ORIGINAL ARTICLE

A comparative study of salivary buffering

capacity, flow rate, resting pH, and salivary
Immunoglobulin A in children with rampant
caries and caries-resistant children
Abstract
Purpose: This study was conducted to identify various
factors in the development of rampant type of dental caries
in South Kerala children, other than high sucrose intake and
poor oral hygiene. This was done by comparing the salivary
buffering capacity(BC), flow-rate(FR), resting pH and salivary
immunoglobulin-A(s-IgA) levels in children who are caries
resistant(CR) and who have rampant dental caries. Materials
and Methods:Two study groups, a rampant caries group(RC)
with more than five active caries lesions in the early stages
and a CR with no caries lesions were selected based on
a specific criteria. Unstimulated whole mixed saliva was
collected directly from the floor of the mouth for a period of
10 min and the FR was calculated. Resting pH of saliva was
measured using color coded pH paper. BC was measured
by calculating the amount of citric acid of pH2.5, required to
lower the initial pH of saliva down to 3. s-IgA levels were also
estimated by immunoturbidometric method after forming a
precipitate of s-IgA with specific anti-IgA antibodies. Result:
The salivary BC, FRs, pH and s-IgA levels were significantly
lower in the RC group when compared to the CR group.
Conclusion: This study showed that salivary BC, flow-rate,
resting pH and levels of s-IgA in saliva are risk factors in the
development of RC in children.

Key words
Buffering capacity, caries risk, flow rate, Immunoglobulin A,
rampant caries, salivary parameters

Introduction
Dental caries is a unique multifactorial, infectious
disease involving internal defense factors such as

Kuriakose S, Sundaresan C1, Mathai V2, Khosla

E3, Gaffoor FMA4
Department of Pedodontics and Preventive Dentistry,
Sri Sankara Dental College, Varkala, Kerala, 1Departments
of Pedodontics and Preventive Dentistry, Sree Mookambika
Institute of Dental Sciences, Kulasekharam, Kanyakumari,
2
Conservative Dentistry and Endodontics, Sree Mookambika
Institute of Dental Sciences, Kulasekharam, Kanyakumari,
3
Department of Pedodontics and Preventive Dentistry, Mar
Baselios Dental College, Kothamangalam, Kerala, 4Department
of Conservative Dentistry and Endodontics, N.I.College of
Dental Sciences, Neyyantinkara, Trivandrum, India
Correspondence:
Dr. Chintu Sundaresan, Department of Pedodontics and
Preventive Dentistry, Mangalya, Era-160, Thottam, Manacaud,
Trivandrum - 695 009, India.
E-mail: chintz_dr@yahoo.co.in
Access this article online
Quick Response Code:

Website:
www.jisppd.com
DOI:
10.4103/0970-4388.115697
PMID:
***

saliva, tooth surface morphology and mineralization,

general health, nutritional and hormonal status, and
a number of external factors such as diet, microbial
flora colonizing the teeth, oral hygiene, and fluoride
availability.[1] Rampant dental caries is an extreme form
of dental caries where multiple caries lesions appear
suddenly, almost all teeth are affected and the disease
process reaches the pulp at very rapid pace. Affected
children are often in great distress due to multiple
pulp exposures, do not eat properly, and become
malnourished. There is no evidence that the mechanism

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69

Kuriakose, et al.: Salivary risk factors in rampant caries

of the decay process is different in rampant caries (RC)

when compared to ordinary caries or that it occurs in
teeth that are malformed or inferior in composition. It
can occur in teeth that were for many years resistant to
decay suggesting that there is a sudden imbalance in the
oral environment. There seems to be an exaggeration
of certain caries-producing factors.
The role of excess consumption of refined carbohydrates,
poor oral hygiene, and accumulation of plaque with
high acid concentration produced by acidogenic bacteria
in the development of RC is well understood. But
even in the presence of these factors, many children
are found to be resistant to rampant dental caries.
Some children who were resistant to caries for many
years may suddenly develop RC even in the absence of
the above-mentioned cariogenic factors. Presence or
absence of protective host factors may be responsible
for the apparent resistance or susceptibility to RC.
Many modern studies have hence introduced a new
approach to dental caries from being a bacteria and
sugar-induced disease to a disease that is greatly
influenced by inherited salivary factors.[1] The dental
caries process is controlled to a large extent by a
natural protective mechanism inherent within the
saliva. The most important caries protective functions
of saliva are the flushing and neutralizing effects
which is dependent on the flow rate (FR) and buffering
capacity (BC) of saliva.[2] It has been shown that a
sudden reduction in the salivary FR can lead rapid
formation of caries lesions.[3] A clear inverse relationship
between salivary BC and caries susceptibility has been
clearly demonstrated.[4] BC is related to the FR as well
as the resting pH of the saliva.[5] BC is one of the
best indicators of caries susceptibility as it reveals the
host response. Saliva acts with its BC as a regulator of
plaque pH, neutralizing acids produced by cariogenic
bacteria. This capacity is based on the phosphate system,
the carbonic acid, and bicarbonate system. Saliva also
contains a number of antibacterial compounds such
as lysozyme, lactoperoxidases, lactoferrin, and various
immunoglobulins which can control the growth of
cariogenic oral microflora.[6] Many studies have shown
that salivary Immunoglobulin A (s-IgA) has a role in
the caries resistance shown by certain individuals and
decrease in IgA can lead to increase in incidence of acute
caries lesions.[7,8]
This study was done to compare the salivary FR, BC,
resting pH, and s-IgA levels in children who show an
inherent resistance to dental caries and children who
70

have rampant dental caries and thereby to identify the

role of various salivary factors in the development of RC.

Materials and Methods

Forty-two children with an age range of 3-5 years
reporting for dental checkup in the Department of
Pedodontics and Preventive dentistry were included
in this study. All the children had a comparable
socio-economic background and belonged to the
southern districts of Kerala and neighboring Tamil
Nadu. They were divided into two study groups, a RC
group and a caries-resistant (CR) group based on the
following criteria.

Rampant caries group

RC was diagnosed based on Masslers definition[9]
of RC.
Children with multiple (5) cervical, proximal,
or lingual white spot or brown spot lesions or
shallow active caries lesions in enamel/dentine were
included.
The subjects had a reasonably good oral
hygiene (plaque score: PlI 1-1.9) and did not have
more than three solid sugar exposures per day based
on a diet history of 3 days.
Baby bottle syndrome cases were excluded.
Children who had any infection during the past
6 months, allergic or other systemic disorders, those
who who underwent tonsillectomy, and those on
medications for systemic ailments were excluded.

Caries-resistant group
Subjects had no visual or radiographic signs of
caries.
Subjects with high plaque scores (PlI 2-3) and
subjects having more than three solid sugar
exposures per day including in-between meal sugar
exposures were included.
Children with a family history of very low dental
caries prevalence were included.

Collection of Saliva
Children and their parents and caretakers were informed
about the procedure and written consent was obtained
before collecting saliva. Unstimulated, resting mixed
saliva was collected for 10 min directly from the floor
of the mouth, using a needleless aspirating syringe
calibrated up to 5 ml. Each subject underwent this
procedure between 8.00 A.M and 9.00 A.M in the
morning. Children were advised not to eat or drink

JOURNAL OF INDIAN SOCIETY OF PEDODONTICS AND PREVENTIVE DENTISTRY | Apr - Jun 2013 | Issue 2 | Vol 31 |

Kuriakose, et al.: Salivary risk factors in rampant caries

of the decay process is different in rampant caries (RC)

when compared to ordinary caries or that it occurs in
teeth that are malformed or inferior in composition. It
can occur in teeth that were for many years resistant to
decay suggesting that there is a sudden imbalance in the
oral environment. There seems to be an exaggeration
of certain caries-producing factors.
The role of excess consumption of refined carbohydrates,
poor oral hygiene, and accumulation of plaque with
high acid concentration produced by acidogenic bacteria
in the development of RC is well understood. But
even in the presence of these factors, many children
are found to be resistant to rampant dental caries.
Some children who were resistant to caries for many
years may suddenly develop RC even in the absence of
the above-mentioned cariogenic factors. Presence or
absence of protective host factors may be responsible
for the apparent resistance or susceptibility to RC.
Many modern studies have hence introduced a new
approach to dental caries from being a bacteria and
sugar-induced disease to a disease that is greatly
influenced by inherited salivary factors.[1] The dental
caries process is controlled to a large extent by a
natural protective mechanism inherent within the
saliva. The most important caries protective functions
of saliva are the flushing and neutralizing effects
which is dependent on the flow rate (FR) and buffering
capacity (BC) of saliva.[2] It has been shown that a
sudden reduction in the salivary FR can lead rapid
formation of caries lesions.[3] A clear inverse relationship
between salivary BC and caries susceptibility has been
clearly demonstrated.[4] BC is related to the FR as well
as the resting pH of the saliva.[5] BC is one of the
best indicators of caries susceptibility as it reveals the
host response. Saliva acts with its BC as a regulator of
plaque pH, neutralizing acids produced by cariogenic
bacteria. This capacity is based on the phosphate system,
the carbonic acid, and bicarbonate system. Saliva also
contains a number of antibacterial compounds such
as lysozyme, lactoperoxidases, lactoferrin, and various
immunoglobulins which can control the growth of
cariogenic oral microflora.[6] Many studies have shown
that salivary Immunoglobulin A (s-IgA) has a role in
the caries resistance shown by certain individuals and
decrease in IgA can lead to increase in incidence of acute
caries lesions.[7,8]
This study was done to compare the salivary FR, BC,
resting pH, and s-IgA levels in children who show an
inherent resistance to dental caries and children who
70

have rampant dental caries and thereby to identify the

role of various salivary factors in the development of RC.

Materials and Methods

Forty-two children with an age range of 3-5 years
reporting for dental checkup in the Department of
Pedodontics and Preventive dentistry were included
in this study. All the children had a comparable
socio-economic background and belonged to the
southern districts of Kerala and neighboring Tamil
Nadu. They were divided into two study groups, a RC
group and a caries-resistant (CR) group based on the
following criteria.

Rampant caries group

RC was diagnosed based on Masslers definition[9]
of RC.
Children with multiple (5) cervical, proximal,
or lingual white spot or brown spot lesions or
shallow active caries lesions in enamel/dentine were
included.
The subjects had a reasonably good oral
hygiene (plaque score: PlI 1-1.9) and did not have
more than three solid sugar exposures per day based
on a diet history of 3 days.
Baby bottle syndrome cases were excluded.
Children who had any infection during the past
6 months, allergic or other systemic disorders, those
who who underwent tonsillectomy, and those on
medications for systemic ailments were excluded.

Caries-resistant group
Subjects had no visual or radiographic signs of
caries.
Subjects with high plaque scores (PlI 2-3) and
subjects having more than three solid sugar
exposures per day including in-between meal sugar
exposures were included.
Children with a family history of very low dental
caries prevalence were included.

Collection of Saliva
Children and their parents and caretakers were informed
about the procedure and written consent was obtained
before collecting saliva. Unstimulated, resting mixed
saliva was collected for 10 min directly from the floor
of the mouth, using a needleless aspirating syringe
calibrated up to 5 ml. Each subject underwent this
procedure between 8.00 A.M and 9.00 A.M in the
morning. Children were advised not to eat or drink

JOURNAL OF INDIAN SOCIETY OF PEDODONTICS AND PREVENTIVE DENTISTRY | Apr - Jun 2013 | Issue 2 | Vol 31 |

Kuriakose, et al.: Salivary risk factors in rampant caries

anything except water before saliva collection and were

not on any sort of medication. Saliva was collected
when they were totally calm. Children were asked to
keep their mouths open and saliva was then collected
in increments. They were allowed to close their mouths
for a few seconds in-between but were instructed not to
swallow any saliva.
The amount of saliva collected during a time period
of 10 min was taken as a measure of the salivary flow
for that individual. Resting salivary pH was estimated
using an Indikrom pH paper, which was placed on
the floor of the mouth with residual saliva, for 10 s.
Indikrom pH papers with a pH range from 5 to 7.5
were used for estimating intraoral salivary pHs. The
BC of the saliva collected was immediately estimated
to prevent CO2 gas from escaping from the sample.
When the quantity of saliva during 10 min was too
small for estimating the BC, saliva was collected for
another 10 min after giving sufficient rest to the child.

Procedure
BC of a sample of saliva was measured as the amount
of acid needed to lower the pH of saliva through a
fixed pH interval as is described inFederation Dentaire
Internationale technical report no. 31.[10] One milliliter
of saliva collected from each subject was dispensed into
a small borosil jar. After noting the initial pH of saliva
with a pH paper which ranges from 5.0 to 7.5, citric
acid of pH 2.5 was poured drop by drop using a small
pipette (one drop0.05 ml) into the saliva in the borosil
jar. Care was taken not to touch the sides of the borosil
jar. After pouring two drops of citric acid, the pH of
saliva was checked with pH paper. This continued till
the pH of saliva dropped to a value of 3. For measuring
lower pHs, Indikrom pH papers which range from 2
to 4.5 were used. The amount of citric acid added was
calculated thereafter (no. of drops added were counted).
This volume was taken as a measure of the BC of that
particular sample of saliva. The initial pH of saliva was
taken as such, i.e., the titration will be till the pH decreased
to 3 irrespective of the initial pH of saliva. Higher initial
pH was given credit for a higher BC.[11] The values were
determined for all the subjects in both the study groups.
They were tabulated and statistically analyzed.
Seventeen children from both the study groups were
recalled after 1 week for an estimation of their s-IgA
values. Saliva was collected again for 10 min from the
floor of mouth as described earlier. The saliva samples
are then transported under refrigerated conditions to the
laboratory where immunological assays are performed.

s-IgA concentrations were determined using the

immunoturbidometric assay. Here, the IgA samples
were suitably diluted first, 2 micro aliquots of each
saliva sample were diluted with 0.9% NaCl applying a
dilution factor of 1:20 using a microliter dispenser, and
then reacted with specific anti-IgA antibodies to form a
precipitate. For this, 50 l of the antibody reagents was
taken in a labeled test tube, 500 l of assay buffer was
pipetted into this test tube, and then specific quantity
of the diluted saliva (50 l) sample, determined by
protein calibration methods was incorporated into
this mixture. The resultant solution was allowed to
stand at room temperature for 30 min in order to
promote immunoprecipitation reaction. Following
immunoprecipitation reaction, each sample suspension
was drawn into the sipper tube of an automatic analyzer,
where a beam of light of 340 nm wavelength impinges
on the reaction mixture and the reduction in transmitted
light is measured using a photo spectrometer. The
amount of light absorbed is converted to units of
concentration using standards of known concentration.

Results
The salivary BC, FR, resting pH, and s-IgA values of
both groups were compared using the unpaired t-test.
When comparing the IgA values of both groups, it
was seen that the mean s-IgA concentration in the
RC group was 9.96 2.83 mg/dl and that in the
CR group was 15.15 2.22 mg/dl, the difference
being statistically significant (P value 0.001 and
t value5.95) [Table 1].
The mean unstimulated FR in the RC group was
0.81 0.45 ml/10 min and 1.37 0.57 ml/10 min
i n t h e C R g r o u p w h i c h w a s s t at i s t i c a l ly
significant (P value0.001, t value3.48) [Table 2].
The mean salivary resting pH value was 6.450.50
in the RC g roup and 7.15 0.30 in the CR
group (statistically significant with a P value0.001
and t value5.43) [Table 3].
When comparing the buffering capacities of both
the groups, the mean salivary BC of the RC group
was 0.430.16 units and that in the CR group was
1.180.30 units (statistically significant t value9.89,
P value0.001) [Table 4].

Discussion
In this study, RC children had a significantly lower
salivary FR, pH, BC, and s-IgA levels compared to

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71

Kuriakose, et al.: Salivary risk factors in rampant caries

Table 1: Comparison of mean immunoglobulin A values

Groups

Mean

SD

Rampant caries 17
Caries resistant 17

9.96
15.15

2.83
2.22

Mean difference t value P value

5.19

5.95

0.001

Table 2: Comparison of mean flow rate

Groups

N Mean SD Mean difference t value P value

Rampant caries 21
Caries resistant 21

0.81
1.37

0.45
0.57

0.56

3.48

0.001

Table 3: Comparison of resting pH values

Groups

N Mean SD Mean difference t value P value

Rampant caries 21

6.45

0.50

Caries resistant 21

7.15

0.31

0.70

5.43

0.001

Table 4: Comparison of mean buffering capacity

Groups

N Mean SD Mean difference t value

Rampant caries 21
Caries resistant 21

0.43
1.18

0.16
0.30

0.75

9.89

P value
0.001

CR children. Only those RC cases where there was

a diet history of 3 solid sugar exposures per day,
no bottle or breast feeding at night/day time, and
where the children maintained reasonably good oral
hygiene (PI-1-1.9) were included. Multiple active caries
lesions (5) in these children aged 3-5 years meant that
other etiological factors were responsible for the rapid
appearance and progress of Carious lesion. Children
who gave a diet history of more than three solid sugar
exposures daily in-between meal sugar exposures,
not maintaining good oral hygiene (PI-2-3), and still
not developing caries lesions were considered CR and
included in the CR group. It was hypothesized that CR
group had more protective salivary host factors than RC
group children. The significantly higher mean values
of salivary FR, pH, BC, and s-IgA, in the CR group,
proved that this hypothesis was correct.
Many studies have reported that caries-free patients
have higher levels of naturally induced s-IgA and that
decrease in IgA levels increases caries incidence.[7,8]
Some studies have shown high levels of IgA in children
with caries susceptibility. Caries lesions accumulated
over a long period of time lodges enormous numbers
of cariogenic bacteria that can stimulate a local immune
response with secondary rise in s-IgA levels.[12] In
this study, care was taken to assess IgA levels at the
initiation of rampant type of dental caries when there
were only cervical, proximal, or lingual white spot
lesions or shallow active caries lesions in enamel and
dentine. There were no long-standing open caries
lesions or root stumps such that only the IgA levels
72

in the primary immune response were assessed.

CR children had significantly higher mean IgA
levels (15.15 mg/dl 2.22 mg/dl) when compared
to (9.962.83) RC children showing the role of IgA
in resisting rampant dental caries.
Specific immune defense against Streptococcus mutans,
considered to be the primary causative agent of
dental caries, is provided largely by s-IgA antibodies
which are generated by the common mucosal immune
systems. [13] This system is functional right from
infancy when infants develop these IgA antibodies as
their mouth gets colonized by oral microorganisms.
s-IgA seems to interfere with sucrose-independent and
sucrose-dependent attachment of S. mutans to tooth
surfaces thereby inhibiting dental caries. They may also
result in agglutination of bacteria and neutralization of
their toxins.[13]
Regarding salivary pH, significantly lower and
more acidic pH values were shown by children in
the RC group (6.45 0.50) when compared to CR
group (7.15 0.30). This is in accordance with the
findings of Sissons et al.[14] Saliva was collected for
10 min as the unstimulated saliva collected during a
period of 1 min was too small for calculating the BC.
The volume collected during the 10 min was taken
as the FR for that individual. A mean difference of
0.56 ml/10 min was seen between the two study groups
with CR group having significantly higher FR. This
result was in agreement with previous studies.[15] Direct
aspiration from the floor of the mouth ensured that the
salivary flow was unstimulated. Spitting onto a tumbler
could have stimulated salivary flow. Unstimulated
FR seems to be more important in RC development
as stimulated flow is seen during mastication only.
Nocturnal flow is also unstimulated.
Jorma Tenovou[15] has reported a negative correlation
between BC and caries activity in a population. Decrease
in salivary BC leads to a drastic increase in caries
susceptibility as the enamel dissolution by plaque acids
is left uncontrolled.[5] A significantly lesser BC was
shown by RC children when compared to CR children
in this study. The technique described by Larsen et al.[16]
was modified and used in this study. Simple inexpensive,
indigenous equipment was used, with citric acid as the
weak acid for measuring the BC of saliva. Citric acid
is one of the byproducts of microbial carbohydrate
metabolism. RC children with known etiological factors
such as poor oral hygiene, uncontrolled sugar intake, and
prolonged bottle or breast feeding were not included in
this study. Hence, it is not possible to conclude that all

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Kuriakose, et al.: Salivary risk factors in rampant caries

RC children have low levels of IgA and low values of

BC, FR, and resting pH. Similarly, it is not possible to
conclude that all CR children have high values of BC,
FR, pH, and IgA levels. Since caries is a multifactorial
disease, a low-sugar diet, good oral hygiene, and low
S. mutans levels can also make a child CR even if the
salivary BC, FR, pH, and IgA levels are low. Other caries
risk factors, such as S. mutans count and composition
and mineralization of enamel, were not assessed in this
study. However, this study has shown conclusively that
a reduction in s-IgA, BC, FR, and resting pH values
can lead to rampant dental caries formation in children.
Further research is required to determine the factors
that may lead to an abrupt reduction in salivary BC,
FR, resting pH, and IgA levels which in turn can lead
to RC formation in preschool children.
Salivary diagnostics is entering the surgery of a
pedodontist, wherein a persons susceptibility to
rampant type of dental caries can be assessed by
measuring the salivary BC, FR, pH, and IgA levels.
A SPIT-KIT, as used in this study, a kit that can be
used to measure various salivary parameters such as
FR, pH, and BC can be useful in identifying high-risk
patients. Estimation of IgA levels in saliva requires
specialized immunological laboratories and cannot be
done as a chair-side procedure and currently there are
no reliable techniques to increase s-IgA levels. However,
IgA studies are important as they will finally help in
the development of a suitable anti-caries vaccine, as
increasing the levels of anti-S. mutans IgA is the basis
of any caries vaccine. Streptococcal antigens like GTF,
antigen 1/11 are being used to develop IgA specific
to S. mutans.[13] In high-risk children, salivary flow
and buffering effect may be increased using sugar-free
chewing gums, sucking tablets, lozenges, etc.[17]

Conclusion
In this study
The RC group children had significantly lower s-IgA
concentration in their saliva when compared to CR
children in their same age group.
The resting salivary pH values of CR children were
significantly higher than RC children.
Salivary BC and FRs are comparatively much
lower in RC children than in children who show a
resistance of dental caries.
In both RC and CR children, the BC and resting pH
values of saliva showed a positive correlation with
each other.

This study has shown that the salivary FR, pH, BC,
and s-IgA concentrations are important risk factors in
the development of rampant dental caries in preschool
children aged 3-5 years. Increase in s-IgA levels, BC,
FR, and resting pH can make a child resistant to dental
caries while a sudden decrease in these parameters can
lead to the development of RC.

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How to cite this article: Kuriakose S, Sundaresan C, Mathai V,

Khosla E, Gaffoor F. A comparative study of salivary buffering
capacity, flow rate, resting pH, and salivary Immunoglobulin A
in children with rampant caries and caries-resistant children. J
Indian Soc Pedod Prev Dent 2013;31:69-73.
Source of Support: Nil, Conflict of Interest: None declared.

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