium,
phosphates, magnesium, sodium, and potassium become part
of the gel-like consistency of plaque and begin to inuence
its mineralization and demineralization. Mineral precipitate
results from a local rise in degree of saturation of calcium
and phosphates in saliva due to (a) increase of pH of saliva
(b) colloidal and particles in saliva which bind to calcium and
phosphates making super-saturated solution.[14,20-22]
Plaque mineralization and calculus formation
Salivary proteins such as esterase, pyrophosphates possibly
acid phosphatase and lysozyme play a role. Calcium crystals
are served by saliva. Persons who are heavy calculus formers are
known to have higher levels of salivary proteins (glycoproteins).
Therefore, oral hygiene instructions should be tailor-made to
suit each child’s need.
Recent concepts
The fact that α-amylase is found in acquired enamel pellicle
suggests that it has a role in bacterial adhesion. If it is so then
α-amylase is double danger, because it binds to bacteria in
the plaque, hold them together, and at the same time provide
additional glucose to those plaque microorganisms, and that too
include proximity to tooth surface. The resulting lactic acid is
added to the pool of acid that is already present.[23]
Saliva and Dental Caries
Evidence shows that saliva from caries-free individuals has higher
values of the following: (Compared to caries prone).
1. The increased rate of ow increased pH and increased
buering.
2. Higher calcium and phosphorous concentrations.
3. Higher ammonia concentration.
4. High concentrations of ATP and fructose diphosphate.
5. Increased aldolase activity and O2 uptake of bacteria.
6. Increased opsonin activity.
7. Increased general antibacterial activity.
8. Increased antibacterial activity specic to lactobacilli and
streptococci.
9. Higher number of intact leukocytes.
10. Dierence in proportion of epithelial cells to leukocytes.[23]
The saliva inuences on the caries process which is
fundamental, and the saliva also aects all the three components
of Keye’s classic Venn diagram of etiology of caries (tooth, plaque,
and substrate). The saliva also aects ow rates and clearance,
pH and buer capacity, calcium phosphate homeostasis and
eects on bacterial metabolism. The obvious manifestation
of the saliva/caries interactions includes adsorption to oral
tissues and elimination from the oral cavity. There are many
studies which had been done to relate certain aspects of salivary
output and composition to caries susceptibility. Most of those
studies were focused at either the physico-chemical properties
of saliva (ow rate, buer capacity) or denite components of
saliva with antimicrobial activity, such as salivary IgA, lactoferrin,
lysozyme and the salivary peroxidase-hypothiocyanite system.
The consensus relationship between caries experience and the
activity of any of the salivary antimicrobial proteins cannot be
validated, except hypothiocyanite system and IgA.[24]
The proline-rich proteins of the human parotid saliva
exhibits inherited polymorphisms [34] that have led to a number
of analysis done to correlate the genetic phenotype with caries
severity. Results have commonly been inconsistent in terms of
determining a relationship between prevalence of dental caries
(DMFS) and genetic phenotype of saliva.[13]
There are number of cross-sectional studies had been done to
correlate the compositions and ow of saliva with dental caries.
However, a basic aw of any such study is that the use of the DMF
index for evaluation of caries activity. The DMF index may be
a lifetime collective index of dental disease and treatment and
should have very little bearing activity at the precise purpose in
time. Similarly, a one-time determination of whole stimulated
salivary ow rate does not pass muster as a comprehensive
analysis of salivary function. Other more sensitive, indicator
of salivary activity have to be compelled to be used, probably
combining in vivo demineralization/remineralization models with
dierent indicators of dental caries activity along with recurrent,
standardized and comprehensive secretion collections.[25]
The use of saliva as a diagnostic uid
There has been a continuing hope over many years that saliva
could provide an alternative to blood for tests which might help
in the diagnosis of disease. This could occur only if a blood
component was transferable across the salivary gland epithelium
in proportion to its concentration in blood. This is true for
urea, glucose and the unbound steroid hormones. Only for the
some of these has saliva proved a useful medium for monitoring
concentrations. Glucose is used by the gland cells and appears in
saliva at around one-hundredth of its plasma concentration - too
low for easy measurement.[26]
Change in salivary composition in salivary gland disease
Sodium and chloride concentrations in the aected gland
secretions are raised in sialadenitis, suggesting that inammation
particularly aects the ductal system. This possibility is
reinforced by the observation that phosphate concentrations are
usually lowered.
Sjogren’s syndrome is a connective tissue disorder which
usually involves reduced secretion from the lacrimal and
salivary glands. Reduced salivary secretion causes a dry mouth
and is termed xerostomia. Again the principal changes in ionic
composition of saliva are increased concentration of sodium and
chloride and decreased concentration of phosphate. In addition,
there are changes in the relative concentrations of some minor
salivary proteins. These may have some diagnostic value. Salivary
gland neoplasms are uncommon, and there are few data available
on their eects on salivary compositions.[26]
Kumar, et al. e composition, function, and role of saliva in maintaining oral health
6
Radiation used in the treatment of neoplasm in the head and
neck region often results in radiation-induced damage to salivary
gland. This is seen as a marked reduction in ow rate, leading
to xerostomia. The small amount of saliva secreted has high
concentrations of sodium, chloride, calcium, and magnesium but
low concentrations of hydrogen carbonate. The low volume of
saliva and its poor buering power are associated with rampant
dental caries in these patients.
The best treatment for xerostomia patients seems
to be frequent use of mouthwashes with a high uoride
concentration.[27]
Conclusion
Clearly, saliva has profound eects on the mouth, however, as
Sreebny has noted, few dental practitioners hassle to raise the
required queries or build the required observations and/or
measurements to work out whether or not there’s any level of
exocrine gland hypofunction in their patients. Unfortunately, a
minimum of a part of the matter is that, for many half, there’s
not an easy x to a broken salivary ow. We will solely hope that
future trends in biological science analysis might permit the
xerostomic patient to regain perform. Until then, dentists ought
to be additional alert to their patient’s salivary function embrace
additional disciplined preventive practices to discourage the
negative eects of reduced salivary ow.
References
1. Cawson RA, Porter OS. Essentials of Oral Pathology and
Oral Medicine. 7thed. London: Churchill Livingstone Elsevier
Science; 2002.
2. Anderson P, Hector MP, Rampersad MA. Critical pH in resting
and stimulated whole saliva in groups of children and adults. Int
J Paediatr Dent 2001;11:266‑73.
3. Alamoudi N, Farsi N, Faris J, Masoud I, Merdad K, MeishaD.
Salivary characteristics of children and its relation to oral
micro‑organism and lip mucosa dryness. Int Clin Pediatr
2004;28:239‑48.
4. Baskar SN. Orban’s Oral Histology and Embryology. 11thed. St.
Louis: Harcourt Asia PIE Ltd., Mosby; 1997.
5. Berkenbilt DA, Bahn AN. Development of antibodies
to cariogenic streptococci in children. J Am Dent Assoc
1971;83:332‑7.
6. Humphrey SP, Williamson RT. A review of saliva: Normal
composition, ow, and function. JProsthet Dent 2001;85:162‑9.
7. Jenkins GN. Physiology and Biochemistry. Oxford: Blackwell
Scientic Publications; 1977.
8. Lovelle CL. Applied Oral Physiology. 2nd ed. London:
Butterworth’s & Co., Publishers Ltd.; 1988.
9. Mandel ID. e functions of saliva. JDent Res 1987;66:623‑7.
10. Tencate AR. Oral History, Development, Structure and
Function. 6thed. St. Louis: Mosby Press; 2004.
11. Sreebny LM. Saliva in health and disease: An appraisal and
update. Int Dent J 2000;50:140‑61.
12. Rayment SA, Liu B, Soares RV, Oner GD, Oppenheim FG,
Troxler RF. e eects of duration and intensity of stimulation
on total protein and mucin concentrations in resting and
stimulated whole saliva. JDent Res 2001;80:1584‑7.
13. Tukia‑Kulmala H, Tenovuo J. Intra‑and inter‑individual
variation in salivary ow rate, buer eect, Lactobacilli, and
Mutans streptococci among 11 to 12year old school children.
Acta Odontol Scand 1993;51:31‑7.
14. Morinushi T, Murayama M, Kinjyo S. Mutans streptococci,
Lactobacilli in saliva and acidity for microorganisms in dental
plaque: Changes aer restorative treatment. JClin Pediatr Dent
2004;28:327‑32.
15. Tenovuo J. Antimicrobial function of human saliva‑
how important is it for oral health? Acta Odontol Scand
1998;56:250‑6.
16. Van Nieuw Amerongen A, Bolscher JG, Veerman EC. Salivary
proteins: Protective and diagnostic value in cariology? Caries
Res 2004;38:247‑53.
17. Azen EA. Genetics of salivary protein polymorphisms. Crit Rev
Oral Biol Med 1993;4:479‑85.
18. Nekrashevych Y, Hannig M, Stösser L. Assessment of enamel
erosion and protective eect of salivary pellicle by surface
roughness analysis and scanning electron microscopy. Oral
Health Prev Dent 2004;2:5‑11.
19. Rantonen PJ, Penttilä I, Meurman JH, Savolainen K, NärvänenS,
Helenius T. Growth hormone and cortisol in serum and saliva.
Acta Odontol Scand 2000;58:299‑303.
20. Bimstein E, Small PA Jr, Magnusson I. Leukocyte esterase and
protein levels in saliva, as indicators of gingival and periodontal
diseases in children. Pediatr Dent 2004;26:310‑5.
21. Saxén L, Tenovuo J, Vilja P. Salivary defense mechanisms in
juvenile periodontitis. Acta Odontol Scand 1990;48:399‑407.
22. Shafer WG, Hine MK, Levy BM. AText Book of Oral Pathology.
4thed. Philadelphia, PA: W.B. Saunder’s Company; 1983.
23. Sullivan A, Borgström MK, Granath L, Nilsson G. Number
of Mutans streptococci or Lactobacilli in a total dental plaque
sample does not explain the variation in caries better than the
numbers in stimulated whole saliva. Community Dent Oral
Epidemiol 1996;24:159‑63.
24. Gelbier MJ, Winter GB. Absence of salivary glands in children
with rampant dental caries: Report of seven cases. Int J Paediatr
Dent 1995;5:253‑7.
25. Moore PA, Guggenheimer J, Etzel KR, Weyant RJ, OrchardT.
Type1 diabetes mellitus, xerostomia, and salivary ow rates. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92:281‑91.
26. Nordgarden H, Jensen JL, Storhaug K. Oligodontia is associated
with extra‑oral ectodermal symptoms and low whole salivary
ow rates. Oral Dis 2001;7:226‑32.
27. Guggenheimer J, Moore PA. Xerostomia: Etiology, recognition
and treatment. JAm Dent Assoc 2003;134:61‑9.
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