Journal of the Ghana Science Association, Vol. 2, No.

2, 2000 1 9

The non-acidogenic potential of two Ghanaian meals

1
1

Frederick Kwaku Addai and 2Isaac Kwasi Nuamah

Department of Anatomy, University of Ghana Medical School, P. O. Box 4236, Accra, Ghana
Private Dental Practitioner, 15 St. Chad Road, Washington, Manchester M20 4WH, England

ABSTRACT
This study tested whether a meal of Ga Kenkey and fried fish with tomato/pepper sauce (kenkey and
fish), or fried ripened plantain with beans (Red-Red) is acidogenic. The pH of baseline saliva given by
volunteers prior to eating a meal, and at specific intervals after the meal (effect saliva) was measured
using a Kent EIL 7020 pH meter. As control, volunteers were given a glucose challenge in which they
rinsed their mouths with a 5% glucose solution for exactly 60 seconds. Changes in pH of effect saliva
were determined with reference to their respective baseline saliva. The mean pH of saliva changed
significantly by negative 0.50 ten minutes after the glucose challenge and negative 0.23 a further five
minutes later. Immediately after a meal of Red-Red the mean pH of saliva significantly changed by
positive 0.45. Ten and 15 minutes after the meal the mean saliva pH changes were positive 0.13 and
positive 0.06, respectively. The mean pH of saliva changed by positive 0.39 fifteen minutes after
volunteers ate kenkey and fish, and twenty-five minutes after the meal the mean change in pH was
positive 0.10. The reduction in pH of saliva below baseline value after the glucose challenge confirmed
its acidogenic potential. Since there was no depression of saliva pH below baseline values after
volunteers had eaten either of the two meals, it is concluded that Red-Red:, as well as kenkey and fish
have non-acidogenic potential. By extension, this suggests that either meal has non-cariogenic or
cariostatic effect.

1.

Introduction

The direct effect of acidogenic challenge

to teeth caused by ingested foods/drinks on
induction and progress of dental caries is well
established. Dental caries develops when oral
microorganisms breakdown remnants of
fermentable carbohydrate food, releasing
organic (lactic, formic, succinate, acetic, and
propionic) acids in the immediate proximity of
the teeth (Felscher, 1993; Anderson et al., 1993;
Pollard et al., 1006). An increase in organic
acid concentration translates into an increase in
hydrogen ion concentration or a decline in pH of
dental plaque (the mixture of noncalcified oral
microorganisms and their substrates/products
that adheres to teeth). The fall in plaque pH
gives rise to dissolution of the inorganic
components of enamel (demineralization) and
loss of mineral salts from the tooth surface
(Margolis et al., 1999). Demineralisation is
followed by enzymatic destruction of dental
protein matrix giving rise to cavitation and direct
bacterial invasion of the tooth. The sequence of
events culminates in tooth decay and subsequent
loss, and was first codified as the chemoparasitic
theory of the tooth decay 110 years ago

(Anderson et al., 1993). In 1978, Geddes and

co-workers demonstrated in vivo that the acid
production by plaque bacteria from fermentable
carbohydrates results in caries-like changes in
dental enamel. Foods that promote plaque acid
production have acidogenic potential, and
because low plaque pH initiates dental carieslike changes (Toumba and Duggal, 1999) they
also have a cariogenic potential.
When the pH of dental plaque rises, it
can result in crystal regrowth or remineralisation
to repair damaged enamel (Leach et al., 1989).
There is thus, equilibrium of de- and
remineralisation that is influenced by a number
of factors, but primarily dependent on the type
and pattern of food intake (Jensen and Wefel,
1989). The balance of de- and remineralisation
is shifted in favour of demineralisation when the
frequency of consumption of fermentable
carbohydrates increases, leading to progression
of dental caries (Jenkins, 1970).
Thielade and Birkhed (1986) identified
the factors in diets that may increase cariogenic
challenge to teeth as follows.

ADDAI & NUAMAH / NON-ACIDOGENIC POTENTIAL OF TWO GHANAIAN MEALS

(i) An overall higher content of rapidly
fermentable carbohydrate, especially sugars
and refined flour;
(ii) an increase in frequency of eating;
(iii) fewer foodstuffs which require vigorous
mastication to produce high levels of
salivary flow, and
(iv) Fewer components in refined foods which
result in caries inhibition.
In a review of the basis of the good
condition of peoples teeth in West Africa Falconer (1992) states that, several authors claim
that diet combined with regular use of chewing
sticks is responsible. In Ghana, a higher
prevalence of dental caries among urban 12year-old children, compared to their peers in the
rural areas was attributed to differences in diet
(Addo-Yobo et. al., 1991).
The authors
suggested that adoption of a Westernized diet
containing relatively higher content of refined
carbohydrates in urban communities, as against
the traditional starchy foods in rural
communities is responsible for the higher
incidence of dental caries among urban school
children.
The present study sought to
scientifically verify the postulate that diets of
traditional starchy foods are non-cariogenic or
do not predispose consumers to dental caries.
We assessed the acidogenic challenge to teeth
(acidogenic potential) of two Ghanaian
traditional meals patronised by Medical students
in their canteen.
Several methods have been recommended
for the assessment of acido/carogenicity of
foods, including total carbohydrate content of
salivary expectorants (Curzon and Pollard,
1996). By far, the most widely used method is
plaque pH measurements (Hussein et al., 1996;
Moynihan et al., 1996; Tahmassebi and Duggal,
1996; Gopinath et al., 1997; Koparal et al.,
1998; Toumba and Duggal, 1999). This requires
specially designed electrodes that are fitted
directly to the tooth, or specialised methods for
harvesting plaque for pH measurements. Lack
of indwelling electrodes, and schedules of both
researchers
and
volunteers
that
were
inauspicious for meticulous plaque harvesting,
made us resort to periodic whole saliva sampling
for pH measurement as an indicator of plaque
acidity. Our choice of saliva pH as an index of
acidogenic potential is supported by well-known
effects of saliva on plaque pH (Englander et al.,
1959; Makinen et al., 1996; Coogan and
Motlekar, 1996; Ittagarun and Wei, 1997) and
dental caries (Mandel, 1989; Vogel et al., 1998).

Also, saliva bathes teeth and their surgace

deposits as well as oral soft tissues and is
considered the natural defence against plaque
acid (Edgar, 1992), and the primary source of
components that regulate plaque pH (Abelson
and Mandel, 1981; Mandel, 1994). Moreover,
Macpherson et al., (1991) showed that saliva pH
correlates with plaque pH. Mandel (1994) noted
that, direct measurement of plaque pH affords a
more convenient estimate of acidogenic and by
extension cariogenic potential. We propose
that analysis of saliva pH at various time
intervals after a sucrose rinse or meal gives a
more comprehensive picture as it incorporates
the natural buffering effects of oral secretions.

2.

Subjects and methods

The acidogenicity of a meal of Ga Kenkey

and fried fish with tomato/pepper sauce (kenkey
and fish), and fried ripened plantain with beans
(Red-Red) was tested in separate experiments.
The direct outcome measure of this study was
the change in pH of whole saliva after eating
either of the two meals, to determine whether or
not a pH decline occurred to suggest that the
meal had an acidogenic potential (and therefore
potentially cariogenic). Healthy volunteers were
drawn from the student population of University
of Ghana Medical School, Korle-Bu, Accra.
There were equal numbers of males and females
in each experiment and selection criteria were
the same for all volunteers. After accepting to
participate in the study when it had been
explained to them, the volunteers were selected
who were not taking any medication for
systemic disease or being treated for medical
problems. They refrained from eating, drinking
and oral hygiene for a minimum of 60 minutes
before salivary collection. The sample size of
each experiment was determined to give a 90%
power of detecting a minimum pH change of 0.4
units. A control experiment was first carried out
to confirm that our methodology and equipment
could detect saliva pH depression caused by
glucose, a known acidogenic (cariogenic) agent
(Yankell and Emling, 1989). At the beginning
of each experiment, the volunteers gave a nonstimulated saliva sample (base-line) by spitting
3-4 times into a pre-cleaned and oven-dried 25
ml conical flask. In the control experiment, the
subjects rinsed their mouths for exactly 60
seconds with 15 ml of a 5% aqueous glucose
solution (i.e., glucose challenge). Ten minutes
after the glucose challenge each volunteer gave a
second saliva sample (effect 1), followed by a

Journal of the Ghana Science Association, Vol. 2, No. 2, 2000

third saliva sample (effect 2) 5 minutes later.
One person (FKA) measured the pH of each
saliva sample, and dealt with saliva from all
subjects within 15 minutes of their collection.
To facilitate pH measurements performed with a
Kent EIL 7020 pH meter, every saliva sample
was diluted with 20 ml of double distilled water
(pH 7.0).
In the experiment involving the meal of
Red-Red, subjects were each given a plate of
the meal to eat after they had given base-line
saliva samples. Fifteen minutes after they
started eating the meal, subjects gave a second
saliva sample designated as effect 1 saliva.
Subsequent saliva samples were taken 10 and 15
minutes later and designated as effect 2 and
effect 3 saliva respectively.
In the third
experiment, subjects were given a plate of
kenkey and fish to eat after giving baseline
saliva samples. Owing to complaints from
volunteers that giving saliva samples
immediately after the meal and/or in the canteen
was off-putting, the second (effect 1) and third
(effect 2) samples of saliva after the meal of
kenkey and fish were taken 15 and 25 minutes
subsequent to the meal, respectively. Thus, the
elapsed time allowed volunteers to return to the
laboratory (in the company of FKA who
ascertained that none ingested/chewed anything
to confound results) where the saliva samples
were given. A one-sample t-test was performed
to determine whether the pH of effect saliva
samples from each experiment was significantly
different from the pH of baseline saliva samples
obtained from volunteers.
The statistical
analysis was done with GraphPad Prism
software on a Gateway personal computer.

3.

Results

The means of saliva pH obtained from

volunteers before and during the three
experiments carried out in this study are
presented in Fig. 1. Table 1 shows the
descriptive statistics for the means presented in
Fig.1. Statistical comparisons of the pH of
baseline and effect saliva in each experiment are
summarised in Table 2. The pH of saliva
obtained 10 minutes (effect 1) and 15 minutes
(effect 2) after volunteers were given the glucose
challenge were significantly lower than the pH

of baseline saliva collected before the treatment

(Table 2).
The pH of saliva obtained
immediately (effect 1) and 10 minutes after
(effect 2) a meal of Red-Red was significantly
higher compared to the neutral pH of baseline
saliva (Table 2). However, the pH of saliva
samples collected 15 minutes after (effect 3) the
meal of Red-Red was not significantly higher
than the pH of baseline saliva. Table 2 also
shows that eating kenkey and fish caused a
significant rise in the pH of saliva obtained from
volunteers 15 (effect 1) and 25 minutes (effect
2) after the meal compared to the pH of their
baseline saliva. A one sample t-test comparison
of the mean baseline saliva pH of volunteers
who ate Red-Red and those who ate kenkey
and fish gave a t-value of 3.954 (75 degrees of
freedom); a two-tailed P =0.0002; the
discrepancy in mean pH was 0.15 with a 95%
confidence interval of negative 0.23 to negative
0.08. A similar comparison of the mean saliva
pH obtained 15 minutes after their meals
produced the following statistics. Students tvalue of 12.69 (75 degrees of freedom); two
tailed P < 0.0001; discrepancy in mean pH of
0.48 with 95% confidence interval of negative
0.55 to negative 0.40.
4.

Discussion

The glucose rinse experiment was carried out to

determine whether or not the Kent EIL 7020 pH
meter and the procedure adopted in this work
could detect significant changes in whole saliva
pH. Our results confirm that of Yankell and
Emling (1989) in which the pH of dental plaque
was found to decrease after a glucose rinse,
indicating its acidogenicity. Owing to the
buffering effects of certain salivary components
(Mandel, 1994; Coogan and Motlekar, 1996;
itthagarun and Wei, 1997) the saliva pH values
obtained in the present work are likely to be
higher than actual plaque pH values. This
implies that whereas the pH drop following the
glucose rinse reported here might be less than
the reality in the closest proximity of teeth, the
rise in pH following meals might also be
exaggerated. But, changes in salivary pH are

ADDAI & NUAMAH / NON-ACIDOGENIC POTENTIAL OF TWO GHANAIAN MEALS

Baseline
Effect 1
Effect 2
Effect 3

7.75

pH of saliva

7.50

7.25

7.00

6.75

6.50
G-rinse

Red-Red

kenkey/fish

Fig. 1. Descriptive statistics of the means of saliva pH obtained from volunteers before (baseline) and after (effect)
glucose rinse or eating two Ghanaian meals. Error bars represent the standard error (SE) of the mean.

Table 1. Descriptive statistics of the means of saliva pH obtained from volunteers before
(baseline) and after (effect) glucose rinse or eating two Ghanaian meals.
(Glucose rinse)
Experimental Status
Minutes elapsing after
Meal

Meal of Red-Red

Baseline Effect 1 Effect 2

-

Parameter/Sample size

10

Baseline Effect1 Effect2 Effect 3

15

--

72

10

15

Meal of Kenkey and

Fish
Baseline Effect 1 Effect 2
--

76

25

56

Mean pH of saliva

7.06

6.56

6.84

7.11

7.56

7.24

7.17

7.26

7.65

7.36

Standard Deviation

0.32

0.45

0.39

0.34

0.40

0.36

0.33

0.29

0.25

0.22

Coefficient of variation (%) 4.50

6.80

5.70

4.80

5.20

5.00

4.6

4.0

3.30

3.00

Lower 95% CI

6.99

6.46

6.74

7.03

7.47

7.16

7.10

7.19

7.59

7.30

Upper 95% CI

7.14

6.67

6.92

7.19

7.65

7.32

7.25

7.34

7.72

7.42

pH are reported to parallel changes in plaque pH, and

effective buffering of saliva can diminish acidogenic
challenge to teeth (Makinen et al., 1996; Vogel et al.,
1998; Kargul et al., 1998). Therefore, it is inferential

that a substance whose ingestion results in a drop in

salivary pH is acidogenic, and that whose ingestion
leads to a rise in salivary pH is non-acidogenic.

Journal of the Ghana Science Association, Vol. 2, No. 2, 2000

Table 2:

Summary of statistical comparisons of means of (effect) saliva pH after glucose

rinse/meals with the respective baseline values in the three experiments.

Statistic

Glucose rinse

Meal of Red-Red

Meal of Kenkey and

Fish

One sample t-test

Effect1

Effect 2

Effect1 Effect2 Effect 3

Effect 1

Effect 2

Baseline means pH (B)

7.06

7.06

7.11

7.11

7.11

7.26

7.26

Mean pH after meal (E)

6.56

6.84

7.56

7.24

7.17

7.65

7.36

Discrepancy (E minus B)

-0.50

-0.23

0.46

0.13

0.06

0.39

0.10

95% Confidence Interval (CI) of

Discrepancy

[-0.61]
[-0.40]

[-0.32]
[-0.14]

[0.36]
[0.55]

[0.05
[0.21

0.01
0.14

0.32
0.46

0.04
0.16

t-value

9.55

9.94

3.18

1.67

11.46

3.32

(degrees of freedom)
Two-tailed P value

4.92
(71)

<0.0001

<0.0001

Thus, our finding that eating Red-Red and

kenkey and fish resulted in significant rises in saliva
pH over baseline levels is very interesting. Other
workers studying the effect of carbohydrate diets on
plaque pH, obtained a lowering of pH (Ferjerskov et
al., 1992; Lingstrom et al., 1993). That saliva pH
rose significantly after eating the two Ghanaian
meals suggests that they are non-acidogenic, and by
extension non-cariogenic or cariostatic.
There
appears to be confirmation in our results for the
thesis that traditional starchy diets are not cariogenic
(Addo- Yobo et al., 1991; McGregor, 1963). By
extension, our results also empirically support the
authors assertion that Westernized dietary habit is
responsible for the higher incidence of decayed,
missing, filled teeth (DMFT) among urban 12-yearold school children compared to their age mates in
rural Ghana who eat traditional starchy foods (such
as those in the meals eaten by volunteers in our
study).
The direct benefit of elevated saliva pH is in
neutralising plaque acid and increasing plaque
calcium and phosphate (Anderson et al., 1993;
Mandel, 1994; Mandel, 1996), thereby inhibiting the
carious process in teeth. Saliva pH rise is also
beneficial because plaque acid control is considered

(75)
<0.0001

0.001

(55)
0.10

<0.0001

0.002

the single most important aspect of the prevention of

inflammatory periodontal disease (Edgar, 1992).
The rise in saliva pH after eating the two meals could
be explained in three possible ways:
i.
Both Red-Red and Kenkey and fish lacked the
simple sugars (such as glucose and fructose) that
constitute the substrate for oral bacteria in plaque
formation (deduction from assertion by
Mcgregor, 1963; Addo-Yobo, 1991; vide supra).
ii.
The combined effect of chewing and swallowing
entailed in eating both meals accelerated
salivation,
which
increased
bicarbonate
concentration of saliva and accounted for the pH
elevation (Jensen and Wefel, 1989, Leach et al.,
1989, Scheie et al., 1998).
iii.
The taste and/or smell of the food stimulated
saliva flow that caused a rise in pH for the reason
given in (2) above (Edgar, 1992).
The first point may not be true of Red-Red
which has a sweet fruity taste. Indeed, biochemical
analysis has shown that ripe plantain contains
glucose (Andoh, 1971). Kenkey, on the other hand,
may not contain simple sugars since it is prepared by
cooking dry, milled and fermented corn. However,
Edgar (1992) noted that cooked starch could give rise
to acid production in human plaque pH experiments.
The author explained that cooking disrupts the

ADDAI & NUAMAH / NON-ACIDOGENIC POTENTIAL OF TWO GHANAIAN MEALS

granules of starch (in cereal and potatoes) which is
otherwise resistant to amylase action, and that
digestion by salivary amylase presumably releases
sufficient maltose (for fermentation by oral bacteria)
to constitute a cariogenic challenge. It is, therefore,
not likely that absence of simple sugars in the two
meals wholly accounted for the significant rise in
saliva pH of subjects after the meals. Besides, the
contribution of other ingredients in the meals (such
as salt, beans, oil, fish, and spices) to the nonacidogenic effects observed in this study remains to
be determined.
On the second point, substantial evidence
suggests that mastication and swallowing result in
increased salivary flow and concomitant rise in pH
owing to increased concentration of bicarbonate
(Dawes and Jenkins, 1964, Jensen and Wefel, 1989;
Scheue et al., 1998). In fact, chewing a flavourless
bolus such as wax or gum leads to a three-fold
increase in saliva flow (Edgar, 1992). We concur
with Edgar (1992), that this phenomenon is a reflex
response in which receptors in the muscles of
mastication; temporomandibular joint, periodontal
ligament and (lingual) mucous membranes detect the
presence of a bolus and its chewing to stimulate the
salivary nuclei to increase para-sympathetic
secretomotor discharge. The fall in pH of (effect 2)
saliva after subjects gave effect 1 saliva samples can
be attributed to the removal of bicarbonate-rich
stimulated saliva, and return to the non-stimulated
salivary flow with a lower content of bicarbonate
ions (Dawes and Jenkins, 1964).
Stimulated
swallowing has also been shown to effectively
reverse plaque pH and pCa changes that were caused
by a glucose rinse (Yankell and Emling, 1989). As
noted by Edgar (1992), it is difficult to account for
empirically dramatic increase in salivary bicarbonate
at high flow rates considering that duct-lining cells
secrete it (bicarbonate). For, in theory, faster flow of
saliva should not allow adequate time for increased
bicarbonate addition by the lining cells within the
ducts of salivary glands. By comparison it is easy to
explain why faster swallowing of saliva accounts for
its neutralising and buffering effect, since this dilutes
and washes away the oral bacteria and their
substrates/products that cause pH elevation.
On the third point, taste (gustatory) and smell
(olfactory) stimulation of saliva secretion and
composition can be demonstrated. The reflex effects

of taste stimuli are quite dramatic, giving rise to

perhaps a ten-fold increase in saliva flow (Edgar,
1992). According to Edgar (1992) sour stimuli are
most effective, followed by sweet, salt and bitter in
accelerating saliva flow. It is interesting, therefore,
that even the baseline saliva for subjects who ate the
kenkey and fish meal was significantly more alkaline
compared to those who ate Red-Red. It is notable
that Ga kenkey has a sour taste and a strong aroma
that stimulates the trigeminal nerves, compared to the
sweet taste and fruity smell of Red-Red. There is
also the effect of pepper on the taste buds. Pepper is
rich in ascorbic acid (Andoh, 1971) and there was
greater amount in the sauce that was eaten with the
kenkey.
The chemical stimulation via chorda
tympani and glossopharyngeal (nerves supplying the
taste buds) to the salivatory nucleus is well known to
be a path for salivary stimulation. In fact, citirc acid
is commonly used to stimulate salivary flow by
directly swabbing a 0.2% solution on the tongue
(Ship et al., 1991, Mandel, 1993). Therefore, the
much higher pH of saliva 15 minutes after kenkey
and fish compared to the same duration after RedRed may be explicable for the above reasons,
although individual differences cannot be discounted
since the volunteers were not the same in the two
experiments.
Specifically, differences between
caries susceptible and caries resistant volunteers
(Mandel, 1994), which we were unable to determine,
could also account for, or contribute to the higher
salivary pH 15 minutes after the meal of kenkey and
fish compared to Red-Red.

5.

Conclusion
It is conjectured that the combined reflex effects
of mastication, swallowing, taste, and smell of RedRed and kenkey and fish accounted for significant
saliva pH elevation after volunteers ate the meals.
This suggests that the two meals are non-acidogenic
or non-cariogenic, but cariostatic. The increase in
salivary pH after eating the meals would also provide
buffering for plaque acid and prevent inflammatory
perodontal disease (Edgar, 1992), We agree with
Jensen and Wefel (1989), that it is sensible to
consider any procedure that reduces acidogenic
challenge to the dentition in caries preventive
programmes. Also, in concurrence with the view
that consumption of protective foods ought to be

Journal of the Ghana Science Association, Vol. 2, No. 2, 2000

considered an important aspect of caries prevention
(Mandel, 1996), we propose that the two meals are
recommendable as diets that may help to prevent bad
oral health, in combination with other strategies. Our
results also suggest that kenkey and fish is the better
of the two meals in its non-acidogenic (cariostatic)
effect.

6.

caries free subjects, J. Dent. Assoc., South

Africa, 51 (12), 823-827.
Curzon, M.E. and Pollard, M.A. (1996).
Integration of methods for determining the
acido/cariogenic potential of foods: a
comparison of several different methods,
Caries Res., 30(2), 126-131.

Acknowledgements

We gratefully acknowledge the financial support

of the Dreyfus Health Foundation (DHF) of New
York, U.S.A. The indispensable and supportive role
of the late Mr. samuel Lawton Ackah-Yensu as the
Ghana Country C0-ordinator for DHF is
acknowledged.
We thank the students who
volunteered as subjects from the year classes 1996,
1997 and 1998 of the University of Ghana Medical
School. The help of our two Research Assistants
Ms. Victoria Andan and Mr. Prince Egyir Yawson
is acknowledged. Finally, we acknowledge the
useful criticisms of the Ethical Committee of the
University of Ghana Medical School on the
Research protocol.

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