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JDRXXX10.1177/0022034519876853Journal of Dental ResearchCaries Inhibition Efficacy of Proximal Resin Infiltration

Research Reports: Clinical

Journal of Dental Research
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Randomized Controlled Clinical Trial DOI: 10.1177/0022034519876853

https://doi.org/10.1177/0022034519876853
journals.sagepub.com/home/jdr

M.C. Peters1 , A.R. Hopkins Jr.2, L. Zhu3, and Q. Yu3

Abstract
This study reports 3-y outcomes of a split-mouth randomized clinical trial. Resin infiltration’s capacity to arrest caries lesion progression
in noncavitated proximal lesions is affirmed. Forty-two consented young adults, blinded to tooth surface allocation, were treated
with resin infiltration on 1 randomly selected surface and concurrently experienced a mock infiltration procedure on another. Both
treatments were provided as an adjunct to the currently accepted standard-of-care regimen (periodic prophylaxis and serial fluoride
varnish applications) appropriate for the management of high caries risk. Challenging periods of low oral hygiene compliance were
expected. The primary outcome measure was 3-y radiographic lesion progression. Blinded investigators evaluated each study surface for
lesion progression with a series of images obtained at intervals over the 3-y course of study. Proportions of progressing lesions were
compared with McNemar’s test. Twenty-nine noncavitated lesion pairs in permanent posterior teeth demonstrating caries penetrating
into inner enamel or outer dentin were included in the analyses. No adverse events were reported. Radiographic progression was
recorded in 4 of 29 infiltrated lesions (14%) and 14 of 29 control lesions (48%, P < .003). Adjunct resin infiltration demonstrated a high
3-y efficacy of 71% (relative risk reduction). The prevented fraction was 86% for infiltration versus 52% for controls. Resin infiltration
was 100% successful in arresting caries progression in inner enamel lesions (E2) and 64% in outer dentin lesions (D1). Supplementary
microinvasive resin infiltration is significantly more efficacious in reducing proximal lesion progression than management by standard
noninvasive therapy alone. Long-term results may shed light on whether this represents the arrest or delay of the caries disease process
(ClinicalTrials.gov NCT01584024).

Keywords: dental caries, permanent dentition, intervention, caries management, patient compliance, sealing

Introduction This study (ClinicalTrials.gov NCT01584024) challenges

Informed clinical practice requires consideration of evidenced
nonsurgical options for the management of early-stage caries
disease affecting uncavitated proximal surfaces of permanent
teeth (Paris et al. 2013). Inclusion of preventive-only and non-
invasive (Peters 2010; Urquhart et al. 2019) to microinvasive
protocols preceding traditional invasive restorative treatment
is becoming a standard of care (SOC; Frencken et al. 2012).
Uninterrupted caries activity may progress and lead to demin-
eralized surface enamel, followed by an initial subsurface
enamel lesion. Continued “watching” may serve to facilitate
development of a cavitated lesion. Microinvasive methods,
such as sealants (Griffin et al. 2008) and resin infiltration (RI;
Paris et al. 2010; Meyer-Lueckel et al. 2016; Peters 2017),
have been shown to arrest the caries disease process and inhibit
caries progression. Systematic reviews are largely in support of
proximal infiltration (Ammari et al. 2014; Dorri et al. 2015;
Doméjean et al. 2015; Chatzimarkou et al. 2018; Krois et al.
2018; Liang et al. 2018). Three clinical studies of proximal
lesion infiltration with different study designs reported a con-
siderable benefit obtained with RI, resulting in a 3-y efficacy
(relative risk reduction [RRR]) of 54% to 91% (Martignon
et al. 2012; Meyer-Lueckel et al. 2012; Arthur et al. 2018).
the efficacy of RI for the nonsurgical management of noncavi-
tated progressing proximal lesions in a high–caries risk (HCR)
population, a population further challenged by exposure to
curriculum-imposed, compliance-challenging periods. Proximal
infiltration was provided as an adjunct to the “golden standard”
of noninvasive management protocol for HCR patients cur-
rently practiced. The 2-y study results (Peters et al. 2018)
showed an efficacy (RRR) of 89%. The present study aimed to
assess the caries-inhibitive effect of proximal lesion infiltration
as a clinical barrier to substrate when combined with currently
accepted SOC preventive measures in this group of high-risk,
1
School of Dentistry, University of Michigan, Ann Arbor, MI, USA
2
Chief, Operative and Comprehensive Dentistry, USADC West Point,
NY, USA
3
Biostatistics Program, Louisiana State University, New Orleans, LA,
USA
A supplemental appendix to this article is available online.
Corresponding Author:
M.C. Peters, School of Dentistry, University of Michigan, 1011 N.
University Avenue, Ann Arbor, MI 48109-1078, USA.
Email: mcpete@umich.edu
2 Journal of Dental Research 00(0)
caries-active adults. It was hypothesized that after 3 y the pro-
gression of infiltrated lesions would be significantly lower as
compared with noninfiltrated control (C) lesions.
Materials and Methods
This within-person, placebo-controlled randomized clinical
trial assessed the efficacy of RI provided as an adjunct to an
SOC fluoride (F) varnish regimen for inhibiting caries lesion
progression in noncavitated proximal surfaces of permanent
premolars and molars. Ethical approval was received from the
governing institutional review board at the University of
Michigan (IRBMED HUM00019821) and at Keller Army
Community Hospital (KACH-IRB 12/006–IRBNet 373988).
HCR volunteers attending the United States Military Academy
were identified and enrolled (A.R.H.). It was anticipated that
the challenges of their curriculum’s arduous field training
would present several periods of compromised compliance or
noncompliance. The study methodology has been comprehen-
sively described in conjunction with the 2-y efficacy data pre-
sented previously (Peters et al. 2018).
After initial general screening, 42 volunteers meeting inclu-
sion criteria provided written consent (generally healthy adult,
at high risk for caries disease and caries progression, having at least
2 active noncavitated proximal carious lesions). Standardized
bitewings (BWs) were taken with digital sensor holders.
Eligible lesions showed a radiographic depth extending into
inner enamel (E2) or outer dentin (D1). In case of multiple
eligible lesions, study lesions were selected following a stan-
dardized process to avoid selection bias. In order of priority,
lesion selection criteria were 1) similar lesion depth (E2/D1),
2) similar tooth type (premolar/molar), and 3) lesion location
with preference for a) same arch left and right, b) over 2 arches
left and/or right, or c) both within same quadrant.
In this split-mouth study, each participant received 1 lesion
management by RI and 1 lesion management by mock infiltra-
tion with tap water as placebo (C). Each C treatment accurately
simulated the infiltration procedure. All participants were
treated by experienced calibrated clinicians; 40 of 42 were
treated by 1 clinician-investigator (A.R.H.). Topical or local
infiltration anesthesia was provided as necessary for focal
hemostasis and patient comfort (rubberdam clamp). Each
lesion pair was randomly allocated to the infiltration (RI) or
placebo (C) group. Computer-derived randomization (M.C.P.;
Urbaniak and Plous 2011) of the lesions was concealed until
the start of the treatment session. Both patients and evaluators
were blinded to the random allocation.
Intervention and Recall
Prior to treatment, standardized BW radiographs were made
with individually customized digital sensor holders. Sensor
exposure was standardized throughout the study. Lesion radio-
lucency was assessed to confirm a baseline lesion depth of
score E2 or D1. Orthodontic separators (3 to 5 d in place) were
removed, and following confirmation of an intact surface and
placement of rubber dam, treatment was provided with
commercially available ICON kits (DMG). The infiltration
protocol (RI) followed the manufacturer’s instructions. The
affected enamel surface was etched (2 min, HCl gel) and rinsed
(30 s), then desiccated with air syringe (10 s), ethanol (30 s),
and air again (30 s). With a fresh applicator, the infiltrant was
placed on the lesion surface and allowed to penetrate for 3 min.
Any flash or excess infiltrant was removed by air and floss,
followed by light curing (≥40 s total) from buccal and lingual
direction. Infiltrant application was repeated (penetration time
1 min) to fill any residual porosity. The mock infiltration pro-
tocol (C) followed the same clinical steps with water instead of
etchant and infiltrant.
All patients received the SOC management protocol for
HCR individuals, including pretreatment dental prophylaxis,
oral hygiene instruction (brushing/flossing), diet counseling, F
toothpaste, and standard F varnish regimen (3 times within first
month after treatment, followed by F varnish application 4
times per year). The study’s infiltration treatments were pro-
vided as adjunct therapy. At recall, consecutive standardized
BW radiographs were taken with the individualized sensor
holder. Digital BWs were obtained annually. Two calibrated
evaluators (M.C.P., A.R.H.), blinded to allocation, scored the
radiographs. In case of differing interpretation between evalu-
ators, consensus was achieved by discussion. Digital images
were visually assessed independently (randomly organized)
and side by side in pairs (baseline to 3 y) at the same screen
resolution and magnification as commonly used in clinical
practice. Single-assessment (lesion depth) and pairwise-com-
parison (PW; lesion progression) data were recorded and ana-
lyzed. The primary endpoint was the proportion of lesions that
progressed as assessed by depth category (E2, D1, D2-Rest
[middle dentin or restored]). If lesions had progressed into the
D2 or D3 stage or had received a restoration, they were scored
as D2-Rest. The secondary endpoint was lesion progression by
PW comparison of the radiographs.
Statistical Methods
The previously reported (Peters et al. 2018) sample size calcu-
lation indicated the need for at least 22 lesion pairs after 3 y to
find differences between the groups. Allowing for a high attri-
tion rate, we enrolled 42 participants. Potential associations
between surfaces involved, baseline scores, and treatment
group and recall/baseline group comparisons were analyzed
with chi-square analysis. Differences in the proportion of pro-
gressed lesions between paired RI/C lesions were analyzed
with McNemar’s test via SAS 9.4 software (SAS Institute
2013). Earlier recorded lesion progression in missing pairs was
mitigated by carrying forward the last documented data of such
pairs. Intra- and interexaminer reliability for assessment of
lesion depth (single radiograph) and progression (PW compari-
son with baseline radiograph) was substantial (kappa >.8;
Landis and Koch 1977).
To address potentially skewed outcomes subsequent to
patients failing recall (Gupta 2011) and to avoid overoptimistic
efficacy estimates (Food and Drug Administration 1988), we
conducted an “intention to treat” (ITT) analysis with 5 cycles
Caries Inhibition Efficacy of Proximal Resin Infiltration 3

of imputations for missing data. For single-

assessment scores, we imputed all missing data
by calculating the probability of increasing with
the complete data. One-year data were imputed
first, then 2-y data, and then 3-y data. For the
comparative assessment, missing 1-y data were
imputed per the filled single assessment and
complete comparative assessment. The same
was done for 2- and 3-y data. Cumulative
assessment was calculated per the imputed
comparative assessment. Imputation was
repeated 5 times to get 5 sets of results.

Results
No adverse events or unwanted incidences were Figure.  Infiltration and control lesions (n = 29 pairs) show progression after 3 y (solid
observed or reported over the 3-y study period. arrows), including development of lesion pairs evaluated only at a previous follow-up
After 3 y, standardized BWs were obtained (dotted lines, asterisk). Lesion depth stages: E2 (inner enamel), D1 (outer dentin), and D2-
from 27 participants (64.3%; Appendix Figure). Rest (middle dentin or restored). Three infiltrated lesions (10.3%) and 7 control lesions
(24.1%) progressed into the next category.
The 3-y recalled group showed similar baseline
characteristics as those originally enrolled.
DMFT values at baseline were similar (mean ± SD: baseline significantly less caries progression than C lesions (McNemar:
group, 6.9 ± 3.0; 3-y recalled group, 6.7 ± 2.9). The dichoto- P = .033, confirmed by ITT analysis: Appendix Table 2).
mous distribution pattern at baseline (Peters et al. 2018) was
mirrored in the baseline DMFT of the recalled group. No sta- Cumulative PW Assessment. Cumulative PW data after 3 y
tistical relationship was found between treatment group and revealed significantly less caries progression in RI lesions (n =
caries stage/lesion depth at baseline (P > .05). Likewise, no 4) than C lesions (n = 14; McNemar: P < .003). These data
relationship was found between treatment group and tooth sur- resulted in a prevented fraction of 87.5% for infiltrated lesions,
faces involved (P > .05). while C lesions showed considerably more lesion progression
(prevented fraction, 46.9%). The P values from 5 imputed data
sets (ITT analysis) were each P < .01 (Appendix Table 3). The
Categorical Analyses odds ratio from observed data was 0.091 with a 95% CI from
Single Assessment.  Lesion depth scores (E2, D1, and D2-Rest) 0.012 to 0.704. The odds of more lesion progression after 3 y
for the recall participants indicated a shift in distribution of in the RI group were 91% less than those in the C group.
lesion stages from 36, 18, and 0 at baseline to 32, 18, and 4 Inhibition failures for enamel and dentin lesions are shown
after 3 y, respectively. In 19 pairs (70.4%), lesion depth was in the Table. For equal lesion pairs (n = 17) both starting in
stable in both C and RI lesions. Two subjects (not attending enamel (E2), all RI lesions were inhibited, while 6 of 17
3-y recall) had shown a category jump in 1 of the 2 lesions (35.3%) of C lesions progressed (McNemar: P < .016; con-
earlier during the study. Carrying forward these 2 pairs, the firmed by 4 of 5 imputations: Appendix Table 4). For 8 equal
percentage of stable lesion pairs dropped to 65.5% (Figure). D1 lesion pairs, no difference was found between groups
Three-year categorical depth scores (n = 29) showed no differ- (McNemar: P > .05; confirmed by 4 of 5 imputations: Appendix
ence between treatment groups (McNemar: P > .05). In terms Table 5).
of ITT analysis, 5 imputed data sets showed each P value >.05,
confirming no difference between the RI and C groups (Appen-
dix Table 1). Discussion
The outcomes of this 3-y RCT support the use of adjunct RI as
an early management therapy for early noncavitated carious
Comparative Analyses
lesions. HCR participants with at least 2 progressing approxi-
PW Assessment.  PW comparison of 3-y recall radiographs and mal carious lesions diagnosed at or near the enamel-dentine
their baseline images included the 2 carry-forward pairs with junction were enrolled. The baseline demographic composition
3.6-y radiographs. This revealed 16 of 29 (48.3%) with stable of the 3-y recalled subjects (n = 27) was homologous to
lesions in both groups. Increased radiolucency was found in 15 descriptors of initially enrolled subjects (n = 42). This similar-
of 58 lesions (25.9%). This included 11 pairs with 1 progress- ity warrants generalization of results. The cohort’s 31.0%
ing lesion (9 C, 2 RI), while 2 pairs showed progression in both lesion progression within its lesions alone evidences RI effi-
lesions (2 C, 2 RI). At 3-y recall, RI lesions showed cacy in an environmental continuum of active caries disease.
4 Journal of Dental Research 00(0)
Table.  Cumulative Progression for Enamel (E2) and Dentin (D1) Lesions: Resin-Infiltrated and Control Groups.
Resin Infiltrated
Location n %
E2 0 of 18  0.0
D1 4 of 11 36.4
Total 4 of 29 13.8
Overall cumulative lesion progression was 31.0% (15 pairs, with 3 pairs showing both lesions progressing). For E2 and D1 lesions, progression was
recorded in 0% and 36.4% for the resin-infiltrated group and 40% and 66.7% for the control group, respectively.
By design, within this HCR-targeted study population, periods
of noncompliance with prescribed oral hygiene measures were
expected. Additional RI-enhanced protection provided to early
lesions may be a helpful means of bridging periods of increased
susceptibility. Timely interception by infiltration of deepening
enamel lesions successfully inhibited disease progression.
While dentin lesions benefited to a lesser extent, many bene-
fited, as evidenced by the reduced number of lesions progress-
ing and by the slower pace of disease progression.
Clinical study outcomes are often based on the number of
participants present for a particular recall. However, excluding
“known failures” in the “missing subject/pair” group might
result in skewed data. To mitigate this effect, we carried for-
ward the last documented data of such pairs. Inclusion of such
early treatment failures from “missing” participants/pairs con-
veys a more complete and clear picture of the actual therapeu-
tic effect of this intervention. Although not unexpected of HCR
populations, the relatively low retention rate may have affected
our results. Techniques including multiple imputations and last
observation carried forward provide ways of imputing missing
data in clinical trials to avoid introducing unknown bias. To
avoid bias, we further investigated the difference between the
groups by ITT analysis with imputation of missing data. This
analysis corroborated the per-protocol analyses of single-
assessment (P > .05) and PW-comparison (P < .05) outcomes.
The confirmative results of conducted ITT analyses strengthen
our study results (Food and Drug Administration 1988; Gupta
2011).
Lesion Depth
After 3 y, 17.2% of lesions showed an increase in depth score
(Figure). Depth of lesion penetration, determined histologi-
cally or clinically, is often used as a reference criterion for
radiographic detection of caries (Hintze et al. 1999). A single
radiograph in conjunction with clinical parameters, such as
papilla inflammation and contact point width, may give infor-
mation regarding probability for caries progression (Ratledge
et al. 2001). The use of set increments (categories), however,
provides a rather coarse approach to recording lesion progres-
sion. Radiographic staging of lesion depth by onetime assess-
ment is useful as a status quo location descriptor for baseline
documentation and stratification purposes only. Despite its fre-
quent use in caries studies, it provides only a one-off depth
score. This coarse approach lacks the accuracy needed to
Control Total
n % n %
8 of 20 40.0   8 of 38 21.1
6 of 9 66.7 10 of 20 50.0
14 of 29 48.3 18 of 58 31.0
capture the typically slow-paced lesion progression of caries
disease (Mejàre et al. 2004).
PW Comparison
In contrast, PW comparison of serial indexed radiographs per-
mits identification of minor progressions within depth catego-
ries. More adept for assessing continued expansion of lesion
radiolucency, PW comparison shows a rather different picture,
almost doubling the total number of failed lesion inhibitions to
31.0%. These data emphasize the essential requirement of con-
secutive serial BW readings for proper diagnosis of early caries
progression or stagnation over time (Kidd et al. 2003).
Comparison of consecutive radiographs is SOC when monitor-
ing lesion inhibition or progression over time. This image-evi-
denced diagnostic approach to treatment planning validates the
selection of non- or microinvasive management strategies.
Although the comparative data of the 3-y recalled groups
showed a significant difference (P = .033) between groups, of
greater significance is the overall cumulative PW comparison
outcome (Table). These data showed considerably more pro-
gression in C lesions (48.3%) when compared with RI lesions
(13.8%), leading to a therapeutic effect of 34.5% for the RI
group. This corroborates earlier outcomes from 2 clinical stud-
ies reporting a slightly higher therapeutic effect of infiltration
of 37.8% (Martignon et al. 2012) and 38.5% (Meyer-Lueckel
et al. 2012). The benefit obtained from adjunct RI in our study
was 71.4% (RRR), lying between the reported efficacy values
of 54% (Martignon et al. 2012) and 91% (Meyer-Lueckel et al.
2012). The positive outcomes shown in this study support the
firm affirmative findings of a recent systematic review sup-
porting RI for the management of proximal carious lesions
(Krois et al. 2018).
Variability in study design and local lesion environment
(e.g., study population, level of caries risk, size of lesions, con-
tinuity in SOC prevention and compliance) makes comparison
between study outcomes difficult. Only 2 comparable clinical
studies have been reported with 3-y results focused on infiltra-
tion of approximal permanent tooth surfaces (Martignon et al.
2012; Meyer-Lueckel et al. 2012). A recent study (Arthur et al.
2018) is not comparable, because of the smaller-sized lesions
selected (only E2 lesions). In addition, that study’s caries con-
trol strategies worked so well that progression rates were low
in both the test and control groups, and no difference between
groups could be found. A less-controlled 18-mo practice-based
Caries Inhibition Efficacy of Proximal Resin Infiltration 5
randomized clinical trial with an HCR subgroup (RRR, 83%
for all subjects) is not considered comparable due to study
design and duration (Meyer-Lueckel et al. 2016). This empha-
sizes the importance of similarity in study design when com-
paring trial outcomes. While our study focused on HCR
individuals receiving the best available preventive care for the
duration of the study, predictable compliance challenges were
anticipated. Both earlier trials enrolled patients with lower
mean DMFT counts (4.9, 6.7 respectively) and lower caries
risk (46% low and 54% moderate-high, Martignon et al. 2012;
moderate, Meyer-Lueckel et al. 2012). Neither study provided
professional hygiene follow-ups with repeated F varnish appli-
cations for the duration of the study.
Importantly, the proportion of D1 lesions in our study was
lower (35%) than in the earlier trials (62%, Martignon et al.
2012; 44%, Meyer-Lueckel et al. 2012). However, RI included
7% more D1 lesions than C, putting the RI group at a disadvan-
tage. While 0 of 18 (0%) E2 lesions and 4 of 11 (36.4%) D1
lesions in our RI group had progressed, the C group showed
progression in 8 of 20 (40%) E2 lesions and 6 of 9 (66.7%) D1
lesions. None of the infiltrated E2 lesions experienced any pro-
gression. The 4 RI lesions that progressed were all D1 lesions at
baseline. In hindsight, 3 of them were borderline D2 lesions.
These results seem to suggest that deeper D1 lesions may not be
reliable candidates for RI. This might be topic of future investi-
gation if a more precise baseline depth could be recorded.
In review, regarding the 4 RI lesions that progressed, 3 part-
ner C lesions had progressed as well. In these cases, an aggres-
sive and sustained cariogenic oral environment may have
overcome the SOC preventive measures and facilitated lesion
progression in both lesion sets. Or, more probably, micropo-
rosities or undiagnosed surface microcavitation may have con-
tributed to disease progression. In addition, lesion progression
probability increases in the presence of a higher proportion of
deeper lesions (Pitts and Rimmer 1992; Hintze et al. 1998).
Our study resulted in a therapeutic effect (absolute value) of
34.5%, which was slightly lower than the earlier reported
37.8% and 38.5%. Despite its lower percentage of D1 lesions,
the overall higher cariogenic challenge suffered by these may
partly explain this outcome.
Infiltration may have a relatively limited additive effect if
other treatments focused on controlling caries activity are suc-
cessful (Arthur et al. 2018). By design, our study enrolled HCR
volunteers, a group with existing oral hygiene compliance
issues and ongoing caries disease.
At times, their oral hygiene compliance would even be
more challenged due to their professional program. The suc-
cessful lesion-inhibitive effect of adjunct infiltration as com-
pared with control lesions shown in this study emphasizes the
importance of study design. The harsh oral environment
elected for this study subjected RI therapy to severe, ethically
sound testing. In 43.7% of participants, the paired lesions did
not progress. This might be credited to the strong SOC mea-
sures taken and participants following through on the profes-
sional advice provided. Increased commitment by study
participants (placebo effect) to oral hygiene and behavioral/
dietary changes may also have played a role. Our SOC preven-
tive activities, professional cleanings, and repeated F varnish
regimen fell short in one-third of this group of young adults.
That alone was not sufficient to curb the disease cycle. In par-
ticular, when periods of noncompliance are anticipated, the
additional 40.6% therapeutic effect of adjunct RI may prevent
incipient lesions from progressing to cavitation. In some more
advanced HCR cases, the potential benefit of infiltration might
be a delay or arrest in progression for any incipient subclinical
caries in adjacent lesions (Basili et al. 2017). The outcomes of
this study show that RI provides an effective strategic solution
for inhibiting initial carious lesions, thereby keeping more treat-
ment options open for future minimally invasive therapeutic
management in cases where focal caries disease may continue.
Adjunct RI demonstrated a high 3-y efficacy of 71% (RRR).
The prevented fraction was 86% for adjunct infiltration versus
52% for controls. RI successfully inhibited disease in enamel
lesions (E2,100%) and outer dentin lesions (D1, 64%). Results
suggest that deeper D1 lesions were more prone to inhibition
failure than those close to the enamel-dentine junction. This
reinforces the need for professional vigilance and, when indi-
cated, early intervention. While not addressed in this study, it
may be inferred that, absent the benefits of this nonsurgical
caries management protocol, radiographic depths evidenced by
progressing control lesions may have been more severe.
Provided concurrently with a preventive SOC HCR regimen,
adjunct RI management of early progressing lesions resulted in
35% more stabilized lesions. Additional longer-term data are
necessary to determine the definitive clinical effectiveness
(inhibition or delay) of adjunct infiltration therapy over time.
Author Contributions
M.C. Peters, contributed to conception, design, data acquisition,
analysis, and interpretation, drafted and critically revised the man-
uscript; A.R. Hopkins, contributed to conception, design, data
acquisition, and interpretation, drafted and critically revised the
manuscript; L. Zhu, contributed to data analysis, critically revised
the manuscript; Q. Yu, contributed to data analysis and interpreta-
tion, critically revised the manuscript. All authors gave final
approval and agree to be accountable for all aspects of the work.
Acknowledgments
We thank the volunteer cadets for participating in this study. We
also thank LTG Robert L. Caslen, the superintendent of the United
States Military Academy; the Keller Army Community Hospital;
and the staff of the Saunders Dental Clinic for their assistance dur-
ing the clinical and recall phases. The study was supported by the
University of Michigan and DMG and conducted in cooperation
with the United States Military Academy. The funding sources
had no involvement in study design, collection, analysis and inter-
pretation of data, decision to publish, or preparation of the manu-
script. The views expressed herein are those of the authors and do
not reflect the position of the United States Military Academy, the
Department of the Army, or the Department of Defense. The
authors declare no potential conflicts of interest with respect to the
authorship and/or publication of this article.
6 Journal of Dental Research 00(0)
ORCID iD
M.C. Peters https://orcid.org/0000-0003-2050-3978
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