RESEARCH REPORTS

Biomaterials & Bioengineering

S. Paris, H. Meyer-Lueckel*,
and A.M. Kielbassa
Dept. of Operative Dentistry and Periodontology,
University School of Dental Medicine, Campus Benjamin
Franklin,
Charit-Universittsmedizin
Berlin,
Assmannshauserstr. 4-6, 14197 Berlin, Germany;
*corresponding author, hendrik.meyer-lueckel@charite.de

Resin Infiltration
of Natural Caries Lesions

J Dent Res 86(7):662-666, 2007

ABSTRACT

INTRODUCTION

Infiltration of non-cavitated caries lesions with

light-curing resins could lead to an arrest of lesion
progression. The aim of this study was to evaluate
the penetration of a conventional adhesive into
natural enamel caries after pre-treatment with two
different etching gels in vitro. Extracted human
molars and premolars showing proximal whitespot lesions were cut across the lesions
perpendicular to the surface. Corresponding lesion
halves were etched for 120 sec with either 37%
phosphoric acid gel (H3PO4) or 15% hydrochloric
acid gel (HCl), and subsequently infiltrated with
an adhesive. Specimens were observed by
confocal microscopy. Mean penetration depths
(SD) in the HCl group [58 (37) m] were
significantly increased compared with those of the
H3PO4 group [18 (11) m] (p < 0.001; Wilcoxon).
It can be concluded that etching with 15%
hydrochloric acid gel is more suitable than 37%
phosphoric acid gel as a pre-treatment for caries
lesions intended to be infiltrated.

uring the development of subsurface caries lesions, mineral is dissolved

out of the enamel, resulting in increased porosities that appear clinically
D
as the so-called 'white-spot' lesions (Ten Cate et al., 2003). Today, these

KEY WORDS: caries, resin infiltration, etching,

acid gel.

Received July 23, 2006; Last revision February 9, 2007;

Accepted March 6, 2007
A supplemental appendix to this article is published
electronically only at http://www.dentalresearch.org.

662

lesions are commonly treated by enhancing remineralization, e.g., by

improving the individual's oral hygiene or fluoridation. However, in noncompliant individuals with cavitated proximal lesions and greater lesion
extension, this strategy has considerable limitations.
A promising alternative therapy for the arrest of caries lesions might be
the infiltration of subsurface lesions with low-viscous light-curing resins.
Since porosities of enamel caries act as diffusion pathways for acids and
dissolved minerals, infiltration of these lesions with resins might occlude the
pathways, thus leading to an arrest of caries progression.
Several studies have demonstrated that artificial caries lesions can be
infiltrated by commercially available adhesives and fissure sealants (Davila
et al., 1975; Robinson et al., 2001; Schmidlin et al., 2004; Meyer-Lueckel et
al., 2006). Moreover, it has been shown that infiltrated artificial lesions do
not progress in a cariogenic environment (Mueller et al., 2006; Paris et al.,
2006). Thus far, only two in vitro studies have addressed the infiltration of
natural lesions. However, these early reports were mainly descriptive
(Davila et al., 1975), or used materials which were not clinically applicable
due to their unsanitary nature (Robinson et al., 1976). Since there are
substantial structural differences between both lesion types, it is not
applicable to transfer findings from artificial to natural lesions.
The surface layer of enamel caries lesions has a lower pore volume
compared with that of the lesion body underneath (Bergman and Lind, 1966;
Silverstone, 1973). Since the infiltration of enamel caries with light-curing
resins is mainly driven by capillary forces, the pore diameter and volume
influence the penetration speed (Paris et al., 2007). Therefore, the surface
layer forms a barrier, which might hamper the infiltration of the lesion body.
From this follows that removing or perforating the surface layer might be
essential for a successful infiltration of the lesion body. In artificial lesions,
brief etching with 37% phosphoric acid enhanced resin penetration (Gray
and Shellis, 2002). With thicker and more mineralized surface layers in
natural lesions (Bergman and Lind, 1966), it was assumed that this etching
procedure would not be effective in eroding the surface layer (MeyerLueckel et al., 2007). The latter study confirmed that etching with 15%
hydrochloric acid gel leads to a more effective erosion of the surface layer
compared with 37% phosphoric acid gel, but did not focus on the
subsequent infiltration of resins into the lesions.
Therefore, the aim of the present study was to evaluate the penetration
of a commercial adhesive into natural proximal caries lesions, without pretreatment and with prior conditioning by two different etching gels in vitro.
The working hypotheses were:
(Hypothesis 1) The surface layer of natural un-cavitated caries is a
diffusion barrier, which hampers the penetration of resin. Therefore, no

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J Dent Res 86(7) 2007

Infiltration of Caries Lesions

663

resin penetration occurs without prior

etching; and (Hypothesis 2) pretreatment for 120 sec with 15%
hydrochloric acid gel leads to a more
pronounced resin penetration
compared with 37% phosphoric acid
gel.

MATERIALS & METHODS

Extracted human molars and premolars
showing proximal white-spot lesions
were used in this study. The study
protocol conformed to the principles
outlined in the Central German Ethics
Committee's statement (2003) focusing
on the use of human body material in
medical research. After being carefully
cleaned of soft tissues, teeth were
stored in 20% ethanol solution until
used. Teeth were examined by 20
stereo microscopy (Stemi SV 11; Carl
Zeiss, Oberkochen, Germany), and
cavitated as well as damaged lesions
were excluded.
For radiographic examination,
teeth were positioned in a silicone base
with the buccal aspects facing a
radiographic tube (Heliodent MD;
Siemens, Bensheim, Germany). To
simulate cheek scatter, we placed a 15mm wall of clear Perspex between the
tube and the teeth. Standardized
radiographs (0.12 sec, 60 kV, 7.5 mA)
were taken of each tooth (Ektaspeed;
Kodak, Stuttgart, Germany) and
developed in an automatic processor
(XR 24-II; Drr Dental, BietigheimBissingen, Germany). The radiographic
lesion depths were independently
assessed by two examiners and scored
(Marthaler and Germann, 1970): no
translucency (R0), translucency
confined to the outer half on enamel
(R1), translucency confined to the inner
half of enamel (R2), translucency
confined to the outer half of dentin
(R3), or translucency confined to the
Figure 1. Representative images of a lesion treated with the adhesive. (A) Clinical aspect of the mesial
inner half of dentin (R4). In case of
surface of a human molar showing a white-spot lesion (dotted line). The lesion was cut in two halves
disagreement in an assessment of
along the dashed line. (B) Aspect of the cut surfaces of the same enamel lesion. (C-E) Confocal
radiographic lesion depth, a consensus
microscopic images of resin-infiltrated lesions (E, sound enamel; SL, surface layer; LB, lesion body; R,
rank was reached.
penetrated resin; S, lesion surface). (C) Deep resin penetration can be observed after etching with
HCl. (D) The surface layer of this H3PO4-etched caries lesion was not eroded completely. Therefore,
The roots of the teeth were
only superficial resin penetration occurred, as indicated by a fine rim of red fluorescence at the tooth
removed, and the crowns were cut
surface. (E) Magnified image of an HCl-etched lesion (40x objective). The outermost 50-100 m of
across the caries lesions perpendicular
prism cores are filled with resin. In non-infiltrated parts of the lesion body, the highly porous prism
to the surface (Band Saw; Exakt
centers show green fluorescence.
Apparatebau, Norderstedt, Germany),
providing two halves of each lesion
outer half of enamel; C2, extension into the inner half of enamel;
(Figs. 1a, 1b). Subsequently, the cut surfaces were examined
or C3, extension into the outer half of dentin. Lesions extending
(stereo microscope, 20 ; Stemi SV 11) and classified with respect
into the inner half of dentin (C4) were excluded. Corresponding
to the histological lesion extension, according to the radiological
lesion halves showing the same grading level (C1-C3) in
grading (Marthaler and Germann, 1970): C1, extension into the
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664

Paris et al.

Figure 2. Mean penetration depths of resin for various pre-treatments

and histological lesion extensions (box and whisker plots with quartiles
and medians; n = 10 per group). Statistically significant differences
between groups are indicated with asterisks (*p < 0.05; **p < 0.01;
***p < 0.001; Mann-Whitney). Abbreviations: C1, caries extension into
the outer half of enamel; C2, caries extension into the inner half of
enamel; C3, caries extension into the outer half of dentin.

histological caries extension were assigned to the treatment (TRT)

group (n = 10 each). In case the corresponding lesion halves
differed in lesion extension, the deeper lesion was used as the
control (CTR; n = 10), and the remaining half was disposed of.
Subsequently, the cut surfaces were covered with nail varnish.
In the treatment (TRT) group, corresponding lesion halves were
etched either with 37% phosphoric acid gel (H3PO4; total etch;
IvoclarVivadent, Schaan, Liechtenstein), or with an experimental
15% hydrochloric acid gel (HCl). The HCl gel contained
hydrochloric acid 15%, glycerol 19%, highly dispersed silicon
dioxide 8%, and methylene blue 0.01% in aqueous solution. After
120 sec, the gels were rinsed thoroughly with water spray for 30
sec. In the control (CTR) group, no acid etching was performed.
Lesions were immersed in pure ethanol for 30 sec and
subsequently dried for 60 sec with oil-free compressed air.
A dental adhesive (Excite; IvoclarVivadent, Schaan,
Liechtenstein) labeled with 0.1% tetramethylrhodamine
isothiocyanate (TRITC; Sigma Aldrich, Steinheim, Germany) was
applied to the lesion surfaces. The resin was allowed to penetrate
the lesions for 5 min. Subsequently, excess material was removed
by means of cotton pellets, and the resin was light-cured for 30 sec
(Translux CL; Heraeus Kulzer, Hanau, Germany) at 400 mW/cm2.
The nail varnish was carefully removed, and specimen halves were
fixed on object holders parallel to the cut surface and polished
(Exakt Mikroschleifsystem, Abrasive Paper 2400, 4000; Exakt
Apparatebau, Norderstedt, Germany). To stain remaining pores,

J Dent Res 86(7) 2007

we immersed the specimens in 50% ethanol solution containing

100 M/L sodium fluorescein (Sigma Aldrich) for 3 hrs.
Specimens were observed by confocal laser scanning
microscopy (CLSM Leica TCS NT; Leica, Heidelberg, Germany)
in dual-fluorescence mode and with a 10x objective. The excitation
light had two wavelength maxima, at 488 and 568 nm. The emitted
light was split by a 580-nm reflection short-pass filter and passed
through a 525/50-nm band-pass filter for FITC and a 590-nm longpass filter for RITC detection. Images with a lateral dimension of
1000 x 1000 m2 and a resolution of 1024 x 1024 pixels were
recorded and analyzed by AxioVision LE software (Zeiss,
Oberkochen, Germany). Penetration depths and thicknesses of the
(residual) surface layer for the lesion halves were measured at up
to 10 defined points (depending on the lesion size; indicated by a
100-m grit), and mean values were calculated. Additionally to
CLSM analysis, acid-etched as well as infiltrated lesion surfaces
were observed by scanning electron microscopy (APPENDIX).
Statistical analysis was performed with SPSS software (SPSS
for Windows 11.5.1; SPSS, Chicago, IL, USA). Data were checked
for normal distribution by the Kolmogorov-Smirnov test. To
analyze differences in penetration depth between lesion halves/acid
gels, we used the Wilcoxon test for paired samples. For
comparison between unpaired groups, we performed MannWhitney and Kruskal-Wallis tests. Penetration depths were
analyzed with regard to possible differences between various
histological lesion extensions (C1-C3) and radiological grades
(R0-R3). The level of significance was set at 5%.

RESULTS
In the CLSM images, the penetrated resin showed a red
fluorescence, whereas remaining pores within the lesion, as
well as dentin, appeared green (Figs. 1c-1e). Solid material,
such as sound enamel or the surface layer, was displayed black.
Penetration depths varied considerably. For lesion halves
etched with HCl gel, the mean penetration depth (standard
deviation) [58 (37) m] was significantly higher compared
with that of those lesions treated with H3PO4 gel [18 (11) m]
(p < 0.001; Wilcoxon) (Fig. 2). Without acid-etching, no resin
penetration was found [0 (1) m]. Within treatment groups, no
significant differences for penetration depths could be observed
between various lesion extensions (C1-C3) (p > 0.05; KruskalWallis).
For radiological grading of lesion extensions, good interobserver agreement could be found ( = 0.804). Similar to
histological lesion extension (C1-C3), no significant
differences in penetration depth could be observed among
different radiological grades (R0-R3) (Table).
For those lesions where the surface layer was completely
removed (CTR, n = 0; H3PO4, n = 2; HCl, n = 8), significantly
higher (p < 0.01; Mann-Whitney) penetration depths [65 (35)
m] could be found compared with those lesions where
residues of the surface layer remained after etching [33 (31)
m]. Surface layer thickness was significantly reduced after
HCl etching [20 (18) m], compared with that in the lesions
etched with phosphoric acid [37 (25) m] and with the nonetched CTR group [42 (23) m] (p > 0.05; Mann-Whitney).

DISCUSSION
In previous studies where confocal microscopy was used, resin
penetration was visualized by labeling of the resin with

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J Dent Res 86(7) 2007

Infiltration of Caries Lesions

665

Table. Mean Penetration Depths [ m (standard deviations)] for the Various

fluorescent dyes (Schmidlin et al., 2004). In another
Radiological Caries Extensions
approach, the remaining (not infiltrated) pores were
marked with a dye-labeled polymer (MeyerGroup\Radiolucency
R0*
R1
R2
R3
Lueckel et al., 2006; Paris et al., 2006), or by
imbibition in a fluorescent solution (GonzlezCTR
0 ( 0)n = 8
0 ( 0) n = 10
1 ( 1) n = 8
0 ( 0) n = 4
Cabezas et al., 1998). In the present study, these
two methods were modified and combined. The
H3PO4
25 (15) n = 6
17 (12) n = 10
16 ( 7) n = 8
16 (10) n = 6
penetration of the resin was visualized by the red
TRT
HCl
47 (27) n = 6
65 (41) n = 10
52 (27) n = 8
67 (52) n = 6
fluorescence of TRITC. The remaining lesion pores
were indicated by the green fluorescence of sodium
* Abbreviations: R0, no radiographic translucency; R1, translucency confined to
fluorescein. Hard tissues with small pore volume
the outer half of enamel; R2, translucency confined to the inner half of enamel;
including the surface layer or sound enamel were
R3, translucency confined to the outer half of dentin; CTR, unetched control
neither infiltrated by the resin nor stained by the
group; TRT, treatment group; H3PO4, phosphoric acid etching; HCl, hydrochloric
green solution and appeared black. Thus, the dualacid etching.
fluorescence technique used in the present study
allowed for the simultaneous observation of the
porous lesion structure, the penetrated resin, as well
could be demonstrated that penetration was significantly
as structures with small pore volume.
increased in those parts of the lesion where the surface layer
Caries infiltration might be a promising approach for the
was completely removed after acid-etching. Therefore,
treatment of uncavitated caries lesions. In contrast to fissure
hypothesis 1 could be corroborated.
sealing, where the diffusion barrier is placed on top of the
Recently, 15% hydrochloric acid gel proved to erode the
(lesion) surface, the infiltration technique aims to create the
surface layer more effectively than 37% phosphoric acid gel
diffusion barrier inside the lesion, replacing lost mineral with
(Meyer-Lueckel et al., 2007). In the present investigation, the
resin. Therefore, the infiltration treatment should be
effects of etching with these acid gels on resin penetration were
differentiated from sealing techniques, where a resin layer
compared. Phosphoric acid (37%) is frequently used in
(Goepferd and Olberding, 1989; Garca-Godoy et al., 1997;
restorative dentistry for adhesive purposes. Hydrochloric acid
Tantbirojn et al., 2000) was established on the caries lesions. A
has been previously used for enamel microabrasion
recent clinical trial, where proximal enamel lesions were
(McCloskey, 1984; Mathewson et al., 1987). Although shortsuperficially sealed with an adhesive, found a significantly
term contact of this strong acid with mucosa has been shown to
reduced but still relatively high (43.5%) lesion progression over
be harmless (Croll et al., 1990), safety precautions, such as a
an 18-month observation period (Martignon et al., 2006).
rubber dam, should be used in clinical practice.
Another clinical investigation did not find any significant
Since significantly higher penetration depths could be
differences in lesion progression between the sealed and the
found after etching with hydrochloric acid, hypothesis 2 could
control group (Gomez et al., 2005). The latter authors
be confirmed as well. However, the surface layer could not be
speculated that treatment failures might be due to incomplete
eroded completely in 67% of lesions in the HCl group. Thus,
sealing or sealant disintegration over time. Moreover,
longer application times should be considered to achieve
laboratory studies confirmed the inferior resistance of unfilled
complete surface layer erosion. However, resin penetration was
resins to mechanical and chemical stress (Schmidlin et al.,
not influenced by macroscopic or radiological lesion extension.
2002, 2006). Therefore, it is questionable whether superficial
The penetration depths observed for Excite in natural
smooth-surface sealing with unfilled resins is, as yet, generally
lesions in the present study were lower compared with those
applicable in daily practice.
observed in artificial lesions (104 m/30 sec) in a previous
Compared with the latter concepts, the infiltration
investigation (Meyer-Lueckel et al., 2006), although a ten-fold
treatment might bear several advantages. With the infiltration
longer penetration time was chosen in the present study. It
technique, excessive resin is removed from the tooth surface
might be argued that the incomplete surface layer erosion in
before light-curing, whereby clinical application is greatly
natural lesions, even for those etched with HCl, could be
simplified. With application strips coated on one side,
responsible for this contradiction. However, in specimens
proximal lesions can be infiltrated without special protection
where the surface layer could be totally removed, mean
for the adjacent tooth, and after only minimal tooth
penetration depths were lower as well. In contrast to artificial
separation, e.g., by means of a wooden wedge or an
lesions, the pores of natural caries might be contaminated with
orthodontic rubber band (unpublished results). Moreover,
organic materials, such as proteins and carbohydrates, that
with this treatment, no sealant margins are produced on the
might hamper resin penetration as well. This underlines that
tooth surface that could enhance plaque accumulation and
findings from artificial lesions cannot necessarily be
cause periodontal inflammation. Furthermore, infiltration of
extrapolated to natural lesions.
the porous lesion structures might strengthen the lesion
It can be concluded that the surface layer of a non-cavitated
mechanically and prevent cavitation.
natural caries lesion is a barrier that significantly hampers the
To infiltrate a caries lesion, the penetrating resin needs
penetration of a light-curing resin. Therefore, no substantial
access to the porous spaces of the lesion body. It was assumed
resin penetration could be observed without prior acidthat the penetration could be hampered by the highly
conditioning. Etching for 120 sec with hydrochloric acid gel led
mineralized surface layer, where the pore volume is
to deeper resin penetration than etching with phosphoric acid
considerably lower. In fact, in the present investigation, no
gel, although surface layers could not be removed in all cases.
penetration was found without prior acid-etching. Moreover, it
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Paris et al.

666

ACKNOWLEDGMENTS
This study was supported by the Deutsche Forschungs gemeinschaft (DFG; PA 1508/1-1). The authors are indebted to
Mrs. Anja Bartels and Mrs. Julia Heinrich (Dept. of Operative
Dentistry and Periodontology, CBF, Charit) for their excellent
contributions to the experiments, to Dr. Herbert Renz (Dept. of
Experimental Dentistry, CBF, Charit) for his assistance with
the SEM, and to Prof. Dr. Harald Stein (Institute for Pathology,
CBF, Charit) for providing the CLSM.
The Charit-Universittsmedizin Berlin holds US
(US10/432,271) and European (EP06021966.4) patent
applications for an infiltration technique for dental caries lesions
in which the authors of this study are appointed as inventors.

REFERENCES
Bergman G, Lind PO (1966). A quantitative microradiographic study
of incipient enamel caries. J Dent Res 45:1477-1484.
Central German Ethics Committee (2003). Statement: [The use of
human body materials for the purposes of medical research].
20.02.2003 http://www.zentrale-ethikkommission.de/10/
31KoerpermatZ.html [site in German].
Croll TP, Killian CM, Miller AS (1990). Effect of enamel
microabrasion compound on human gingiva: report of a case.
Quintessence Int 21:959-963.
Davila JM, Buonocore MG, Greeley CB, Provenza DV (1975).
Adhesive penetration in human artificial and natural white spots. J
Dent Res 54:999-1008.
Garca-Godoy F, Summitt JB, Donly KJ (1997). Caries progression of
white spot lesions sealed with an unfilled resin. J Clin Pediatr
Dent 21:141-143.
Goepferd SJ, Olberding P (1989). The effect of sealing white spot
lesions on lesion progression in vitro. Pediatr Dent 11:14-16.
Gomez SS, Basili CP, Emilson CG (2005). A 2-year clinical evaluation
of sealed noncavitated approximal posterior carious lesions in
adolescents. Clin Oral Investig 9:239-243.
Gonzlez-Cabezas C, Fontana M, Dunipace AJ, Li Y, Fischer GM,
Proskin HM, et al. (1998). Measurement of enamel remineralization using microradiography and confocal microscopy. A
correlational study. Caries Res 32:385-392.
Gray GB, Shellis P (2002). Infiltration of resin into white spot carieslike lesions of enamel: an in vitro study. Eur J Prosthodont Restor
Dent 10:27-32.
Marthaler TM, Germann M (1970). Radiographic and visual
appearance of small smooth surface caries lesions studied on
extracted teeth. Caries Res 4:224-242.
Martignon S, Ekstrand KR, Ellwood R (2006). Efficacy of sealing
proximal early active lesions: an 18-month clinical study
evaluated by conventional and subtraction radiography. Caries
Res 40:382-388.

J Dent Res 86(7) 2007

Mathewson RJ, Morrison JT, Carpenter R (1987). Modification of

stained enamel surfaces: use of hydrochloric acid and pumice
mixture. J OK Dent Assoc 77:22-25.
McCloskey RJ (1984). A technique for removal of fluorosis stains. J
Am Dent Assoc 109:63-64.
Meyer-Lueckel H, Paris S, Mueller J, Colfen H, Kielbassa AM (2006).
Influence of the application time on the penetration of different
dental adhesives and a fissure sealant into artificial subsurface
lesions in bovine enamel. Dent Mater 22:22-28.
Meyer-Lueckel H, Paris S, Kielbassa AM (2007). Surface layer
erosion of natural caries lesions with phosphoric and hydrochloric
acid gels in preparation for resin infiltration. Caries Res 41:223230.
Mueller J, Meyer-Lueckel H, Paris S, Hopfenmuller W, Kielbassa AM
(2006). Inhibition of lesion progression by the penetration of
resins in vitro: influence of the application procedure. Oper Dent
31:338-345.
Paris S, Meyer-Lueckel H, Mueller J, Hummel M, Kielbassa AM
(2006). Progression of sealed initial bovine enamel lesions under
demineralizing conditions in vitro. Caries Res 40:124-129.
Paris S, Meyer-Lueckel H, Colfen H, Kielbassa AM (2007).
Penetration coefficients of commercially available and
experimental composites intended to infiltrate enamel carious
lesions. Dent Mater 23:742-748.
Robinson C, Hallsworth AS, Weatherell JA, Kunzel W (1976). Arrest
and control of carious lesions: a study based on preliminary
experiments with resorcinol-formaldehyde resin. J Dent Res
55:812-818.
Robinson C, Brookes SJ, Kirkham J, Wood SR, Shore RC (2001). In
vitro studies of the penetration of adhesive resins into artificial
caries-like lesions. Caries Res 35:136-141.
Schmidlin PR, Gohring TN, Sener B, Lutz F (2002). Resistance of an
enamel-bonding agent to saliva and acid exposure in vitro assessed
by liquid scintillation. Dent Mater 18:343-350.
Schmidlin PR, Zehnder M, Pasqualetti T, Imfeld T, Besek MJ (2004).
Penetration of a bonding agent into de- and remineralized enamel
in vitro. J Adhes Dent 6:111-115.
Schmidlin PR, Kluck I, Zimmermann J, Roulet JF, Seemann R (2006).
Caries-preventive potential of an adhesive patch after
thermomechanical loadinga microbial-based in vitro study. J
Adhes Dent 8:7-12.
Silverstone LM (1973). Structure of carious enamel, including the
early lesion. Oral Sci Rev 3:100-160.
Tantbirojn D, Rozzi SM, Mitra SB, Kedrowski BL, Douglas WH
(2000). In vitro inhibition of enamel demineralization by a
polymerizable amphiphilic film. Eur J Oral Sci 108:564-568.
Ten Cate JM, Larsen MJ, Pearce EIF, Fejerskov O (2003). Chemical
interactions between the tooth and oral fluids. In: Dental caries.
Fejerskov O, Kidd EAM, editors. Oxford: Blackwell Munksgaard,
pp. 49-69.

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