The Effect of Sucrose on Plaque pH in the Primary and Permanent Dentition of Caries-inactive and -active Kenyan Children 0. FEJERSKOV, A.Aa. SCHEIE', and F. MANJI2 Department of Oral Anatomy, Dental Pathology and Operative Dentistry, The Royal Dental College, Vennelyst Boulevard, DK8000 Aarhus C, Denmark; 'Department of Microbiology, Faculty of Odontology, University of Oslo, Norway; and 2IDRC Regional Office, Health Science Division, Nairobi, Kenya The hypothesis that the Stephan pH responses of dental plaque would be different in caries-active and -inactive individuals was tested in 20 seven-year-old and 19 14-year-old Kenyan children. In each age group, half the children had . 2 dentin cavities; the other half had no such lesions. With a palladium-touch microelectrode, interdental plaque pH was monitored between m,/m2 in each quadrant in the primary dentition and in the four molar/premolar regions in the permanent dentition. pH was also monitored in caries cavities in the occlusal surfaces of lower first molars and on the tongue. pH was measured before and up to 60 min after the children rinsed with 10 mL of 10% sucrose. Caries status of the individual was unrelated to plaque pH in comparable non-carious sites in both of the age groups. The pH minimum in the maxilla was about 0.5 pH units lower than that in the mandible. Active occlusal caries lesions had a resting pH value ofabout 5.5, about 1 pH unit lower than that ofsound surfaces. The pH dropped to about 4.5 in caries lesions and recovered slowly. In sound occlusal sites, a pH drop to about 6.0 was followed by a relatively rapid return to the resting value. Thus, when the mean values were considered, the classic Stephan curve response was evident. However, when the pH changes at single sites were considered at various time intervals, a substantial, erratic fluctuation was observed. The tongue had a resting pH value of 7.0, which dropped to about pH 5.5 and remained low for more than 60 min. J Dent Res 71(1):25-31, January, 1992
Introduction. Since the excellent studies of Stephan (1940, 1944), rather few studies have dealt with plaque pH variations at various sites in the oral cavity (Kleinberg and Jenkins, 1964), and attempts to associate plaque pH with the actual caries status of individuals and sites examined are few and inconclusive (Englander et al., 1956; Rosen and Weisenstein, 1965; Turtola and Luoma, 1972). However, the methods used in assessing plaque pH have differed, as have the operational definitions of dental caries and caries activity. Although there is a large body of literature on the different aspects of plaque acidogenesis, plaque pH alone has been questioned as a reliable measure of cariogenicity, and it has been suggested that there are theoretical grounds for questioningthe relative significance of plaque pH measurements as indicators of caries activity (Bibby, 1981). Nevertheless, it has been claimed that "measurements of pH have made it possible to examine dental plaque as a metabolic unit and to identify the Stephan pH response as an important indicator of caries activity" (Kleinberg et al., 1982). The purpose of this study was to test the hypothesis that the in Received for publication February 14, 1991 Accepted for publication August 20, 1991 The present study is part of The Primary Oral Health Care Project Kenya conducted in collaboration between the Kenya Medical Research Institute, Nairobi, and the WHO Collaborating Centre on Oral Health Care Planning and Research at the Royal Dental College, Aarhus, Denmark, financed by DANIDA.
situ pH responses ofdental plaque to a sucrose rinse in caries-active and -inactive children would be different.
Materials and methods. Study group.-All children aged six to seven and 13 to 15 years attending a primary school in a sublocation ofMeru district, Kenya, were screened for the presence or absence of frank caries cavities. All children presented with poor oral hygiene and had never had fillings or tooth extractions. From each age group, children were assigned to either a "cariesinactive" group, group A (no frank cavities), or a "caries-active" group, group B (at least two teeth with deep caries cavities reaching dentin). This selection procedure continued until there were 20 seven-year-olds and 20 14-year-olds, each age group consisting of ten "caries-active" and ten "caries-inactive" children. On the following days, all children selected (except one 14-yearold who did not attend) were subjected to measurements of plaque pH, followed by a detailed clinical caries examination based on the criteria previously described (Manji et al., 1989). The children had been asked not to eat or drink for three h prior to the examinations. Plaque pH was measured prior to (i.e., resting pH), and at two, five, ten, 15, 20, 30, 40, 50, and 60 min following a one-minute rinse with 10 mL of a 10% (w/w) sucrose solution. When the starting (presucrose) plaque pH value was reached, further measurements were stopped. Measurements were made in the following sites: In the seven-year-olds, plaque pH was measured in the interproximal sites between the deciduous molars in all four quadrants, provided that these sites were sound. In the 14-year-olds, plaque pH was measured at the interproximal space between the second premolar and first molar in both mandibular quadrants, at the interproximal space between the first and second premolar in the maxillary right quadrant, and between the canine and first premolar in the maxillary left quadrant, provided, again, that the sites were sound. In the caries-active groups, plaque pH was also measured in occlusal cavities where present, preferably in the mandible, where there is easy access. In the caries-inactive groups, comparable sound occlusal sites were used as controls. pH measurements.-Two examination teams with a complete pH measurement set-up performed the investigation. The pH measurements were performed with a palladium-touch microelectrode (diameter, 0.1 mm; Beetrode MEPH- 1, W-P Instruments, New Haven, CT) connected to a battery-run Orion SA 720 pH/ISE Meter (Orion Research, Inc., Cambridge, MA). A porous glass electrode (Beetrode MERE-1) was used as a reference electrode. A reference salt bridge was created by having the test subject dip one finger into a 3 mol/L KCl solution containing the reference electrode. Immediately prior to, and after, each examination period (one to two min), the electrodes were calibrated against standard pH buffers at pH 7 and 4. If calibration measurements showed a drift of the electrode exceeding 0.05 pH units in any of the two standard buffers, the readings in between were adjusted according to calibration curves. The pH-meter readings were noted by an independent assistant. The two examiners exchanged electrodes at various intervals during the examination period. For further details, see Scheie et al. (1992).
25 Downloaded from jdr.sagepub.com at Univ of Connecticut / Health Center / Library on May 21, 2015 For personal use only. No other uses without permission.
J Dent Res
FEJERSKOVet al.
26
7 YEAR OLDS
pH
January 1992
14 YEAR OLDS
pH 7-
7-
6.5 -
6.5
MAN DIB3.U LA'S
MANDIBULAR
6-
6-
5.5 -
5.5 -
.........L A
I...........
MAXI LLARY 5-
5-
4..o e
Ad
I
I 0
5
I
I
10 15 20 25 30 35 40 45 60
TIME
-
I
65
-
--
60
4.5
-
I
0
5 10 15 20 25 30 35 40 45 50 5 60
TIME - MINUTES
MINUTES
Fig. 1-The Stephan response curves obtained in sound approximal maxillary and mandibular sites of seven-year-olds and 14-year-olds following a sucrose rinse. Bars indicate standard errors.
In order for pH responses over time between groups to be compared, an area under the curve was calculated, as arbitrarily defined by: the curve connecting pH values obtained from time 0 to time 30, a horizontal line through pH 3.5, a vertical line through time 0 min, and a vertical line through time 30 min (Area30). Between-group differences were tested by a two-tailed Student t test.
Results. Tables 1A and 1B present the mean plaque pH values for each sound site at different times. After a sucrose rinse, the mean pH at each sound site dropped by about one pH unit, and, after 30 min, the mean pH values were approaching the starting values of time 0. In these sites, there were no differences between the inactive and active groups in pH response over time. In both age groups, there was a slight, but statistically non-significant, tendency for the caries-active children (group B) to have resting pH values lower than those of the caries-inactive children (group A). There were no statistically significant differencesbetween the caries activity groups in the values of Area30. In both age groups, the pH response was more pronounced in sound maxillary sites than in sound mandibular sites throughout the 60 min (Fig. 1). There was a remarkable similarity between the two age groups in the pH response in mandibular sites. In the maxilla, the pH drop was more pronounced for the 14-year-olds as compared with the younger group. Fig. 2 shows the frequency distribution of the pH changes in single sites at various time intervals during the first 20 min following the sucrose rinse for maxillary and mandibular sites separately. During the first two min, the distribution of pH changes was highly skewed, such that the probability ofa pH drop exceeding one pH unit was 0.42 in maxillary sites and 0.24 in mandibular sites (Fig. 2). Although most sites showed pH drops during the first two min, 11% of maxillary sites and 20% of mandibular sites showed
unchanged or even increased pH values. In the following time intervals, the distribution of the pH changes approached a symmetrical distribution, such that both pH drops and pH increases were likely to occur. Thus, at any time interval, except for two min after sucrose rinsing, pH fluctuated in either direction. Fig. 3 shows that the mean pH values at time 0 and throughout the 60 min following a sucrose rinse were lower in active occlusal caries lesions than in sound occlusal surfaces (Area30, p < 0.001). The response curves for the three occlusal cavities that were classified as "inactive" (dark brown but hard when probed) were rather similar to those of sound surfaces and very different from those of "active lesions" (with soft floors). The pH response of the microbial plaque located on the dorsum ofthe tongue is shown in Fig. 4. The initial drop from mean pH 7 to pH 5.5 occurred within the first two min, and the shape ofthe curve was very similar to that seen in active caries lesions (Fig. 3). Thus, mean pH on the tongue remained low for up to 20 min and was still about one pH unit lower than the resting value one h after the sucrose rinse.
Discussion. Our study showed that the "Stephan pH responses" of microbial deposits in "non-carious" interproximal sites in the posterior parts of the oral cavity of caries-active and -inactive children were indistinguishable. However, there were marked differences between the average pH responses of carious and sound sites following a sucrose rinse. The demonstrated lack ofdifference between plaque pH responses in caries-active and -inactive children apparently contrasts with some of the earlier literature. However, this probably reflects differences in the way plaque pH was measured and how cariesactive individuals were defined. In Stephan's extensive study(1944) of 65 individuals [most likely adults (Stephan, 1940)], five subjects
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Vol. 71 No. 1
..
PLAQUE pH AND CARIES ACTIVITYIN CHILDREN
OBSERVED PROBABILITY
0.46
27
OBSERVED PROBABILITY 0.46, 0.40-
MANDIBULAR SITES
. . . . . . . .I.
0.36-
0.30-
0.26
-
0.20-
0.16
0.10
0.06
=I II 11112-....
=
--ma
onn0 -M __-
0% 0%oh
1
.
.
.
.
.
.
.
.
.
1
98 7 6 6432 1 0 1 234667 89
CHANGE IN pH; pH UNITS
-
0.30 -
-
O.SO
0.260.20-
0.10
-
0.06 -
0.00O
0.36'
0.30 0.26 0.20 0.16 0.10
0.06 U.W0
.
.
.
.
.
.
.
.
.
.
.
1
.
987 66432 1 01 23466760 CHANGE IN pH; pH UNITS
+
..
... ...
0.26
.
0.20
. ............
-.-...............
.....................
......................
0.10 .....................
h.........................................
|'-M 'IN ||N 0
ML .'AN
0.06 0.06
-
s | r ~~~~~~~~~~~ ~~~~~~~~ . ........ . ........
'i . .s .
.
.
.
.
.
.
.
0 8 7 6 6 4 32101 2 3 4 66 7 i 09
-
0.40
.
.......................
0.16
I
in AS
.
0.40 . .................
0.36-
0.16
.
.
.
OBSERVED PROBABILITY
0.4
0.40-
.
-
OBSERVED PROBABILITY
0.45
0.30
4.
.
CHANGE IN pH; pH UNITS
I
..
+
3BSERVED PROBABILITY
.
.
.
.
.
.
.
087664321
I. 2346670
CANGE IN p pH1 UNITS
-
0.46
601
+
OBSERVED PROBABILITY
Ia] * -o min
0.40-
0.36-
..
.....................................
0.30- .............. ...
....
0.26-
0.20-
......l[
0.10-
nn~~~~~ Unnnnn .II
.
.
.
. -
.
.
.
96766432 i
I
"I
I.
II
,"
*
6i0 2346676
CHANGE IN pH; pH UNITS
...... . . . . . . . . . . . . . . . . . . . . . . . . ....................
0.16-
...H.. _ .'
1
........................................................
.
0.06 -
n i l -,-l~l~lAl ..f i,. i.R0 ..
1
I. .
IIIY
0.00 I-
I
1 ..
.
.
.
.
.
iI
.
nn inn i I
.
8766432 16 1 23466760
+-
CHANGE IN PK pH UNITS
1
+
Fig. 2-The relative frequency distribution of changes in pH at sound maxillary and mandibular sites during the time intervals 0 to two min, two to five min, and 15 to 20 min, respectively. pH changes have been calculated as pH(t+l) - pH(t). Numbers on x-axes denote midpoints of pH intervals. Negative sign indicates pH drop from one measurement to the next. Downloaded from jdr.sagepub.com at Univ of Connecticut / Health Center / Library on May 21, 2015 For personal use only. No other uses without permission.
J Dent Res
FEJERSKOV et al.
28
January 1992
pH 7
6.5
6.5 6
6 5.5
5.5 _ 5
5_ 4.5
0
5
10 15 20 26 30 35 40 45 50
55
60
TIME (MINUTES) Fig. 3-The Stephan response curves obtained from sound occlusal surfaces, inactive occlusal caries lesions, and deep, active occlusal caries lesions following a sucrose rinse. Bars indicate standard errors.
4.5
were caries-free (group I), and 11 subjects had caries but showed no new lesions or enlargement of established ones over a two-year period (group II). In group III (26 individuals), there was a definite increase in the size of one or more lesions, and/or the development of small new cavities. Fifteen subjects exhibited rapid caries development and progression (group IV), and the remaining eight subjects had extensive caries, with active caries lesions on labial surfaces of the anterior teeth (group V). Although Stephan found an association between increased caries activity and a more acidic plaque response, resting pH values were similar in all groupsexcept in the extreme caries group (V). In the latter, pH measurements were most likely performed in plaque covering caries lesions (Stephan, 1944), and the pH response curves were remarkably similar to those observed for caries lesions in this study. Our caries-active group corresponded to groups II and III of the Stephan study (1944), and when account is taken of the variance about the means in both data sets, it may be seen that the plaque pH trends were rather similar. The different plaque pH responses claimed to exist between caries-free individuals and caries-active subjects (Englander et al., 1956; Moore et al., 1956; Clement et al., 1956; Turtola and Luoma, 1972; Kleinberg et al., 1982) may well be the result of the pooling of plaque samples from all sites before extra-oral pH measurement. When plaque is pooled, the pH measurements in caries-active subjects are therefore likely to include measurements of plaque from a varying number of caries lesions. The data recently published by Rankine et al. (1989) support this interpretation. Rankine et al. (1989) compared pH changes in plaque fluid aftervarious challenges, including sucrose, and found no differences between children with low caries activity and children with a six-month incidence of four or more new caries lesions-when all lesions had been restored before the study. It is of particular interest for the results of the study by Dirksen et al. (1962) to be compared with our data, even taking into account the differences in techniques used for pH measurements. The pH changes over time in our few inactive caries lesions were similar to
Fig. 4-The pH curve from the dorsum ofthe tongue after a sucrose rinse. Bars indicate standard errors.
I
0
5 10 15 20 25 30 35 40 45 50 55 60
TIME (MINUTES)
those which Dirksen et al. (1962) obtained from 34 cavities with "wide clinical openings and a thin layer of pigmented decayed dentine often hard and polished". The present study showed that the occlusal plaque in lower molars exhibited a fermentative response to a sucrose rinse similar to that obtained in the interdental molar/premolar spaces in the mandible (Figs. 3 and 4). The size of the microelectrode was such that it allowed pH measurements to be made even at the entrances to deep fissures (Fejerskov et al., 1973). This is important, since the majority of the early caries lesions developing in occlusal fissures are located immediately deep to the fissure entrance and along the lateral walls of the fissure (Thomsen et al., 1988). The within-mouth variation, with the maxillary sites showing a lower pH level and a slowerreturn to restingvalues thanmandibular sites, is in accordance with Stephan's original findings (1944) from incisor regions, and with the very detailed 'plaque pH-mapping" in adults, as performed by Kleinberg and Jenkins (1964). The possible physiological explanation for this is that, in a non-chewing and nontalking subject, the velocity of the 0.1-mm-thick salivary film is up to about 10 x less in the maxilla as compared with the mandible (Dawes et al., 1989). As suggested by these authors, the slow movement of the salivary film of unstimulated saliva allows for accumulation of diffusants from dental plaque which may prolong the clearance time of metabolic products such as acids. The possible relative importance of saliva in both buffering and removing plaque acids has been extensively considered (Edgar, 1976; Dawes, 1989), as have the related complex problems of diffusion properties of dental plaque (Dibdin, 1984; Dibdin and Shellis, 1988). It is tempting to compare our caries cavity plaque pH behavior with that observed on the dorsum ofthe tongue. The levels of resting pH and minimum pH reached after a sucrose rinse were
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Vol. 71 No. 1
PLAQUE pH AND CARIES ACTIVITYIN CHILDREN
29
TABLE 1A
MEAN pH (± S.D.) IN SOUND SITES MEASURED IN 20 SEVEN-YEAR-OLD CHILDREN FOLLOWING A SUCROSE RINSE Time
Group A
Group B*
Group A
Group B*
(min)
Site 55/54
Site 55/54
Site 64/65
Site 64/65
Mean
S.D.
n
Mean
0
6.25
(0.79)
10
2
5.37
(0.34)
5
5.38
10
S.D.
n
Mean
5.60
(0.75)
9
10
5.44
(0.69)
(0.35)
10
5.53
5.36
(0.52)
10
15
5.63
(0.56)
20
5.69
30
S.D.
n
Mean
6.38
(0.70)
10
9
5.44
(0.53)
(0.76)
9
5.60
5.24
(0.67)
9
10
5.38
(0.78)
(0.57)
10
5.54
5.98
(0.62)
10
40
5.84
(0.62)
50
5.85
60
Area,,
S.D.
n
6.09
(0.52)
5
10
5.24
(0.51)
5
(0.62)
10
5.22
(0.43)
5
5.50
(0.74)
10
5.37
(0.35)
5
9
5.67
(0.74)
10
5.29
(0.51)
5
(0.65)
9
5.73
(0.86)
10
5.41
(0.63)
5
5.76
(0.66)
9
5.87
(0.81)
10
5.96
(0.78)
5
7
5.79
(0.74)
9
5.79
(0.81)
7
5.77
(0.78)
5
(0.55)
7
6.06
(0.48)
8
5.91
(0.59)
7
6.04
(0.48)
5
6.02
(0.56)
4
6.01
(0.67)
6
6.12
(0.67)
4
6.06
(0.72)
4
63.65
(13.44)
10
59.77
(16.58)
9
65.57
(19.52)
10
58.77
(11.40)
5
Group A Site 85/84
Time
(min) Mean
S.D.
n
Mean
0
6.38
(0.68)
10
2
5.76
(0.54)
5
5.54
10
Group B*
Group A
Site 85/84
Site 74/75
S.D.
n
Mean
6.02
(0.30)
9
10
5.69
(0.57)
(0.39)
10
5.74
5.64
(0.56)
10
15
5.62
(0.72)
20
6.00
30 40
Group B* Site 74/75
S.D.
n
Mean
6.48
(0.71)
10
9
5.53
(0.45)
(0.53)
9
5.60
5.85
(0.65)
9
10
5.96
(0.44)
(0.53)
10
6.12
6.21
(0.49)
10
6.16
(0.55)
7
S.D.
n
6.22
(0.76)
7
10
6.21
(0.32)
7
(0.76)
10
6.00
(0.67)
7
5.94
(0.66)
10
6.16
(0.42)
7
9
6.17
(0.59)
10
5.97
(0.62)
7
(0.51)
9
6.30
(0.63)
10
6.42
(0.61)
7
6.12
(0.35)
9
6.35
(0.64)
10
6.39
(0.38)
7
6.25
(0.55)
9
6.31
(0.57)
7
6.49
(0.28)
7
8 6.33 7 6.74 6 (0.59) (0.45) (0.35) 4 60 5.64 4 6.06 4 6.52 6.43 5 (0.38) (0.66) (0.52) (0.39) 70.26 (13.21) 10 73.82 (11.44) 9 81.51 (11.26) 7 77.21 (15.47) 10 Area30 * The full complement of these sites was not always available, since such sites with caries lesions were excluded. "n" denotes the number of each type of site measured at each time point. Area30 indicates the area under the pH curve, from time 0 to time 30. Group A, caries-inactive; Group B, caries-active. 50
6.09
(0.64)
7
6.17
obviously different, which most likely reflects the very different microbial compositions on the two sites (Carlsson, 1967), resulting in different diffusion properties (Dibdin and Shellis, 1988). Of particular importance, however, is that microbial deposits on the tongue respond to a sucrose rinse with a plaque pH drop of 1.5 units and demonstrate a "recovery profile" similar to that of the caries cavity plaque. Both sites, we suggest, have equal access to saliva
and a low salivary film velocity (Dawes, 1989). However, the tongue plaque differs from microbial deposits on an intact tooth surface in that it lacks an underlying mineral phase. Since the pH measured in caries cavity plaque does not reflect the pH deep within the front of demineralization in the dentin, the "caries plaque" should also be considered as lacking an underlying mineral phase. The very slow elimination of acids from plaque covering both the tongue and the
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30
J Dent Res
FEJERSKOV et al.
January 1992
TABLE 1B
MEAN pH (± S.D.) IN SOUND SITES MEASURED IN 19 14-YEAR-OLD CHILDREN FOLLOWING A SUCROSE RINSE Group B* Group A Group B* Group A Time Site 23/24 Site 23/24 Site 14/15 Site 14/15 (min) Mean
S.D.
n
Mean
S.D.
n
Mean
S.D.
n
Mean
S.D.
n
0
5.99
(0.41)
10
5.76
(0.57)
8
6.13
(0.62)
10
6.20
(0.68)
9
2
5.20
(0.57)
10
5.24
(0.45)
8
4.91
(0.49)
10
5.21
(0.55)
9
5
5.05
(0.58)
10
5.20
(0.41)
8
5.04
(0.72)
10
5.13
(0.75)
9
10
5.05
(0.44)
10
5.17
(0.67)
8
5.01
(0.60)
10
4.96
(0.75)
9
15
5.41
(0.50)
10
5.44
(0.73)
8
5.19
(0.74)
10
5.40
(0.64)
9
20
5.53
(0.40)
10
5.42
(0.63)
8
5.29
(0.54)
10
5.51
(0.60)
9
30
5.52
(0.41)
10
5.75
(0.61)
8
5.60
(0.56)
10
5.78
(0.74)
9
40
5.73
(0.37)
10
5.64
(0.72)
6
5.74
(0.72)
10
6.07
(0.72)
7
50
5.79
7
5.90
(0.55)
4
5.70
(0.43)
7
6.27
(0.46)
4
60
5.68
(0.15) (0.57)
3
6.73
-
1
5.77
(0.52)
3
6.25
(0.33)
2
55.55
(8.82)
10
57.07
(13.40)
8
52.24
(13.81)
10
56.83
(17.74)
9
Area,
Group B* Site 45/46
Group A Site 45/46
Time
(min) Mean
S.D.
n
Mean
S.D.
n
Mean
Group A
Group B*
Site 35/36
Site 35/36
S.D.
n
Mean
S.D.
n
0
6.13
(0.67)
10
6.10
(0.71)
6
7.00
(0.58)
2
6.47
(0.18)
7
2
5.54
(0.59)
10
5.78
(0.56)
6
6.44
(0.39)
2
5.99
(0.45)
7
5
5.37
(0.47)
10
5.70
(0.79)
6
6.34
(0.61)
2
5.88
(0.70)
7
10
5.66
(0.70)
10
5.45
(0.55)
6
7.02
(0.39)
2
6.03
(0.39)
7
15
5.70
(0.61)
10
5.76
(0.59)
6
6.84
(0.01)
2
6.19
(0.27)
7
20
5.81
(0.51)
10
5.87
(0.56)
6
6.71
(0.50)
2
6.28
(0.51)
7
30
6.06
10
6.21
(0.69)
6
6.62
(0.34)
2
6.38
(0.18)
7
40
6.15
(0.43) (0.52)
10
6.26
(0.35)
4
6.59
(0.27)
2
6.70
(0.19)
5
50
6.36
(0.25)
7
6.35
(0.20)
3
6.71
(0.63)
2
6.55
(0.24)
3
60
6.24
(0.14)
3
6.45
6.83
(0.16)
2
-
1
Area30
2 96.12 (7.48) 67.17 (12.73) 10 69.46 (16.28) 6 80.11 7 (9.71) The full complement of these sites was not always available, since such sites with caries lesions were excluded. "n" denotes the number of each type of site that was measured at each time point. Area30 indicates the area under the pH curve, from time 0 to time 30. Group A, caries-inactive; Group B, caries-active. *
softened caries lesion, we therefore suggest, is a result of the effect of unstimulated saliva of low velocity combined with the buffers of the microbial deposits. The much more rapid return to resting pH values on non-carious tooth sites after a sucrose rinse may be due to the buffering effect of the underlying apatite. This hypothesis should also be tested by comparison of the acid profiles in the different plaques and sites, as well as of the biochemical and
chemical conditions within the enamel as caries lesions develop. We have recently drawn attention to the erratic fluctuations of pH both in starved resting plaque and in plaque which has been challenged with a sucrose rinse (Scheie et al., 1992), a phenomenon also commented on by Newmanet al. (1979) and compensated for in telemetric studies (Imfeld, 1983). The present method requires that the electrode be re-positioned at exactly the same site. Although
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Vol. 71 No. 1
PLAQUE pHAND CARIES ACTIVITYIN CHILDREN
great effort was made to do so, it could be argued that some of the fluctuations observed in Fig. 2 represent the error of the method rather than a true biological variation. As stressed above, however, telemetry demonstrates fluctuations of similar magnitude within short time intervals. Moreover, although it is plausible that marked variations mayexistin the pH ofplaque measured at small distances apart, no such data have so far been published. It is common to think of the pH response in plaque following a sucrose rinse as a classic Stephan-type response. However, Stephan curves reflect an average response, but are more complex, as demonstrated in the present study. In spite ofthe apparent random fluctuations in pH at any given time, the Stephan response curves can nevertheless be elicited. It is noteworthy that, except for two min after a sucrose rinse, it is not possible at any given time to predict whether the subsequent measurement will show an increase or a drop in pH. The consequence of these observations for understanding the nature of caries lesion development should be explored further.
Acknowledgments. We thank M. Kj0lby and A. Kuseler for organizing the field arrangements and for their role as recorders in this study. Also, thanks to Drs. D. Birkhed and P. Lingstrom for valuable assistance. REFERENCES BIBBY, B.G. (1981): Foods and Dental Caries. In: Foods, Nutrition and Dental Health, J.J. Hefferren and H.M. Koehler, Eds., Park Forest South, IL: Pathotox Publishers Inc., pp. 257-278. CARLSSON, J. (1967): Presence of Various Types of Non-haemolytic Streptococci in Dental Plaque and in other Sites of the Oral Cavity in Man, Odontol Revy 18:55-74. CLEMENT, A.J.; PLOTKIN, R.; and FOSDICK, L.S. (1956): The Formation of Lactic Acid in Dental Plaques. II. Oral Conditions of Primitive Bushmen of the Western Kalahari Desert, JDent Res 35:786-791. DAWES, C. (1989): An Analysis of Factors Influencing Diffusion from Dental Plaque into a Moving Film of Saliva and the Implications for Caries, J Dent Res 68:1483-1488. DAWES, C.; WATANABE, S.; BIGLOW-LECOMTE, P.; and DIBDIN, G.H. (1989): Estimation ofthe Velocity ofthe Salivary Film at Some Different Locations in the Mouth, JDent Res 68:1479-1482. DIBDIN, G.H. (1984): A Brief Survey of Recent in vitro Work on Diffusion of Small Ions and Molecules in Dental Plaque. In: Cariology Today, B. Guggenheim, Ed., Basel: Karger, pp. 191-198. DIBDIN, G.H. and SHELLIS, R.P. (1988): Physical and Biochemical Studies of Streptococcus mutans Sediments Suggest New Factors Linking the Cariogenicity of Plaque with its Extracellular Polysaccharide Content,
JDent Res 67:890-895.
31
DIRKSEN, T.R.; LITTLE, M.F.; BIBBY, B.G.; and CRUMP, S.L. (1962): The pH of Carious Cavities. I. The Effect ofGlucose and Phosphate Buffer on Cavity pH, Arch Oral Biol 7:49-58. EDGAR, W.M. (1976): The Role of Saliva in the Control of pH Changes in Human Dental Plaque, Caries Res 10:241-254. ENGLANDER, H.R.; CARTER, W.J.; and FOSDICK, L.S. (1956): The Formation of Lactic Acid in Dental Plaques. III. Caries-immune Individuals, JDent Res 35:792-799. FEJERSKOV, O.; MELSEN, B.; and KARRING, T. (1973): Morphometric Analysis of Occlusal Fissures in Human Premolars, Scand J Dent Res 81:505-510. IMFELD, T.N. (1983): Identification ofLow Caries Risk Dietary Components. In: Monographs in Oral Science, H.M. Myers, Ed., Basel: Karger, pp. 1-198. KLEINBERG, I. and JENKINS, G.N. (1964): The pH of Dental Plaques in the Different Areas of the Mouth Before and After Meals and Their Relationship to the pH and Rate ofFlow ofResting Saliva,Arch OralBiol 9:493-516. KLEINBERG,I.;JENKINS,G.N.;CHATTERJEE,R.;andWIJEYEWEERA, L. (1982): The Antimony pH Electrode and Its Role in the Assessment and Interpretation of Dental Plaque pH, J Dent Res 61:1139-1147. MANJI, F.; FEJERSKOV, O.; and BAELUM, V. (1989): Pattern of Dental Caries in an Adult Rural Population, Caries Res 23:55-62. MOORE, B.W.; CARTER, W.J.; DUNN, J.K.; and FOSDICK, L.S. (1956): The Formation of Lactic Acid in Dental Plaques. I. Caries-active Individuals, J Dent Res 35:778-785. NEWMAN, P.; MacFADYEN, E.E.; GILLESPIE, F.C.; and STEPHEN, K.W. (1979): An In-dwelling Electrode for in-vivo Measurement of the pH of Dental Plaque in Man, Arch Oral Biol 24:501-507. RANKINE, C.A.N.; PRIHODA, T.J.; ETZEL, KR.; and LABADIE, D. (1989): Plaque Fluid pH, Calcium and Phosphorus Responses to Calcium Food Additives in a Chewable Candy, Arch Oral Biol 34:821-824. ROSEN, S. and WEISENSTEIN, P.R. (1965): The Effect of Sugar Solutions on pH of Dental Plaques from Caries-susceptible and Caries-free Individuals, J Dent Res 44:845-849. SCHEIE,A.Aa.; FEJERSKOV, O.; BIRKHED, D.; LINGSTROM, P.; MANJI, F.; and BAELUM, V. (1992): Use of a Palladium Microelectrode under Field Conditions for in vivo Assessment ofDental Plaque pH in Children, Carries Res (in press). STEPHAN, R.M. (1940): Changes in Hydrogen-ion Concentration on Tooth Surfaces and in Carious Lesions, JAm Dent Assoc 27:718-723. STEPHAN, R.M. (1944): Intra-oral Hydrogen-ion Concentration Associated with Dental Caries Activity, JDent Res 23:257-266. THOMSEN, J.; TAGESEN, J.; and FEJERSKOV, 0. (1988): Prevalence and Distribution of Fissure Caries in Clinically 'Sound" Premolars, Danish Dent J 92:1-6. TURTOLA, L.O. and LUOMA, H. (1972): Plaque pH in Caries-active and Inactive Subjects Modified by Sucrose and Fluoride, with and without Bicarbonate-phosphate, Scand J Dent Res 80:334-343.
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Introduction. Since the excellent studies of Stephan (1940, 1944), rather few studies have dealt with plaque pH variations at various sites in the oral cavity (Kleinberg and Jenkins, 1964), and attempts to associate plaque pH with the actual caries status of individuals and sites examined are few and inconclusive (Englander et al., 1956; Rosen and Weisenstein, 1965; Turtola and Luoma, 1972). However, the methods used in assessing plaque pH have differed, as have the operational definitions of dental caries and caries activity. Although there is a large body of literature on the different aspects of plaque acidogenesis, plaque pH alone has been questioned as a reliable measure of cariogenicity, and it has been suggested that there are theoretical grounds for questioningthe relative significance of plaque pH measurements as indicators of caries activity (Bibby, 1981). Nevertheless, it has been claimed that "measurements of pH have made it possible to examine dental plaque as a metabolic unit and to identify the Stephan pH response as an important indicator of caries activity" (Kleinberg et al., 1982). The purpose of this study was to test the hypothesis that the in Received for publication February 14, 1991 Accepted for publication August 20, 1991 The present study is part of The Primary Oral Health Care Project Kenya conducted in collaboration between the Kenya Medical Research Institute, Nairobi, and the WHO Collaborating Centre on Oral Health Care Planning and Research at the Royal Dental College, Aarhus, Denmark, financed by DANIDA.
situ pH responses ofdental plaque to a sucrose rinse in caries-active and -inactive children would be different.
Materials and methods. Study group.-All children aged six to seven and 13 to 15 years attending a primary school in a sublocation ofMeru district, Kenya, were screened for the presence or absence of frank caries cavities. All children presented with poor oral hygiene and had never had fillings or tooth extractions. From each age group, children were assigned to either a "cariesinactive" group, group A (no frank cavities), or a "caries-active" group, group B (at least two teeth with deep caries cavities reaching dentin). This selection procedure continued until there were 20 seven-year-olds and 20 14-year-olds, each age group consisting of ten "caries-active" and ten "caries-inactive" children. On the following days, all children selected (except one 14-yearold who did not attend) were subjected to measurements of plaque pH, followed by a detailed clinical caries examination based on the criteria previously described (Manji et al., 1989). The children had been asked not to eat or drink for three h prior to the examinations. Plaque pH was measured prior to (i.e., resting pH), and at two, five, ten, 15, 20, 30, 40, 50, and 60 min following a one-minute rinse with 10 mL of a 10% (w/w) sucrose solution. When the starting (presucrose) plaque pH value was reached, further measurements were stopped. Measurements were made in the following sites: In the seven-year-olds, plaque pH was measured in the interproximal sites between the deciduous molars in all four quadrants, provided that these sites were sound. In the 14-year-olds, plaque pH was measured at the interproximal space between the second premolar and first molar in both mandibular quadrants, at the interproximal space between the first and second premolar in the maxillary right quadrant, and between the canine and first premolar in the maxillary left quadrant, provided, again, that the sites were sound. In the caries-active groups, plaque pH was also measured in occlusal cavities where present, preferably in the mandible, where there is easy access. In the caries-inactive groups, comparable sound occlusal sites were used as controls. pH measurements.-Two examination teams with a complete pH measurement set-up performed the investigation. The pH measurements were performed with a palladium-touch microelectrode (diameter, 0.1 mm; Beetrode MEPH- 1, W-P Instruments, New Haven, CT) connected to a battery-run Orion SA 720 pH/ISE Meter (Orion Research, Inc., Cambridge, MA). A porous glass electrode (Beetrode MERE-1) was used as a reference electrode. A reference salt bridge was created by having the test subject dip one finger into a 3 mol/L KCl solution containing the reference electrode. Immediately prior to, and after, each examination period (one to two min), the electrodes were calibrated against standard pH buffers at pH 7 and 4. If calibration measurements showed a drift of the electrode exceeding 0.05 pH units in any of the two standard buffers, the readings in between were adjusted according to calibration curves. The pH-meter readings were noted by an independent assistant. The two examiners exchanged electrodes at various intervals during the examination period. For further details, see Scheie et al. (1992).
25 Downloaded from jdr.sagepub.com at Univ of Connecticut / Health Center / Library on May 21, 2015 For personal use only. No other uses without permission.
J Dent Res
FEJERSKOVet al.
26
7 YEAR OLDS
pH
January 1992
14 YEAR OLDS
pH 7-
7-
6.5 -
6.5
MAN DIB3.U LA'S
MANDIBULAR
6-
6-
5.5 -
5.5 -
.........L A
I...........
MAXI LLARY 5-
5-
4..o e
Ad
I
I 0
5
I
I
10 15 20 25 30 35 40 45 60
TIME
-
I
65
-
--
60
4.5
-
I
0
5 10 15 20 25 30 35 40 45 50 5 60
TIME - MINUTES
MINUTES
Fig. 1-The Stephan response curves obtained in sound approximal maxillary and mandibular sites of seven-year-olds and 14-year-olds following a sucrose rinse. Bars indicate standard errors.
In order for pH responses over time between groups to be compared, an area under the curve was calculated, as arbitrarily defined by: the curve connecting pH values obtained from time 0 to time 30, a horizontal line through pH 3.5, a vertical line through time 0 min, and a vertical line through time 30 min (Area30). Between-group differences were tested by a two-tailed Student t test.
Results. Tables 1A and 1B present the mean plaque pH values for each sound site at different times. After a sucrose rinse, the mean pH at each sound site dropped by about one pH unit, and, after 30 min, the mean pH values were approaching the starting values of time 0. In these sites, there were no differences between the inactive and active groups in pH response over time. In both age groups, there was a slight, but statistically non-significant, tendency for the caries-active children (group B) to have resting pH values lower than those of the caries-inactive children (group A). There were no statistically significant differencesbetween the caries activity groups in the values of Area30. In both age groups, the pH response was more pronounced in sound maxillary sites than in sound mandibular sites throughout the 60 min (Fig. 1). There was a remarkable similarity between the two age groups in the pH response in mandibular sites. In the maxilla, the pH drop was more pronounced for the 14-year-olds as compared with the younger group. Fig. 2 shows the frequency distribution of the pH changes in single sites at various time intervals during the first 20 min following the sucrose rinse for maxillary and mandibular sites separately. During the first two min, the distribution of pH changes was highly skewed, such that the probability ofa pH drop exceeding one pH unit was 0.42 in maxillary sites and 0.24 in mandibular sites (Fig. 2). Although most sites showed pH drops during the first two min, 11% of maxillary sites and 20% of mandibular sites showed
unchanged or even increased pH values. In the following time intervals, the distribution of the pH changes approached a symmetrical distribution, such that both pH drops and pH increases were likely to occur. Thus, at any time interval, except for two min after sucrose rinsing, pH fluctuated in either direction. Fig. 3 shows that the mean pH values at time 0 and throughout the 60 min following a sucrose rinse were lower in active occlusal caries lesions than in sound occlusal surfaces (Area30, p < 0.001). The response curves for the three occlusal cavities that were classified as "inactive" (dark brown but hard when probed) were rather similar to those of sound surfaces and very different from those of "active lesions" (with soft floors). The pH response of the microbial plaque located on the dorsum ofthe tongue is shown in Fig. 4. The initial drop from mean pH 7 to pH 5.5 occurred within the first two min, and the shape ofthe curve was very similar to that seen in active caries lesions (Fig. 3). Thus, mean pH on the tongue remained low for up to 20 min and was still about one pH unit lower than the resting value one h after the sucrose rinse.
Discussion. Our study showed that the "Stephan pH responses" of microbial deposits in "non-carious" interproximal sites in the posterior parts of the oral cavity of caries-active and -inactive children were indistinguishable. However, there were marked differences between the average pH responses of carious and sound sites following a sucrose rinse. The demonstrated lack ofdifference between plaque pH responses in caries-active and -inactive children apparently contrasts with some of the earlier literature. However, this probably reflects differences in the way plaque pH was measured and how cariesactive individuals were defined. In Stephan's extensive study(1944) of 65 individuals [most likely adults (Stephan, 1940)], five subjects
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Vol. 71 No. 1
..
PLAQUE pH AND CARIES ACTIVITYIN CHILDREN
OBSERVED PROBABILITY
0.46
27
OBSERVED PROBABILITY 0.46, 0.40-
MANDIBULAR SITES
. . . . . . . .I.
0.36-
0.30-
0.26
-
0.20-
0.16
0.10
0.06
=I II 11112-....
=
--ma
onn0 -M __-
0% 0%oh
1
.
.
.
.
.
.
.
.
.
1
98 7 6 6432 1 0 1 234667 89
CHANGE IN pH; pH UNITS
-
0.30 -
-
O.SO
0.260.20-
0.10
-
0.06 -
0.00O
0.36'
0.30 0.26 0.20 0.16 0.10
0.06 U.W0
.
.
.
.
.
.
.
.
.
.
.
1
.
987 66432 1 01 23466760 CHANGE IN pH; pH UNITS
+
..
... ...
0.26
.
0.20
. ............
-.-...............
.....................
......................
0.10 .....................
h.........................................
|'-M 'IN ||N 0
ML .'AN
0.06 0.06
-
s | r ~~~~~~~~~~~ ~~~~~~~~ . ........ . ........
'i . .s .
.
.
.
.
.
.
.
0 8 7 6 6 4 32101 2 3 4 66 7 i 09
-
0.40
.
.......................
0.16
I
in AS
.
0.40 . .................
0.36-
0.16
.
.
.
OBSERVED PROBABILITY
0.4
0.40-
.
-
OBSERVED PROBABILITY
0.45
0.30
4.
.
CHANGE IN pH; pH UNITS
I
..
+
3BSERVED PROBABILITY
.
.
.
.
.
.
.
087664321
I. 2346670
CANGE IN p pH1 UNITS
-
0.46
601
+
OBSERVED PROBABILITY
Ia] * -o min
0.40-
0.36-
..
.....................................
0.30- .............. ...
....
0.26-
0.20-
......l[
0.10-
nn~~~~~ Unnnnn .II
.
.
.
. -
.
.
.
96766432 i
I
"I
I.
II
,"
*
6i0 2346676
CHANGE IN pH; pH UNITS
...... . . . . . . . . . . . . . . . . . . . . . . . . ....................
0.16-
...H.. _ .'
1
........................................................
.
0.06 -
n i l -,-l~l~lAl ..f i,. i.R0 ..
1
I. .
IIIY
0.00 I-
I
1 ..
.
.
.
.
.
iI
.
nn inn i I
.
8766432 16 1 23466760
+-
CHANGE IN PK pH UNITS
1
+
Fig. 2-The relative frequency distribution of changes in pH at sound maxillary and mandibular sites during the time intervals 0 to two min, two to five min, and 15 to 20 min, respectively. pH changes have been calculated as pH(t+l) - pH(t). Numbers on x-axes denote midpoints of pH intervals. Negative sign indicates pH drop from one measurement to the next. Downloaded from jdr.sagepub.com at Univ of Connecticut / Health Center / Library on May 21, 2015 For personal use only. No other uses without permission.
J Dent Res
FEJERSKOV et al.
28
January 1992
pH 7
6.5
6.5 6
6 5.5
5.5 _ 5
5_ 4.5
0
5
10 15 20 26 30 35 40 45 50
55
60
TIME (MINUTES) Fig. 3-The Stephan response curves obtained from sound occlusal surfaces, inactive occlusal caries lesions, and deep, active occlusal caries lesions following a sucrose rinse. Bars indicate standard errors.
4.5
were caries-free (group I), and 11 subjects had caries but showed no new lesions or enlargement of established ones over a two-year period (group II). In group III (26 individuals), there was a definite increase in the size of one or more lesions, and/or the development of small new cavities. Fifteen subjects exhibited rapid caries development and progression (group IV), and the remaining eight subjects had extensive caries, with active caries lesions on labial surfaces of the anterior teeth (group V). Although Stephan found an association between increased caries activity and a more acidic plaque response, resting pH values were similar in all groupsexcept in the extreme caries group (V). In the latter, pH measurements were most likely performed in plaque covering caries lesions (Stephan, 1944), and the pH response curves were remarkably similar to those observed for caries lesions in this study. Our caries-active group corresponded to groups II and III of the Stephan study (1944), and when account is taken of the variance about the means in both data sets, it may be seen that the plaque pH trends were rather similar. The different plaque pH responses claimed to exist between caries-free individuals and caries-active subjects (Englander et al., 1956; Moore et al., 1956; Clement et al., 1956; Turtola and Luoma, 1972; Kleinberg et al., 1982) may well be the result of the pooling of plaque samples from all sites before extra-oral pH measurement. When plaque is pooled, the pH measurements in caries-active subjects are therefore likely to include measurements of plaque from a varying number of caries lesions. The data recently published by Rankine et al. (1989) support this interpretation. Rankine et al. (1989) compared pH changes in plaque fluid aftervarious challenges, including sucrose, and found no differences between children with low caries activity and children with a six-month incidence of four or more new caries lesions-when all lesions had been restored before the study. It is of particular interest for the results of the study by Dirksen et al. (1962) to be compared with our data, even taking into account the differences in techniques used for pH measurements. The pH changes over time in our few inactive caries lesions were similar to
Fig. 4-The pH curve from the dorsum ofthe tongue after a sucrose rinse. Bars indicate standard errors.
I
0
5 10 15 20 25 30 35 40 45 50 55 60
TIME (MINUTES)
those which Dirksen et al. (1962) obtained from 34 cavities with "wide clinical openings and a thin layer of pigmented decayed dentine often hard and polished". The present study showed that the occlusal plaque in lower molars exhibited a fermentative response to a sucrose rinse similar to that obtained in the interdental molar/premolar spaces in the mandible (Figs. 3 and 4). The size of the microelectrode was such that it allowed pH measurements to be made even at the entrances to deep fissures (Fejerskov et al., 1973). This is important, since the majority of the early caries lesions developing in occlusal fissures are located immediately deep to the fissure entrance and along the lateral walls of the fissure (Thomsen et al., 1988). The within-mouth variation, with the maxillary sites showing a lower pH level and a slowerreturn to restingvalues thanmandibular sites, is in accordance with Stephan's original findings (1944) from incisor regions, and with the very detailed 'plaque pH-mapping" in adults, as performed by Kleinberg and Jenkins (1964). The possible physiological explanation for this is that, in a non-chewing and nontalking subject, the velocity of the 0.1-mm-thick salivary film is up to about 10 x less in the maxilla as compared with the mandible (Dawes et al., 1989). As suggested by these authors, the slow movement of the salivary film of unstimulated saliva allows for accumulation of diffusants from dental plaque which may prolong the clearance time of metabolic products such as acids. The possible relative importance of saliva in both buffering and removing plaque acids has been extensively considered (Edgar, 1976; Dawes, 1989), as have the related complex problems of diffusion properties of dental plaque (Dibdin, 1984; Dibdin and Shellis, 1988). It is tempting to compare our caries cavity plaque pH behavior with that observed on the dorsum ofthe tongue. The levels of resting pH and minimum pH reached after a sucrose rinse were
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Vol. 71 No. 1
PLAQUE pH AND CARIES ACTIVITYIN CHILDREN
29
TABLE 1A
MEAN pH (± S.D.) IN SOUND SITES MEASURED IN 20 SEVEN-YEAR-OLD CHILDREN FOLLOWING A SUCROSE RINSE Time
Group A
Group B*
Group A
Group B*
(min)
Site 55/54
Site 55/54
Site 64/65
Site 64/65
Mean
S.D.
n
Mean
0
6.25
(0.79)
10
2
5.37
(0.34)
5
5.38
10
S.D.
n
Mean
5.60
(0.75)
9
10
5.44
(0.69)
(0.35)
10
5.53
5.36
(0.52)
10
15
5.63
(0.56)
20
5.69
30
S.D.
n
Mean
6.38
(0.70)
10
9
5.44
(0.53)
(0.76)
9
5.60
5.24
(0.67)
9
10
5.38
(0.78)
(0.57)
10
5.54
5.98
(0.62)
10
40
5.84
(0.62)
50
5.85
60
Area,,
S.D.
n
6.09
(0.52)
5
10
5.24
(0.51)
5
(0.62)
10
5.22
(0.43)
5
5.50
(0.74)
10
5.37
(0.35)
5
9
5.67
(0.74)
10
5.29
(0.51)
5
(0.65)
9
5.73
(0.86)
10
5.41
(0.63)
5
5.76
(0.66)
9
5.87
(0.81)
10
5.96
(0.78)
5
7
5.79
(0.74)
9
5.79
(0.81)
7
5.77
(0.78)
5
(0.55)
7
6.06
(0.48)
8
5.91
(0.59)
7
6.04
(0.48)
5
6.02
(0.56)
4
6.01
(0.67)
6
6.12
(0.67)
4
6.06
(0.72)
4
63.65
(13.44)
10
59.77
(16.58)
9
65.57
(19.52)
10
58.77
(11.40)
5
Group A Site 85/84
Time
(min) Mean
S.D.
n
Mean
0
6.38
(0.68)
10
2
5.76
(0.54)
5
5.54
10
Group B*
Group A
Site 85/84
Site 74/75
S.D.
n
Mean
6.02
(0.30)
9
10
5.69
(0.57)
(0.39)
10
5.74
5.64
(0.56)
10
15
5.62
(0.72)
20
6.00
30 40
Group B* Site 74/75
S.D.
n
Mean
6.48
(0.71)
10
9
5.53
(0.45)
(0.53)
9
5.60
5.85
(0.65)
9
10
5.96
(0.44)
(0.53)
10
6.12
6.21
(0.49)
10
6.16
(0.55)
7
S.D.
n
6.22
(0.76)
7
10
6.21
(0.32)
7
(0.76)
10
6.00
(0.67)
7
5.94
(0.66)
10
6.16
(0.42)
7
9
6.17
(0.59)
10
5.97
(0.62)
7
(0.51)
9
6.30
(0.63)
10
6.42
(0.61)
7
6.12
(0.35)
9
6.35
(0.64)
10
6.39
(0.38)
7
6.25
(0.55)
9
6.31
(0.57)
7
6.49
(0.28)
7
8 6.33 7 6.74 6 (0.59) (0.45) (0.35) 4 60 5.64 4 6.06 4 6.52 6.43 5 (0.38) (0.66) (0.52) (0.39) 70.26 (13.21) 10 73.82 (11.44) 9 81.51 (11.26) 7 77.21 (15.47) 10 Area30 * The full complement of these sites was not always available, since such sites with caries lesions were excluded. "n" denotes the number of each type of site measured at each time point. Area30 indicates the area under the pH curve, from time 0 to time 30. Group A, caries-inactive; Group B, caries-active. 50
6.09
(0.64)
7
6.17
obviously different, which most likely reflects the very different microbial compositions on the two sites (Carlsson, 1967), resulting in different diffusion properties (Dibdin and Shellis, 1988). Of particular importance, however, is that microbial deposits on the tongue respond to a sucrose rinse with a plaque pH drop of 1.5 units and demonstrate a "recovery profile" similar to that of the caries cavity plaque. Both sites, we suggest, have equal access to saliva
and a low salivary film velocity (Dawes, 1989). However, the tongue plaque differs from microbial deposits on an intact tooth surface in that it lacks an underlying mineral phase. Since the pH measured in caries cavity plaque does not reflect the pH deep within the front of demineralization in the dentin, the "caries plaque" should also be considered as lacking an underlying mineral phase. The very slow elimination of acids from plaque covering both the tongue and the
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30
J Dent Res
FEJERSKOV et al.
January 1992
TABLE 1B
MEAN pH (± S.D.) IN SOUND SITES MEASURED IN 19 14-YEAR-OLD CHILDREN FOLLOWING A SUCROSE RINSE Group B* Group A Group B* Group A Time Site 23/24 Site 23/24 Site 14/15 Site 14/15 (min) Mean
S.D.
n
Mean
S.D.
n
Mean
S.D.
n
Mean
S.D.
n
0
5.99
(0.41)
10
5.76
(0.57)
8
6.13
(0.62)
10
6.20
(0.68)
9
2
5.20
(0.57)
10
5.24
(0.45)
8
4.91
(0.49)
10
5.21
(0.55)
9
5
5.05
(0.58)
10
5.20
(0.41)
8
5.04
(0.72)
10
5.13
(0.75)
9
10
5.05
(0.44)
10
5.17
(0.67)
8
5.01
(0.60)
10
4.96
(0.75)
9
15
5.41
(0.50)
10
5.44
(0.73)
8
5.19
(0.74)
10
5.40
(0.64)
9
20
5.53
(0.40)
10
5.42
(0.63)
8
5.29
(0.54)
10
5.51
(0.60)
9
30
5.52
(0.41)
10
5.75
(0.61)
8
5.60
(0.56)
10
5.78
(0.74)
9
40
5.73
(0.37)
10
5.64
(0.72)
6
5.74
(0.72)
10
6.07
(0.72)
7
50
5.79
7
5.90
(0.55)
4
5.70
(0.43)
7
6.27
(0.46)
4
60
5.68
(0.15) (0.57)
3
6.73
-
1
5.77
(0.52)
3
6.25
(0.33)
2
55.55
(8.82)
10
57.07
(13.40)
8
52.24
(13.81)
10
56.83
(17.74)
9
Area,
Group B* Site 45/46
Group A Site 45/46
Time
(min) Mean
S.D.
n
Mean
S.D.
n
Mean
Group A
Group B*
Site 35/36
Site 35/36
S.D.
n
Mean
S.D.
n
0
6.13
(0.67)
10
6.10
(0.71)
6
7.00
(0.58)
2
6.47
(0.18)
7
2
5.54
(0.59)
10
5.78
(0.56)
6
6.44
(0.39)
2
5.99
(0.45)
7
5
5.37
(0.47)
10
5.70
(0.79)
6
6.34
(0.61)
2
5.88
(0.70)
7
10
5.66
(0.70)
10
5.45
(0.55)
6
7.02
(0.39)
2
6.03
(0.39)
7
15
5.70
(0.61)
10
5.76
(0.59)
6
6.84
(0.01)
2
6.19
(0.27)
7
20
5.81
(0.51)
10
5.87
(0.56)
6
6.71
(0.50)
2
6.28
(0.51)
7
30
6.06
10
6.21
(0.69)
6
6.62
(0.34)
2
6.38
(0.18)
7
40
6.15
(0.43) (0.52)
10
6.26
(0.35)
4
6.59
(0.27)
2
6.70
(0.19)
5
50
6.36
(0.25)
7
6.35
(0.20)
3
6.71
(0.63)
2
6.55
(0.24)
3
60
6.24
(0.14)
3
6.45
6.83
(0.16)
2
-
1
Area30
2 96.12 (7.48) 67.17 (12.73) 10 69.46 (16.28) 6 80.11 7 (9.71) The full complement of these sites was not always available, since such sites with caries lesions were excluded. "n" denotes the number of each type of site that was measured at each time point. Area30 indicates the area under the pH curve, from time 0 to time 30. Group A, caries-inactive; Group B, caries-active. *
softened caries lesion, we therefore suggest, is a result of the effect of unstimulated saliva of low velocity combined with the buffers of the microbial deposits. The much more rapid return to resting pH values on non-carious tooth sites after a sucrose rinse may be due to the buffering effect of the underlying apatite. This hypothesis should also be tested by comparison of the acid profiles in the different plaques and sites, as well as of the biochemical and
chemical conditions within the enamel as caries lesions develop. We have recently drawn attention to the erratic fluctuations of pH both in starved resting plaque and in plaque which has been challenged with a sucrose rinse (Scheie et al., 1992), a phenomenon also commented on by Newmanet al. (1979) and compensated for in telemetric studies (Imfeld, 1983). The present method requires that the electrode be re-positioned at exactly the same site. Although
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Vol. 71 No. 1
PLAQUE pHAND CARIES ACTIVITYIN CHILDREN
great effort was made to do so, it could be argued that some of the fluctuations observed in Fig. 2 represent the error of the method rather than a true biological variation. As stressed above, however, telemetry demonstrates fluctuations of similar magnitude within short time intervals. Moreover, although it is plausible that marked variations mayexistin the pH ofplaque measured at small distances apart, no such data have so far been published. It is common to think of the pH response in plaque following a sucrose rinse as a classic Stephan-type response. However, Stephan curves reflect an average response, but are more complex, as demonstrated in the present study. In spite ofthe apparent random fluctuations in pH at any given time, the Stephan response curves can nevertheless be elicited. It is noteworthy that, except for two min after a sucrose rinse, it is not possible at any given time to predict whether the subsequent measurement will show an increase or a drop in pH. The consequence of these observations for understanding the nature of caries lesion development should be explored further.
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