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Journal

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Dentistry
Journal of Dentistry 28 (2000) 265270
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Relative susceptibility of deciduous and permanent dental hard tissues to


erosion by a low pH fruit drink in vitro
M.L. Hunter a,*, N.X. West b, J.A. Hughes b, R.G. Newcombe c, M Addy b
a

Dental Health and Development, University of Wales College of Medicine Dental School, Heath Park, Cardiff CF14 4XN, UK
b
Restorative Dentistry, University of Bristol Dental School, Lower Maudlin Street, Bristol BS1 2LY, UK
c
Medical Computing and Statistics, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, UK
Received 26 April 1999; received in revised form 1 October 1999; accepted 23 November 1999

Abstract
Objectives: The objectives of this study were two-fold: (1) to determine (by surfometry) loss of deciduous and permanent enamel and
dentine following 15 days exposure to a single low pH orange drink; and (2) to determine (by surfometry) loss of deciduous and permanent
enamel and dentine following exposure to the product 2 versus 4 times per day for 15 days.
Methods: This in vitro study employed the validated methodology described by West and co-workers [Journal of Dentistry, 1998;26:329
335.]
Results: In all four tissues, erosion was progressive over time, though this pattern was more linear in enamel than in dentine. In general,
erosion of enamel was greater in the deciduous tissue, while erosion of dentine was greater in the permanent tissue. However, these
differences were rarely of statistical significance. Increasing frequency of exposure resulted in a non-proportional increase in tissue loss.
Conclusions: Differences in susceptibility of deciduous and permanent tissues to erosion by a low pH drink in vitro appear to exist, though
these may not be of statistical significance. Care may be indicated in the delivery of dietary advice, since reduced frequency of exposure to a
low pH drink does not appear to result in a proportional reduction in tissue loss. q 2000 Elsevier Science Ltd. All rights reserved.
Keywords: Erosion; Enamel; Dentine

1. Introduction
In recent years, the dental profession has noted an
increase in the number of children and adolescents presenting with localised loss of anterior tooth tissue to which an
erosive aetiology has been ascribed [2,3]. A number of
epidemiological studies published during the last 5 years
have examined the prevalence of erosion in these younger
age groups [49], but it is perhaps in those focusing on preschool and younger school-age children [4,68] that the
most disturbing statistics lie.
The early supervention of sensitivity, or even frank exposure, in the deciduous dentition has usually been attributed
to the reduced amount of tooth tissue present [10], though
this may be an over-simplification. While the enamel and
dentine layers of the primary dentition are certainly known
to be much thinner than those of its permanent successor
* Corressponding author. Tel. 144-2920-742458; fax: 144-2920742421.
E-mail address: hunterml@cf.ac.uk (M.L. Hunter BDS, MScD, FDS
(Paed) RCS (Edinburgh)).

[11,12], other differences between deciduous and permanent


tissues may also be of importance. For example, deciduous
teeth demonstrate a higher degree of enamel porosity [13]
and a lower degree of mineralisation [1416] than permanent teeth. In addition, deciduous enamel has repeatedly
been noted to have a higher content of carbon dioxide and
carbonate, as well as a lower content of phosphorous than
the permanent tissue [14,1721].
Featherstone and Melberg [22] and Tyler and co-workers
[23] have demonstrated that deciduous teeth are more
susceptible to caries-like acid attack than permanent teeth
in vitro. Lending support to this observation, Shellis [24]
found that, on average, artificial caries-like lesions in deciduous teeth were 75% deeper than in permanent tissue. It is
therefore logical to question whether the susceptibility of
deciduous and permanent tissues to erosion, for example by
low pH drinks, is also inherently different. If this were to be
so, care would be indicated in the extrapolation to the
deciduous dentition of data derived from experiments
using specimens derived from permanent teeth.
No published study has specifically examined the relative
susceptibility of deciduous and permanent hard tissues to

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M.L. Hunter et al. / Journal of Dentistry 28 (2000) 265270

erosion by low pH drinks, though Johansson and co-workers


[25] have recently investigated the susceptibility of deciduous and permanent enamel to erosion by 2% citric acid. In
this latter study, the microhardness of the two tissues was
shown to be statistically significantly different both before
and after exposure. The authors concluded that deciduous
enamel seemed to be more susceptible to dental erosion than
its permanent analogue.
The primary aim of this study was therefore to examine
the existence of a difference in susceptibility of deciduous
and permanent enamel and dentine to erosion by a single
low pH drink. The primary objective was to determine the
amount of deciduous and permanent enamel and dentine lost
by erosion following 15 days exposure to an orange drink
(Asda Farm Stores No Added Sugar Orange Squash. Asda
Stores Limited, Leeds, UK) in vitro. Determination of tissue
loss at 5 and 10 days was considered to be a secondary
objective.
As with caries, frequency, rather than total consumption,
of low pH drinks is thought to be critical to the erosive
process. However, until now, there has been a dearth of
evidence to support this assumption [26]. Therefore, as a
secondary aim, this study also sought to determine the role
of frequency in the erosion of deciduous and permanent
enamel and dentine. This was accomplished by comparing
the amount of tissue loss resulting from two versus four
exposures per day.

2. Methods
Specimens of permanent enamel and dentine were
derived from recently extracted, caries free, unerupted
third permanent molars. These were collected from patients
aged between 18 and 30 years of either gender. Specimens
of deciduous enamel and dentine were derived from recently
extracted, caries free, deciduous canines. These were
collected from children of either gender who were undergoing their extraction for the relief of crowding. At the time
of extraction, donors were resident in areas where the water
supplies contained less than 0.3 ppm fluoride. However,
details of previous residence were not available and it is
also likely that fluoride-containing toothpaste were being
used.
Following extraction, each tooth was soaked for at least
24 h in 50% sodium hypochlorite before being scraped of
any remaining tissue with a scalpel. It was then rinsed in
copious amounts of distilled water. Finally, the crown was
sectioned from the root and both portions cut vertically to
produce approximately equal sections of enamel and
dentine, respectively. In the case of the third permanent
molars, four or six equal sections were cut from the crown
of each tooth, depending on its size. However, due to differences in both size and morphology, it was only possible to
cut two sections from the crown of each deciduous canine.
Each section was embedded in a vacuum-formed poly-

urethane mould filled with epoxy resin. Twenty-four hours


later, when the epoxy resin had cured, the specimen was
removed and, using an automatic lapping and polishing
unit (Kermet International, Maidstone, UK), ground to fit
a stainless steel jig. This had been specifically constructed to
hold the specimen precisely during surfometry and ensure
that a stable horizontal platform was maintained. Using
abrasive discs of decreasing coarseness (Kermet International Ltd., Maidstone, UK), a smooth, flat area of buccal
or lingual/palatal enamel or dentine (as required) was
exposed, care being taken to remove the minimum amount
of tissue. This process was monitored by surfometry,
employing an SF200 surfometer (Planer Products Ltd.,
Sunbury-on-Thames, UK). Each specimen was only
accepted for use when two consecutive readings across the
exposed area fell within the range 20.3 to 10.3 mm. Thirtytwo specimens of each tissue were prepared in this way.
Following acceptance, each specimen was given a unique
reference number which was recorded on its reverse side in
indelible ink. It was then stored in isotonic saline at room
temperature in an eppendorf tube marked with the same
reference number, and its two baseline surfometry measurements recorded for future reference. Immediately before
use, an area of enamel or dentine was delineated by placing
PVC insulating tape (RF Components Ltd., Corby, UK)
over the specimen, leaving a 2 mm wide zone of hard tissue
exposed.
On each of 15 consecutive working days, the sugar free
concentrate was diluted 1:4 with bottled mineral water
(Volvic, Premier Waters Ltd, London, UK). Prior to each
exposure, at least 1 l of the prepared drink was warmed to
378C in a water bath. Specimens of deciduous and permanent enamel and dentine were placed in large glass beakers.
The four tissues were segregated, the beakers being clearly
marked with the nature of the tissue which they contained.
Two hundred millilitres of the prepared, previously warmed
drink were added to the specimens, and the beakers placed
in a water bath at 378C. The mixture was then stirred with an
overhead paddle stirrer for 10 min, a stopwatch being used
for monitoring. Following each exposure, the specimens
were removed from the drink, rinsed in a total of 1 l of
distilled water, and finally stored in isotonic saline at
room temperature. The used drink was discarded. Following the first exposure, the treated area was marked using
indelible ink. This aided the repositioning of the tapes
following measurement of tissue loss.
Sixteen specimens of each tissue were exposed to the
drink at 0900 and 1100 h. The remaining sixteen specimens
of each tissue were exposed to the drink at 0900, 1100, 1300
and 1500 h. Overnight, and at weekends, the specimens
were stored in isotonic saline at room temperature. This
was contained in sealed beakers clearly marked with the
nature of the tissue therein.
At completion of days 5, 10 and 15, the PVC tape was
removed from each specimen and tissue loss determined by
surfometry as described by West and co-workers [1]. Two

M.L. Hunter et al. / Journal of Dentistry 28 (2000) 265270

267

Table 1
Progression of erosion (in mm) over time by frequency of exposure
Tissue

Exposures/day

Day 5 Mean (SD)

Day 10 Mean (SD)

Day 15 Mean (SD)

Deciduous enamel

2
4
2
4
2
4
2
4

212.35 (5.82)
218.90 (7.40)
210.84 (3.80)
214.71 (5.79)
212.23 (2.20)
219.00 (4.27)
212.07 (3.94)
219.44 (3.32)

221.29 (7.26)
239.80 (12.30)
217.99 (4.32)
234.14 (5.93)
217.45 (5.04)
223.43 (6.65)
217.20 (5.38)
228.94 (8.88)

231.70 (10.30)
254.50 (11.70)
227.58 (5.99)
256.15 (7.35)
216.83 (3.30)
224.76 (7.85)
220.04 (3.64)
229.48 (7.04)

Permanent enamel
Deciduous dentine
Permanent dentine

surface profiles were taken from each specimen. Each


profile was taken from just within the taped zone on one
side, across the exposed area and just into the opposite taped
zone. This enabled the instrument to calculate the average
gain (1) or loss (2) of the exposed area compared to two
chosen fixed points in the previously taped zones, i.e. corresponding to the original baseline height. Following
measurement on days 5 and 10, the area to be exposed
was once more delineated with PVC tape.
It was possible to evaluate differences between deciduous
and permanent teeth and the effect of frequency of exposure.
Enamel and dentine were considered separately. The
primary outcome measure was mean tissue loss on each
measurement day. This was calculated by taking the mean
of the two replicate readings on days 5, 10 and 15 and
subtracting the mean of the two replicate readings at baseline. Unpaired t tests were employed to examine differences
between erosion in deciduous and permanent tissues and
between the two frequencies of exposure.

3. Results
Two specimens each of deciduous enamel, deciduous
dentine and permanent dentine were not measured at day
15. In the case of the deciduous enamel specimens, it was
evident that erosion had progressed into dentine, while in
that of the dentine specimens, it was considered that the
PVC tapes had moved, thereby significantly altering the
area to be measured. There were no other missing data.
Means for erosion at days 5, 10 and 15 are presented in
Table 1. This illustrates progression of erosion over time for
all four tissues and for both exposure frequencies. In
general, erosion in all four tissues was progressive over
Table 2
Statistical significance of differences between erosion of specimens
subjected to two versus four exposures per day
Tissue

Day 5 P value

Day 10 P value

Day 15 P value

Deciduous enamel
Permanent enamel
Deciduous dentine
Permanent dentine

0.0096
0.035
0.0000
0.0000

0.0000
0.0000
0.0079
0.0001

0.0000
0.0000
0.0029
0.0002

time, though this pattern was more linear in enamel than


in dentine. In deciduous dentine, at least 70% of the total
erosion had occurred by day 5; in permanent dentine, at least
60% of the total erosion had occurred by the same time
point. It is apparent, though not tested formally, that, at
day 15, in vitro erosion was much more severe in enamel
than in dentine. Generally, deciduous enamel was seen to
erode more severely than permanent enamel, whereas deciduous dentine showed less erosion than permanent dentine.
The statistical significance of these differences was determined using unpaired t tests. Differences between deciduous
and permanent enamel did not reach conventional levels of
statistical significance. Differences between deciduous and
permanent dentine were statistically significant only at day
15 and at the lower exposure frequency p 0:016:
Tissue loss was consistently greater in specimens exposed
four times daily than in those exposed twice daily. The
difference between the two regimes was always statistically
significant, often highly so (Table 2). However, it should be
noted that in only one case (day 15 for permanent enamel)
did doubling the frequency of exposure actually result in
doubling the amount of erosion recorded. Further, no
consistent ratio for the degree of erosion produced by 4
versus 2 exposures per day emerged.
4. Discussion
From the results of Johansson and co-workers [25] one
might logically have expected the degree of erosion seen in
deciduous enamel to be greater than that in permanent
enamel. However, although deciduous enamel was generally seen to erode more severely than permanent enamel,
while deciduous dentine showed less erosion than permanent dentine, only one contrast in each case reached a conventional level of statistical significance. The whole pattern
could therefore simply be regarded as a chance finding.
Despite the absence of statistical significance, one inevitably starts looking for explanations for these observations.
With regard to deciduous and permanent enamel, the most
obvious assumption is that differences in the rate of erosion
arise from the differences in structure which are known to
exist between the two tissues. Unfortunately, structural
differences between deciduous and permanent dentine do

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M.L. Hunter et al. / Journal of Dentistry 28 (2000) 265270

not appear to have been investigated previously. This is


clearly an area which may repay attention.
Though already noted, it should be reiterated here that
deciduous enamel exhibits a higher degree of enamel porosity [13]. Shellis [24] postulated that this difference might
arise from variations in the relative volume contributions of
(a) the prism junctions and (b) the interprismatic enamel. In
his study, he showed that the interprismatic fraction and the
prism-junction density were indeed significantly greater in
deciduous enamel than its permanent analogue p , 0:001:
These results supported, and provided a structural basis for,
the hypothesis that differences in caries lesion formation
between deciduous and permanent teeth can be accounted
for in terms of enamel porosity [27]. We would venture to
suggest that differences in porosity might also contribute, at
least in part, to the observed variation in rate of erosive
lesion formation.
The process of diffusion plays a central role in the
progression of erosion. Of likely importance in explaining
the results of the studies reported here, Linden and co-workers [28] have produced data suggesting that the apparent
diffusion coefficient (Da) is greater for deciduous enamel
than for the permanent tissue, an observation consistent
with the relative mineral contents [16].
An index, determined by magnetic spin resonance and
related to the degree of dispersion of crystal orientation
within the enamel, has also been found to be greater in
deciduous than in permanent enamel [29,30]. In addition,
carbonate substitutions in the hydroxyapatite crystals are
also known to change both the charge and solubility of the
surface [3133].
Although increased frequency of exposure resulted in
increased erosion of all tissues, the effect was clearly not
proportional. Patients receiving dietary advice aimed at
controlling their erosion not infrequently (subjectively at
least) initially respond by suggesting that they cut down
rather than cut out their consumption of erosive drinks.
From this study, doubling the frequency of exposure did
not result in double the amount of erosion. However, it is
important to emphasise that this observation can also be
interpreted as reducing the frequency of exposure by half
does not result in half the amount of erosion. If this observation were to be replicated in an in situ or in vivo study,
there would clearly be important implications for the delivery of dietary advice.
The somewhat surprising observation that erosion in
dentine appeared to progress in a less linear manner than
in enamel is of particular interest, since this phenomenon
does not appear to have been reported previously.
For reasons of availability, both deciduous and permanent
dentine specimens employed in this study were prepared
from sectioned roots. Fogel and co-workers [34] have
shown the hydraulic conductance of radicular dentine to
be much lower than that of coronal dentine, this difference
being largely attributable to variations in tubule diameter
and density. Since convection or hydraulic conductance

varies with the fourth power of the tubule radius, while


diffusion only varies with its square [35], hydraulic conductance results tend to be more pronounced than would be
expected for diffusion data. However, the results of Fogel
and co-workers [34] would predict that diffusive permeation
across radicular dentine would also be lower than that
measured in coronal dentine in a manner analogous to
their relative hydraulic conductance.
It is not possible to explain our observations on the basis
of variations in the relative hydraulic conductance of inner
and outer radicular surfaces. Indeed, Fogel and co-workers
[34] showed the hydraulic conductance of inner radicular
dentine to be approximately 20% that of coronal dentine,
while outer radicular dentine has a hydraulic conductance
approximately 2% that of coronal dentine. Since it was the
outer surface of the root dentine which was exposed, one
might therefore have expected tissue loss to increase over
time, rather than decrease as observed.
It is obviously tempting to suggest that the marked
dentine loss observed in the first five days was due to
removal of the smear layer, since this is known to be extremely acid labile [36,37], being readily removable by exposure to dietary fluids known to contain organic acids [38].
The depth of the smear layer varies widely depending on
whether the dentine is cut wet or dry, the amount and
composition of the irrigant, and the instrumentation
employed. The thickest smear layers reported (,10
15 mm) are those produced in vitro with a coarse diamond
blade mounted in a metallurgical saw [39]. The specimens
used in these experiments were prepared using silicon
carbide discs irrigated with copious amounts of water.
Although no data are available relating to the depth of
smear layer thus created, it seems more likely that this
would fall at the lower end of the range (15 mm) noted
for clinically-produced smear layers [40]. In our opinion,
removal of the smear layer cannot be the sole explanation
for the loss of at least 60% of the tissue in the first five days.
Clearly, further research is required to establish the aetiology of such non-linear tissue loss.
The aim of this study was to determine whether deciduous and permanent tissues differed in their susceptibility to
erosion. Consequently, differences between enamel and
dentine per se were not tested formally. It was anticipated
that enamel would be far more resistant to acid attack than
dentine, though it was noted that Davis and Winter [41] had
found that the rate of erosion in enamel was often as fast as
that for dentine. In the light of this expectation, the results of
this in vitro study were somewhat surprising. At day 15,
erosion was much more severe in enamel than in dentine,
though this relationship was not the same at all measurement points. At the present time, it is not possible to explain
why this should have occurred. However, it may be postulated that the reduced hydraulic conductance (and by
extrapolation, the reduced diffusion) associated with radicular dentine [34], might have, in some way, limited the
amount of erosion which could take place in vitro. It is

M.L. Hunter et al. / Journal of Dentistry 28 (2000) 265270

our suggestion that this in vitro study be repeated using


coronal dentine, albeit accepting the logistic problems
which this poses.
In relation to the erosion of enamel, it has been recognised that the particular in vitro methodology used here
dramatically over-estimates the amount of tissue loss
which can be expected in the oral environment [1]. During
treatment, the drink has total contact with the specimens,
whereas in situ or in vivo, the drink is diluted with saliva
both before and after it reaches the latter [4244], thereby
altering its thermodynamic properties [45]. Further, the
effect of the drink is not limited by the buffering capacity
of saliva. During storage, the specimens have no access to
CaPO4 to facilitate remineralisation. These shortcomings
may be addressed by the use of artificial (or natural) saliva
in the treatment and storage of specimens, thus simulating
the oral environment. However, it is difficult to see how one
can replicate the dynamics of the latter.
Pellicle (and plaque) formation undoubtedly confers
some benefit in with respect to erosion of enamel [46,47].
However, it should be emphasised that little information is
available on the characteristics of pellicle formation on
dentine and its possible protective effects. Maupome and
co-workers [48] have emphasised that the introduction of
carefully controlled saliva environments and salivary pellicles is necessary if we are to achieve a more realistic simulation of how an erosive challenge posed by frequent soft
drink consumption is met in situ or in vivo. In retrospect, it
may have been preferable to incorporate the development of
salivary pellicles in this study.

5. Conclusions
From the results of this in vitro study, it can be concluded
that differences in susceptibility of deciduous and permanent tissues to erosion by a low pH drink appear to exist.
Though not of consistent statistical significance, the
increased susceptibility of deciduous enamel to erosion is
of clinical significance. Deciduous teeth have a maximum
covering of 11.3 mm of enamel [11]. Indeed, a recent
study by Harding and co-workers [12], seeking to examine
the thickness of human deciduous incisor enamel, found that
the mean thickness of enamel (in millimetres) of the buccal
incisal and cervical thirds was 0:39 ^ 0:08 and 0:15 ^ 0:05;
respectively, with the mean palatal thickness being 0:22 ^
0:04: Such a thin covering of enamel coupled with an
increased rate of wear would appear to render deciduous
teeth more likely to exhibit exposure of dentine (or pulp)
during their lifetime. From this point of view, our findings
perhaps go a long way towards explaining the high percentage of 5- and 6-year-olds in whom the palatal surfaces of
the maxillary deciduous incisors are seen to be eroded into
dentine or pulp [6].
Increasing frequency of exposure to a low pH drink

269

appears to result in a non-proportional increase in erosion.


Likewise, halving the frequency of exposure does not result
in a similar reduction in tissue loss. This observation may
prove to be of relevance in the delivery of dietary advice to
those in our care.
It is recognised that in vitro methodology is incapable of
replicating the biological variations of the oral environment
and that actual erosion in vivo largely depends on consumption practices. The results of this study are of limited value if
they cannot be correlated with those arising from an in situ
or in vivo study. Therefore, it is our recommendation that
this study be replicated in the oral environment.

References
[1] West NX, Maxwell A, Hughes JA, et al. A method to measure clinical
erosion: the effect of orange juice consumption on erosion of enamel.
Journal of Dentistry 1994;26:32935.
[2] Bishop K, Briggs P, Kelleher M. The aetiology and management of
localized anterior tooth wear in the young adult. Dental Update
1994;21:15360.
[3] Shaw L, Smith A. Erosion in children: an increasing clinical problem.
Dental Update 1994;21:1036.
[4] Millward A, Shaw L, Smith A. Dental erosion in four-year-old children from differing socioeconomic backgrounds. ASDC Journal of
Dentistry for Children 1994;61:2636.
[5] Milosevic A, Young PJ, Lennon MA. The prevalence of tooth wear in
14-year-old school children in Liverpool. Community Dental Health
1994;11:836.
[6] OBrien M. Childrens dental health in the United Kingdom, 1993.
London: HMSO, 1994.
[7] Hinds K, Gregory JR. National diet and nutrition survey; children
aged 1 1/2 to 4 1/2 years. Report of the dental survey, vol. 2. London:
HMSO, 1995.
[8] Jones SG, Nunn JH. The dental health of 3-year-old children in East
Cumbria. Community Dental Health 1995;12:1616.
[9] Bartlett DW, Coward PY, Nikkah C, et al. The prevalence of tooth
wear in a cluster sample of adolescent schoolchildren and its relationship with potential explanatory factors. British Dental Journal
1998;184:1259.
[10] Nunn J, Shaw L, Smith A. Tooth weardental erosion. British
Dental Journal 1996;180:34952.
[11] Huszar G. Observations sur lepaisseur de lemail (Studies on the
thickness of dental enamel). Bulletin Du Group International Pour
La Recherche Scientifique En Stomatologie Et Odontologie
1971;14:15567.
[12] Harding AM, Satanovskiy Y, Simmelink JW, et al. Thickness of
human primary incisor enamel. Journal of Dental Research
1996;75:196.
[13] Fejerskov O, Stephen KW, Richards A, et al. Combined effect of
systemic and topical fluoride treatments on human deciduous
teethcase studies. Caries Research 1987;21:4529.
[14] Naujoks R, Schade H, Zelinka F. Chemical composition of different
areas of the enamel of deciduous and permanent teeth. (The content of
Ca, P, CO2, Na and N2.) Caries Research 1967;1:13743.
[15] Thylstrup A, Fejerskov O, Joost Larsen M. Polarized light microscopy
of enamel structure in incisors from newborn infants. Scandinavian
Journal of Dental Research 1976;84:24354.
[16] Wilson PR, Beynon AD. Mineralization differences between human
deciduous and permanent enamel measured by quantitative microradiography. Archives of Oral Biology 1989;34:858.
[17] LeGeros Z, Trautz OR, LeGeros JP, et al. Apatite crystallites: effects
of carbonate on morphology. Science 1967;155:140911.

270

M.L. Hunter et al. / Journal of Dentistry 28 (2000) 265270

[18] Cutress TW. The inorganic composition and solubility of dental


enamel from several specified population groups. Archives of Oral
Biology 1972;17:93109.
[19] Ingram GS. The role of carbonate in dental mineral. Caries Research
1973;6:21730.
[20] Feagin F, Thiradilok S, Aponte-Merced L. The carbonate and fluoride
in surfaces of remineralised enamel. Journal of Oral Pathology
1977;6:33842.
[21] Nelson DGA. The influence of carbonate on the atomic structure and
reactivity of hydroxyapatite. Journal of Dental Research
1981;60:16219.
[22] Featherstone JDB, Mellberg JR. Relative rate of progress of artificial
caries lesions in bovine, ovine and human enamel. Caries Research
1981;15:10914.
[23] Tyler JE, Poole DFG, Shellis RP. Artificial carious lesion formation in
human enamel: deciduous/permanent and high/low fluoride comparisons. Journal of Dental Research 1982;61:562.
[24] Shellis RP. Relationship between human enamel structure and the
formation of caries-like lesions in vitro. Archives of Oral Biology
1984;29:97581.
[25] Johansson A-K, Sorvari R, Meurman JH, et al. In vitro effect of citric
acid on deciduous and permanent enamel. Caries Research
1998;32:310.
[26] Milosevic A. Toothwear: aetiology and presentation. Dental Update
1998;25:611.
[27] Poole DFG, Shellis RP, Tyler JE. Rates of formation in vitro of dental
caries-like enamel lesions in man and some non-human primates.
Archives of Oral Biology 1981;26:4137.
[28] Linden L-A, Bjorkman W, Hattab F. The diffusion in vitro of fluoride
and chlorhexidine in the enamel of human deciduous and permanent
teeth. Archives of Oral Biology 1986;31:337.
[29] Cevc G, Cevc P, Schara M, Skaleric U. The caries resistance of
human teeth is determined by the spatial arrangement of hydroxyapatite microcrystals in the enamel. Nature 1980;286:4256.
[30] Skaleric U, Ravnik C, Cevc P, et al. Microcrystal arrangement in
human deciduous dental enamel studied by electron paramagnetic
resonance. Caries Research 1982;16:4750.
[31] Kibby CL, Hall WK. Surface properties of calcium phosphate. In:
Hair ML, editor. The chemistry of biosurfaces, 2. New York: Marcel
Dekker, 1972. p. 663729.
[32] Besic FC, Bayard M, Wiemann MR, et al. Composition and structure

[33]
[34]

[35]

[36]

[37]

[38]
[39]
[40]
[41]
[42]
[43]
[44]
[45]
[46]

[47]

[48]

of dental enamel: elemental composition and crystalline structure of


dental enamel as they relate to its solubility. Journal of the American
Dental Association 1975;91:594600.
Arends J, Jongebloed WL. Dislocations and dissolutions in apatites:
theoretical considerations. Caries Research 1977;11:1867.
Fogel HM, Marshall FJ, Pashley DH. Effects of distance from the pulp
and thickness on the hydraulic conductance of human radicular
dentine. Journal of Dental Research 1988;67:13815.
Merchant MJ, Livingston MJ, Pashley DH. Dentin permeation:
comparison of diffusion with filtration. Journal of Dental Research
1977;56:11614.
Pashley DH. The influence of dentin permeability and pulpal blood
flow on pulpal solute concentrations. Journal of Endodontics
1979;5:35561.
Addy M, Absi EG, Adams D. Dentine hypersensitivity. The effects in
vitro of acids and dietary substances on root planed and burred
dentine. Journal of Clinical Periodontology 1987;14:2749.
Absi EG. Studies on the aetiology, appearance, and treatment of
hypersensitive dentine. (Thesis), University of Wales, 1989.
Pashley DH, Michelich V, Kehl T. Dentin permeability: effects of
smear layer removal. Journal of Prosthetic Dentistry 1981;46:5317.
Brannstrom M. Dentin and pulp in restorative dentistry. London:
Wolfe Medical Publications, 1982.
Davis WB, Winter PJ. The effect of abrasion on enamel and dentine
and exposure to dietary acid. British Dental Journal 1980;148:2536.
Speirs RL. Saliva and dental health (1). Dental Update 1984;11:541
2.
Speirs RL. Saliva and dental health (1). Dental Update 1984;11:544.
Speirs RL. Saliva and dental health (1). Dental Update 1984;11:546.
Ireland AJ, McGuiness N, Sherriff M. An investigation into the ability
of soft drinks to adhere to enamel. Caries Research 1995;29:4706.
Meurman JH, Frank RM. Scanning electron microscopic study of the
effect of salivary pellicle on enamel erosion. Caries Research
1991;25:16.
West NX. Dentine hypersensitivity; clinical and laboratory studies of
toothpastes, their ingredients and acids, Thesis. University of Wales
College of Medicine, 1995.
Maupome G, Diez-de-Bonilla J, Torres-Villasenor G, et al. In vitro
quantitative assessment of enamel microhardness after exposure to
eroding immersion in a cola drink. Caries Research 1998;32:14853.

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