closing the gap between oral hygiene and minimally

VOLUME 40 • NUMBER 8 • SEPTEMBER 2009 663

QUINTESSENCE INTERNATIONAL

Undoubtedly, after the advent of dentistry as

an academic discipline at the end of the 19th

century, the profession was influenced by a

mechanical era (with high-speed rotary cut-

ting instruments) and predominantly used a

surgical approach to remove caries. This

included radical removal of diseased por-

tions of the tooth, along with (material-driven)

geometric extensions to areas that were

assumed to be caries resistant; this concept

of extension for prevention was introduced

by Webb1 (and slightly modified by Black2

later on), and has influenced dentistry for

more than 120 years, even though this regi-

men was never scientifically based and was

misleading. Notwithstanding, already in

1922, it was recommended that restorative

treatment for these lesions should be con-

servative and that there is no need to remove

Closing the gap between oral hygiene and minimally invasive dentistry: A review on the resin infiltration technique of incipient (proximal) enamel lesionsAndrej M. Kielbassa, Dr Med Dent1/Jan Müller, Dr Med Dent2/

Christian R. Gernhardt, Dr Med Dent3

Dental caries on (proximal) tooth surfaces is still a problem in many industrialized coun-

tries. The objectives of this review were to present the scientific basis and the principles of

the resin infiltration concept, to discuss the inherent clinical applications, and to describe

how these backgrounds can be integrated into the concept of minimal intervention den-

tistry. Data were identified by searches of the Cochrane Registers, Medline, and Scopus.

Articles published in English and German through December 2008 were selected, and

most up-to-date or relevant references were chosen. Cross-referencing of significant arti-

cles identified additionally relevant articles written in other languages and those of histori-

cal value. A total of 23 in vitro studies (focusing on penetration depths or demineralization

prevention) were found, and 3 clinical studies (involving 122 subjects) could be retrieved;

these studies were not comparable. With an increased understanding of the caries

process, it is now recognized that demineralized but noncavitated enamel lesions can be

arrested or remineralized in many situations. The clinical research evidence on the resin

infiltration technique currently is of moderate extent to reach any decisive conclusions;

however, based on available laboratory and clinical studies, it seems convincing that resin

infiltration of enamel lesions should reduce (or even stop) the progress of white spot

lesions. Combining this ultraconservative restorative approach (which is considered

microinvasive) with a substantial caries remineralization program may provide therapeutic

benefits and significantly reduce both long-term restorative needs and costs, thus comple-

menting the concept of minimal intervention dentistry. (Quintessence Int 2009;40:663–681)

Key words: enamel, fluoride, minimal intervention dentistry, remineralization,

resin infiltration, subsurface caries lesion

1Professor and Head, Department of Operative Dentistry and

Periodontology, CharitéCentrum 3, University School of Dental

Medicine, Charité—Universitätsmedizin Berlin, Berlin, Germany.

2Assistant Medical Director, Department of Operative Dentistry

and Periodontology, CharitéCentrum 3, University School of

Dental Medicine, Charité—Universitätsmedizin Berlin, Berlin,

Germany.

3Associate Professor, Assistant Medical Director, Department of

Operative Dentistry and Periodontology, University School of

Dental Medicine, Martin-Luther-University Halle-Wittenberg,

Halle, Germany.

Correspondence: Dr Andrej M. Kielbassa, Abteilung für

Zahnerhaltungskunde und Parodontologie, CharitéCentrum 3

für Zahn-, Mund- und Kieferheilkunde, Aßmannshauser Straße

4-6, D-14197 Berlin, Germany. Fax: 49-30-450 562 932. Email:

[email protected]

© 2009 BY QUINTESSENCE PUBLISHING CO, INC. PRINTING OF THIS DOCUMENT IS RESTRICTED TO PERSONAL USE ONLY. NO PART OF THIS ARTICLE MAY BE REPRODUCED OR TRANSMITTED IN ANY FORM WITHOUT WRITTEN PERMISSION FROM THE PUBLISHER.

664 VOLUME 40 • NUMBER 8 • SEPTEMBER 2009


Kielbassa et a l

sound tooth structure in the name of preven-

tion.3 Nowadays, such surgical techniques

are considered maximally invasive, destruc-

tive, and outmoded.4

In modern dentistry, it has been widely

accepted that no cavity design or restorative

material will cure caries. For sure, once there

is a cavitation on the enamel surface, surgi-

cal intervention will be justified; in these

situations, minimally invasive techniques

(restricted to the actual damage) reduce the

amount of destruction; biomimetic restora-

tive materials (imitating nature while adhe-

sively luted) allow for a satisfying clinical and

esthetic outcome (Fig 1), and, concomitantly,

the intervention will enable control of the

local microflora (by modifying the local envi-

ronment, and thus revealing that operative

and restorative dentistry is but a true part of

prevention). Nonetheless, minimally invasive

approach is late in the disease process and

destructive as well, and restorative materials

are neither a perfect nor an everlasting

replacement for original tooth structure.

Thus, in view of the mean lifetime of any

restoration type, the original anatomy,

strength, and esthetics are lost forever (even

with modern preparation concepts like slot,

tunnel, or minibox restorations), and this will

lead to the continuum of replacement den-

tistry,5,6 with repeatedly enlarged restorations

and increased damage of hard tissues.

Moreover, invasive and even minimally or

microinvasive restorative procedures might

be associated with postoperative sensitivity

or pathogenic pulpal reactions, sometimes

requiring highly destructive endodontic treat-

ment solutions.

However, a cavity is but a symptom of the

disease, because the term caries means

rather the process than simply a lesion

resulting from that process. Therefore, dis-

covering a frank cavity is not equivalent to

caries diagnosis, and caries diagnosis—if

defined as an intellectual course of collecting

and consolidating data obtained by clinical

Fig 1a to 1f (a) Initial bitewing radiograph revealing a proximal caries lesion at the distal aspect of the mandibular first molar.(b) Preoperative view with undermining caries visible distally. (c) Intraoperative view with rubber dam placement.(d) Etching of completed cavity preparation (matrix, wooden wedge, and G-ring to ensure tight proximation). (e) CompletedClass 2 restoration after finishing. (f) Clinical view 1 week after placement of restoration.

a cb

d fe




Kielbassa et a l

and radiographic examination along with the

use of objective diagnostic armamentarium,

biologic knowledge, and information gained

from anamnesis—will be much more than

detecting breakdown of surfaces.6 Indeed,

the concept of minimum intervention den-

tistry should be tantamount to preservative

dentistry, and should embody at least 5 gen-

eral principles7,8:

• Scientifically oriented caries diagnosis of

early lesions using adequate diagnostic

devices

• Disease control by reduction of cariogenic

bacteria/modification of the oral flora and

patient education

• Remineralization of the earliest lesions

• Minimum surgical intervention of cavitat-

ed lesions

• Repair in favor of replacement of defective

restorations

Proximal caries constitutes a large health

problem for high-risk patients; at the age of

21 years, up to 50% of patients show carious

or restored proximal surfaces,9 and lack of

compliance with preventive behavior by

these patients is still a major problem.10,11 In

recent decades, a much more tissue-

preserving approach to arrest and control

proximal or smooth-surface caries lesions

has been studied extensively; this concept

aims at occluding the highly porous struc-

tures of incipient enamel lesions by means of

low-viscosity resins, and has been called

penetration,12 plastification,12 (therapeutic)

sealing,13,14 infiltration,12,15 impregnation,12,16

noninvasive,17 or ultraconservative18 tech-

nique. In medicine, infiltration means the act

or process of infiltrating (as of liquids) into the

pores or cavities of a substance; thus, this

term seems most appropriate to describe the

treatment approach using low-viscosity resin

mixtures with high penetration capabilities

on subsurface enamel lesions.

The purpose of this article is to present the

scientific basis and the principles of the resin

infiltration technique, to discuss the inherent

clinical applications (which are considered

microinvasive), and to describe how these

backgrounds can be transferred into clinical

practice.

DATA SOURCES AND STUDY SELECTION

We searched The Cochrane Library, Medline,

and Scopus for relevant articles up to

December 2008. The search was supple-

mented by manual searching of reference

lists from each relevant article identified. The

main search terms were adhesive, demineral-

ization, artificial caries, enamel, sealant, sub-

surface lesion, and white spot lesion. Articles

published in English and German through

December 2008 were selected, and most

up-to-date or relevant references were cho-

sen. Cross-referencing of significant articles

identified additional relevant articles written in

other languages and those of historic value.

The research resulted in 23 experimental and

3 clinical articles.

Three fields of interest were identified—

reaction of resin with artificial enamel lesions,

13 studies; natural enamel lesions, 4 studies;

and sound enamel, 7 studies. Only original

experimental articles were considered (see

compilation of in vitro studies, Table 1), but

for completeness reasons, interim and case

reports or abstracts were not excluded from

this review.

INITIATION OF THECARIES PROCESS—SUBSURFACE WHITESPOT FORMATION

The roles of plaque and saliva in the initiation

and progression of dental caries are summa-

rized schematically in Fig 2. A central feature

is the generation of organic acids by acido-

genic plaque bacteria following the dietary

intake of carbohydrates such as sucrose.

Saliva performs 2 direct functions to combat

enamel dissolution by these acids: (1) The

continuous flow of saliva acts to clear the

acids from the mouth, and (2) a number of

diverse salivary constituents have “caries-

protective activity.” The latter constituents

can act on the acids themselves (via buffer-

ing or neutralization), on the bacteria (via inhi-

bition of the metabolic processes involved in

acid production), and on the enamel (by



Kielbassa et a l

maintaining chemical supersaturation in the

adjacent plaque fluid). A key indirect function

of saliva is as a medium for the transfer of

potentially active therapeutic agents, such as

fluoride, to the site of action.

From a recent study, it seems that good

oral hygiene habits, established in early child-

hood, provide a foundation for a low experi-

ence of proximal caries in adolescents.11

Moreover, overweight and obese adoles-

cents had more proximal caries than normal-

weight individuals. Thus, the frequent con-

sumption of snack products during early

childhood appears to be a risk indicator for

caries at age 15.11

Demineralization and remineralization are

2 dynamic processes of dental caries in

which chemical composition plays a key role.

Type of Commercially available/

Evaluation

Pub. Ref. No. of Type ofdemineralization

Surface experimental Inhibition ofyear no. teeth enamel Gel Solution etch material Penetration demineralization

1989 110 15 Human x H3PO4 (37%; 60 s) Com. Resin tags Yes1992 87 48 Human x H3PO4 (36%; 60 s) Com. Yes (strong bond, Not studied

withstands thermocycling)

1997 65 20 Human x H3PO4 (37%; 20 s) Com. Not studied Yes2001 86 27 Human x H3PO4 (10%; 15 s) Com./Exp. Yes Yes2002 94 40 Human x H3PO4 (36%; 5 s) Com. Yes Not studied2003 109 15 Human x H3PO4 (37%; 60 s) Com. Not studied Yes2004 101 10 Human x H3PO4 (35%; 120 s) Com. Yes Not studied2005 95 27 Bovine x H3PO4 (20%; 5 s) Com. Yes Not studied2006 96 27 Bovine x H3PO4 (20%; 5 s) Com. Yes (best with Not studied

prolonged application time)

2006 106 27 Bovine x H3PO4 (20%; 5 s) Com. Yes Yes2006 107 27 Bovine x H3PO4 (20%; 5 s) Com. Yes Yes (not with

all resins)2007 97 27 Bovine x H3PO4 (20%; 5 s) Com. Yes (best with Not studied

high penetration coefficient)

2008 98 40 Bovine x H3PO4 (37%; 5 s) Com./Exp. Yes (best with Yeshigh penetration coefficient)

1975 12 24 Human Artificial/natural lesions H3PO4 (50%) Exp. Yes (if surface Not studiedetched)

1976 15 25 Human Natural lesions HCl (1 N; 5/10 s) Exp. Yes Not studied2007 93 30 Human Natural lesions HCl (15%; 120 s) Exp. Yes (best with Not studied

HCl etching)2008 108 40 Human Natural lesions HCl (15%; 120 s) Com./Exp. Yes (best with Not studied

high penetration coefficient)

1996 112 40 Human Sound enamel No information Com. Inhibition of demineralization2000 100 60 Human Sound enamel H3PO4 (35%; 60 s) Com. Full penetration of commercial

material with low viscosity2000 111 8 Bovine Sound enamel Citric acid (10%; 15 s) Exp. Inhibition of demineralization2003 109 10 Human Sound enamel H3PO4 (37%; 60 s) Com. Inhibition of demineralization2005 105 80 Bovine Sound enamel H3PO4 (35%; 60 s) Com./“Patch” Inhibition of demineralization2005 113 32 Human Sound enamel H3PO4 (35%; 30 s) Com. Inhibition of demineralization2005 115 40 Human Sound enamel H3PO4 (37%; 60 s) Com. Inhibition of demineralization

(H3PO4) Phosphoric acid; (HCl) hydrogen chloride.*Experimental design and main outcome of resin infiltration on artificially demineralized specimens and natural caries or sealants on sound enamel are given.

Table 1 Compilation of in vitro studies*

666 VOLUME 40 • NUMBER 8 • SPETEMBER 2009




Kielbassa et a l

The driving force for de- and remineralization

of tooth mineral is the degree of saturation

with respect to dental minerals in the adja-

cent liquid. The main inorganic anions are

chloride and inorganic phosphate, while

short-chain organic acids include lactic,

acetic, propionic, succinic, formic, pyruvic,

and butyric acids.19 The main cationic com-

ponents are ammonium, potassium, magne-

sium, and calcium. After repeated episodes

of prolonged exposure to acidic conditions

consistently below the critical pH (5.5) for

enamel dissolution, demineralization starts

as dissolution of apatites from the enamel

prisms. In the face of failure to remove

plaque from retentive tooth areas, with a diet

high in refined carbohydrates, the dynamic

equilibrium between demineralization and

remineralization will be tipped toward dem-

ineralization, and this will result in clinically

detectable white spot lesions.20

Without regular mechanical disturbance

of dental plaque,21 and with continuing de-

mineralization (and without the benefit of re-

mineralization), an initial subsurface lesion

will appear, and 2 zones of demineralization

can be histologically visualized now (Figs 3a

and 3b): the translucent zone (1% pore vol-

ume) at the advancing front, and the body of

the lesion (up to 25% pore volume).22

Dissolution may start at the prism cores,23

and mineral losses of up to 50% have been

observed at interprismatic areas and from

the prism peripheries.24 Moreover, 2 zones of

remineralization are present: the dark zone

(2% to 4% pore volume), and the surface

zone (< 5% pore volume) forming the

pseudointact surface overlying the lesion.22

The surface layer has a varying thickness of

some 40 µm and a mineral content of up to

82 vol%.25 These values are considerably

higher than with artificial lesions.26

TRADITIONAL TREATMENT OPTIONS

As long as the initial white spot lesion has an

intact surface (see Figs 3a and 3b), the most

effective means of caries control is an ade-

quately performed oral hygiene including the

complete removal of dental plaque using

mechanical means such as toothbrushing

and flossing.27 However, while flossing in par-

ticular seems to be a reasonable recommen-

dation for proximal surfaces, its preventive

effect has not been supported by evidence

up to now, neither with regard to gingival

health28 nor proximal caries,29 and only the

professional use on a supervised basis has

been identified to reduce caries risk (in chil-

dren).29,30 This way, arrest of the lesion may

be achieved, and remineralization becomes

possible; remineralization is the natural repair

process for noncavitated lesions (occurring

daily to repair the smallest demineraliza-

tions), and it relies on calcium and phos-

phate ions assisted by fluoride. However,

optimal conditions are mandatory to ensure

repair or healing by deposition of mineral on

existing damaged crystals or nucleation and

de novo crystal formation.20

Moreover, the additional use of antimicro-

bials (ie, chlorhexidine) should limit bacterial

growth and increase oral health.27 However,

caries-preventive properties of chlorhexidine

mouthrinses are limited, and most results are

inconclusive. A recent in situ study did not

Fig 2 Schematic diagram of the plaque-tooth interface (adapted andmodified from Duckwork and Gao19). Reprinted with permission fromS. Karger AG, Basel, Switzerland.

Pellicle

Saliva

Sugar

Acid

Enamel

Demineralization

Ions

Buffers

HCO3-

PI

PI

Ca2+

Ca2+CL-

K+

Dentalplaque




Kielbassa et a l

show any preventive effects of mouth rinsing

with 0.2% chlorhexidine, neither on acid

production of plaque samples nor enamel

demineralization.31 Moreover, chlorhexidine

obviously hampers fluoride accumulation

on tooth hard substances.32 Based on the

available literature, chlorhexidine rinses

(along with chlorhexidine gels and varnishes)

do not seem to be recommendable for caries

prevention.33

The use of topical fluorides to enhance

remineralization of demineralized proximal

enamel has been advocated.27 Application of

fluoride varnish every third month significantly

reduced the progression of proximal caries

lesions in premolars and molars. The most

obvious reduction of caries progression was

observed among children with moderate

caries risk, while children with high caries

activity (more than 9 new proximal lesions) did

not benefit from proximal caries reduction.34

However, in a recent study, caries prevention

of fluoride varnish treatment twice a year at 6-

month intervals was 69% in high-risk areas,

66% in medium-, and 20% in low-risk areas.35

Additionally, with fluoride mouth rinsing,

reduced caries incidence on proximal sur-

faces could be observed in adolescents with

low to moderate caries risk as well.36 All in all,

fluorides have been considered as an excel-

lent caries prevention strategy for proximal

surfaces in adolescents at the caries risk

ages of 13 to 16 years, and as a supplement

to oral home care and preventive efforts at

dental clinics.37 However, fluorides are not

able of completely preventing onset or pro-

gression of proximal caries in the long

term.9,38

There is some evidence that the use of

topical fluorides reduces the occurrence and

severity of white spot lesions, for example,

during orthodontic treatment; unfortunately,

Figs 3a and 3b (a) Proximal caries lesion with a smaller extent than the one treated in Fig 1. (b) Polarizingmicrograph of the slab from the same tooth (imbibed with quinoline), depicting a lesion not confined toenamel.

a b




Kielbassa et a l

it remains unclear which method or combi-

nation of methods to deliver the fluoride is

the most effective. Based on current best

practice in other areas of dentistry for which

there is evidence, it has been recommended

that patients with fixed brackets rinse daily

with a 0.05% sodium fluoride mouthrinse.39

These observations emphasize that the use

of fluorides is mainly a primary prevention

component, because fluoride aims to ham-

per demineralization and have a preventing

effect on developing lesions.

Indeed, studies on true remineralization of

proximal lesions are limited to only a few arti-

cles.40–42 It has been pointed out that even

with noncavitated proximal lesions, the caries

process may gradually progress to cavita-

tions if no preventive treatment is undertak-

en.43 Thus, because the enamel surface will

not be restored by salivary repair mecha-

nisms once a substantial loss of surface min-

erals has occurred (and surface discontinuity

is evident), plaque accumulation is regarded

as unavoidable in this situation. This might

explain why even small radiolucencies tend

to progress, albeit slowly.44

Therefore, close follow-ups should strong-

ly be recommended when considering a

preventive treatment regimen with small radi-

olucencies of proximal surfaces. The

process of caries development occurs over a

substantial length of time: Indeed, average

survival times of proximal lesions confined to

enamel of up to 8 years have been report-

ed.45 With regard to the treatment decision,

great variations in the thresholds of interven-

tion based upon lesion depth seen in radi-

ographic images among clinicians from vari-

ous countries have been observed. A con-

siderable number of professionals still tend

to practice invasive techniques; with lesions

confined to enamel, the decision to prepare

a cavity ranged from 19% in Norway46 to

nearly 50% in Mexico47 and Brazil,48,49 but

with even higher proportions in other coun-

tries.50,51 These values indicate an interven-

tionist attitude, which clearly could result in

overtreatment when remembering the slow

progression of enamel lesion development.

REMINERALIZATION OF (PROXIMAL) LESIONS

Due to the relative thickness and the consid-

erably high mineral contents, the pseudoin-

tact surface layer has been suspected to

inhibit remineralization. Therefore, the use of

acid etching52 and the acidulation of calcified

fluids53 have been investigated in vitro and

found to increase the surface porosity and to

facilitate remineralization.54 These proce-

dures obviously created a more pronounced

remineralization effect, thus indicating that

the surface of an incipient lesion constitutes

a barrier for remineralizing fluids; recently, an

effective reduction in the surface layer of nat-

ural enamel caries was achieved by etching

with a hydrochloric acid gel (15%; 90 to 120

seconds).55 Indeed, a 10-week remineraliza-

tion study using this acid-etch strategy

showed significant differences in lesion

depth, mineral content at the surface layer,

and integrated mineral loss between etched

and nonetched groups. However, addition of

fluoride accelerated the remineralization

process only in the beginning; in later stages,

the process leveled out and even reached a

plateau in all the groups, and it was conclud-

ed that full remineralization was not achieved

by etching, the addition of fluoride, or the

combination of treatments.56

Clinically, the degree of remineralization

seems to be limited, and this has been attrib-

uted to the presence of organic substances

attaching to the enamel surface and possibly

occluding the underlying pores in the caries

lesion.20,57,58 Moreover, the role of possible

remineralization inhibitors is not clearly

understood; the ability of albumin to bind and

to inhibit growth of calcium phosphate crys-

tals raises the question as to the possible role

of such molecules in the development of

caries lesions.59 Notwithstanding, mucins

have been shown to inhibit demineralization60

and to promote remineralization.61 In minimal

intervention dentistry (Fig 4), remineralization

or arrest of lesions should be utilized to a

maximum, because there is no real substitute

for natural tooth structure.




Kielbassa et a l

CLINICAL OBSERVATIONSON WHITE SPOT LESIONS

Concerning the fate of initial caries lesions

on smooth surfaces, the article by Backer

Dirks,62 showing that some 51% of early

white spot lesions might disappear after sev-

eral years, has been cited innumerable

times. A large part of the quoting articles

referred almost exclusively to remineraliza-

tion effects, and since that time, the profes-

sion has been increasingly attracted by the

concept of remineralization.63 Interestingly, in

a study similar to that of Backer Dirks62 only

13% of white spot lesions disappeared, while

50% showed no changes.64 In these 2

(uncontrolled) studies,62,64 the authors did

not clearly differentiate between active

(chalky, rough surface) and inactive (shiny,

hard surface) lesions, and lesion disappear-

ance has been attributed to either elimination

of caries challenge or remineralization.65

In a randomized clinical trial comparing

treatment with fluoride varnish and profes-

sional tooth cleaning for remineralization of

white spot lesions in caries-active adoles-

cents, there was a significant difference in

mean change in fluorescence between the 2

test groups; however, for lesion areas, no sig-

nificant differences could be observed.66 In

another study, adjunctive weekly brushing

with amine fluoride gel achieved no signifi-

cant enhancement of remineralization of

active white spot lesions monitored with the

Quantitative Light Fluorescence (QLF)

method, when compared to brushing alone

with amine fluoride dentifrice.67 This was cor-

roborated in another randomized clinical

study; here, long-existing white spot lesions

were observed over 6 months. The effective-

ness of dentifrices containing either sodium

fluoride (1,500 ppm) or amine fluoride (1,250

ppm) was not significantly different, and the

long-existing white spot lesions were stable

concerning fluorescence loss over the lesion

area. Moreover, fluorides did not seem to

have any effect on long-existing white spot

lesions.68

In a clinical study on postorthodontic de-

mineralized white spot lesions, demineralized

areas reduced by approximately half their

original size during the 6 months after treat-

ment.69 Again, the intervention using a low

fluoride test mouthrinse and dentifrice com-

bination compared with a nonactive control

combination failed to show any differences

or therapeutic effect; however, once formed,

many of these early lesions appear to be sur-

face demineralization, rather than a subsur-

face lesion with an intact surface zone,69 and

in these situations, abrasive effects are very

common. This would be in accordance with

other observations indicating that superficial

lesions seen after orthodontic treatment will

tend to disappear (“remineralize”) more rap-

idly and completely than deeper lesions on

removal of the cariogenic challenge.70

In his original work, Backer Dirks62 specu-

lated on either remineralization, abrasion, or

even both when trying to explain the clinically

observable disappearance of the smooth-

surface white spot lesions after several years.

When considering that white spot lesions on

smooth surfaces disappeared while proximal

caries obviously did not,62 and abrasion and

early recession are common in patients with

good oral care,71 the results of a previous

study seem to support the idea that tooth-

brushing on smooth surfaces might con-

tribute to abrasion of initial caries, in particular,

if vigorous toothbrushing is implemented as a

part of oral hygiene.26

Fig 4 Essential aspects of diagnosis and treatment planning. Resininfiltration fills the gap between oral hygiene and minimally invasivedentistry and can be integrated into the minimal intervention conceptof operative dentistry (adapted and modified from Mount and Ngo5).

Minimal intervention dentistry

Evaluation

SalivaMicrofloraDietSurface riskGeneral health

Diseasecontrol

Prevention Remineralization

Infiltration

Maximization of remineralization potentialDisruption of demineralization cyclesEducation and motivation

Maintain toothintegrityBiomimetic materialElimination cavitation

Treatmentneed

Adequate diseasecontrolCompromisedtooth integrityPatient agreement

Damagerepair




Kielbassa et a l

This would agree with scanning electron

microscopy (SEM) observations on demin-

eralized areas that formed beneath orthodon-

tic bands.70 Here, developmental white opaci-

ties had a higher luminance (ie, were whiter),

and the boundaries were more circular than

the postorthodontic caries lesions.72 Exam-

ination of definite white spot lesions revealed

characteristic patterns of initial tissue destruc-

tion. Focal holes and an accentuation of the

perikymata were observed affecting the

enamel surface zone (an area previously con-

sidered to remain relatively intact during the

development of a caries lesion).70 Another

SEM study on the fate of subsurface lesions

revealed a general tendency toward leveling

of the surface of the lesion indicating a loss of

porous tissue,73 probably by attrition/abrasion

due to functional wear and/or toothbrushing.74

These findings confirmed that removal of car-

iogenic challenge results in arrest of further

demineralization. However, the gradual regres-

sion of the lesion at the clinical level was

believed to be primarily a result of surface

abrasion.73,75

With proximal caries, it has been argued

that once a lesion is cavitated, it can no longer

be cleaned with flossing by the patient and,

hence, tends to progress,76,77 because the

constantly metabolically active biofilm cannot

be controlled. Therefore, from this threshold

an operative intervention is generally recom-

mended to prevent further lesion progression.

Unfortunately, the bitewing radiograph does

not give any direct information on the surface

integrity of proximal lesions. Clinical stud-

ies78–81 found comparably few cavitations in

R3 (radiolucency reaching the outer dentin on

bitewings) lesions (22% to 52%), while several

laboratory studies confirmed a considerably

earlier cavitation, with breakdown of surfaces

in up to 100% of R3 lesions (for review, see

Kielbassa et al44,82). Interestingly, gingival

bleeding has been shown to be related to sit-

uations with progressing proximal caries,83

and, according to the thoughts presented

here, possibly with breakdown of surfaces

(and higher accumulation of plaque). Caries

may be a multifactorial disease, but dental

plaque remains the only cause. Indeed, this

might be an explanation for the slow (but often

constant) progression of proximal lesions.43

Reliability of diagnosing precavitated

caries lesions for smooth (and proximal)

tooth surfaces has been shown to be poor.84

In this context, in clinical studies access to

the proximal space often is limited, thus lead-

ing to a possible underreporting of cavita-

tions. Moreover, a previous study reported a

sensitivity of only 76% for the clinical obser-

vation of R3 lesions with the naked eye after

tooth separation.85 Accordingly, it might be

speculated that clinical recording of small

cavities is extremely difficult during prepara-

tion procedures (Fig 5).

THE RESIN INFILTRATIONCONCEPT

Laboratory studies on penetrationdepthsFrom early histologic experiments, it is well

known that enamel lesions can be imbibed (in

water or quinoline; see Fig 3), because of the

increased microporosities of the different his-

tologic zones. Moreover, these tiny porous

openings and widened intercrystalline spaces

act as diffusion pathways for acids and dis-

solved minerals. With this in mind, it should be

possible to infiltrate incipient lesions with

other liquids, ie, with low-viscosity resins.

Thus, instead of removing the porous carious

tissue at a relatively late stage in the disease

process, attempts have been made to “fill” the

microporosities of lesions at a much earlier

stage of lesion development. This would not

only reduce the microporosities (and there-

fore the access of acid), but also afford some

mechanical support to the tissue.86

Early descriptive studies from the

1970s12,13 indicated that the adhesive encom-

passes the residual (in)organic materials of

the demineralized portions, thus transform-

ing the lesion into an acid-resistant unit.12

While artificial lesions can be infiltrated with a

comparable outcome, natural white spot

lesions have to be acid etched before infiltra-

tion.12,15,55 This obviously is due to the thick-

ness, and the low porosity/high mineral con-

tent of the surface layer (see above),25 and

due to organic substances found in natural

caries.59 However, it was found that a resin




Kielbassa et a l

infiltration depth of 60 µm was sufficient to

prevent further demineralization, even if the

surface coating had been dislodged.12

In a pioneering attempt at resin infiltrants,

well-defined requirements for potentially use-

ful materials were characterized. These mate-

rials should be:

• Hydrophilic

• Highly surface active and with low viscosity

• Bacteriostatic

• Nontoxic to oral tissues

• Polymerizable to a solid state

• Resistant against chemical and mechani-

cal challenges of the oral cavity

• Cosmetically acceptable15

Successful infiltration of materials into

lesions was demonstrated using resorcinol-

formaldehyde,15 which, however, was clinical-

ly unacceptable. Nevertheless, the results

showed that up to 60% of the lesion pore vol-

ume had been occluded following infiltration

and that this treatment was capable of reduc-

ing further acid demineralization.15

Acid conditioning of artificial subsurface

lesions with phosphoric acid revealed an

etching pattern similar to sound enamel.

Bonding to etched subsurface lesions

proved to be reliable, and was able to with-

stand thermocycling. Thus, it was concluded

that subsurface lesions are an acceptable

and suitable substrate for resin adhesion.87

However, the surface of natural white spot

lesions has been revealed to be more resist-

ant to phosphoric acid etching than adjacent

sound enamel.88

Further experiments revealed that viscosi-

ty, surface tension, and contact angle on

human enamel influence the penetration of

restorative resins into acid-etched enamel;

however, viscosity of the monomer mixture

was not shown to be a limiting factor for the

penetration of restorative resin monomers

into the pores of etched enamel surfaces,89

and depth of penetration decreased only

slightly with changing viscosity. Interestingly,

tag lengths (representing the penetration

depth) of up to 50 µm or more were observed

with composite as well as with non–composite

resins on (noncarious) phosphoric acid–

etched enamel.90–92 In a recent article, similar

penetration depths after surface conditioning

with hydrochloric acid were found in natural

lesions.93 Some commercially available adhe-

sives (sealants, bonding agents) have been

shown to be suitable for infiltration of artificial-

ly induced subsurface lesions, as well,94–96 but

significant differences could be revealed with

artificial lesions, when various resin infiltrants

Figs 5a and 5b Mesial surface of a maxillary premolar revealing a radio-lucency confined to the outer half of enamel (R1). The clinical situation(a) indicates a roughened surface and accentuated imbrication lines.SEM of the same lesion (b), depicting a breakdown of surface and micro-pores not considered remineralizable.

a

b




Kielbassa et a l

with differing penetration coefficients were

used.97 This has been corroborated with natu-

ral lesions recently,98 thus indicating that resin

infiltrants with high penetration coefficients99

are able to penetrate more deeply into sub-

surface lesions. In Fig 6, a typical example of

a resin infiltrated lesion is shown.

A previous SEM study on sealant penetra-

tion into etched fissures seems to confirm

these observations. Here, a low-viscosity

sealant penetrated fully and formed a resin-

infiltrated layer in enamel beyond the etched

depth. However, the high-viscosity sealants

used in that study did not penetrate enough

to ensure that the acid-etched enamel was

infiltrated sufficiently by the sealant to insure

good marginal seals.100

Another factor seems to be the degree of

microporosities. Penetration of an unfilled

resin into enamel was considerably influ-

enced by the degree of dental hard tissue

mineralization. Resin tags in demineralized

enamel were significantly longer (some 60

µm) than in other groups, and penetration

decreased significantly in remineralized areas

or after use of fluoride; however, this was still

significantly deeper than in control sites, and

remineralized enamel also allowed good pen-

etration of the unfilled bonding agent.101

Various modifications (additionally to acid

concentration and etching time) of the appli-

cation technique have been proposed to

improve the penetration depths in sound but

etched enamel. Ultrasonic treatment during

Figs 6a to 6c Light microscopic (a) aspects of a perpendicularly cut proximal surface of a molar showing a white spotlesion. Confocal laser scanning micrograph (b) of corresponding lesion confined to outer enamel, depicting the principle ofresin infiltration into subsurface lesions and revealing resin-infiltrated parts of the lesion (green, resin infiltrant labeled withfluorescent dye, fluorescein isothiocyanate [FITC]). SEM of the same lesion (c), confirming obturation of demineralized areas(note that at deeper lesion aspects, micropores have not been occluded).

a b c




Kielbassa et a l

etching procedure and drying of etched fis-

sures by means of acetone increased the

mechanical interlocking considerably.102 Re-

cently, it has been shown that conventional

phosphoric acid etching (if used alone) has

some limitations, and a deproteinization pre-

treatment using sodium hypochlorite (5.25%;

60 seconds) before etching revealed favor-

able results with regard to the retentive sur-

face.103 The additional use of alcohol has also

been advocated to dry the lesion areas,94 and

future studies should evaluate these addition-

al pretreatment regimens with regard to a

possibly increased penetration depth of resin

infiltrants. In Table 1, the respective studies

on penetration of subsurface lesions are

compiled.

Laboratory studies on preventionof lesion progressThe initiative to arrest caries by infiltration of

resins has been followed since the initial

studies mentioned above,12,13,15 and the

advent of dental adhesives with potentially

suitable properties has prompted a reexami-

nation of this concept in recent years.

In an early study resembling the infiltration

technique, the applied resin was aggressive-

ly air thinned to ensure oxygen inhibition

throughout the external surface film thick-

ness. In the absence of a polymerized outer

surface film, the infiltrated lesions showed a

reduced degree of demineralization, and an

experimental fluoride resin did not produce

statistically significant differences when com-

pared to a fluoride-free resin.104 Several

recent studies on artificial carieslike lesions

have demonstrated that commercially avail-

able adhesives having infiltrated the micro-

pores of the demineralized areas revealed a

considerable reduction of lesion progression

by either double application86,105,106 or extend-

ed penetration times (30 seconds compared

to 15 seconds).107 Using infiltrants with high

penetration coefficients facilitated inhibition

of lesion progression, thus showing that resin

infiltration sufficiently occludes the acids’ path-

ways and hampers demineralization.108 This

beneficial effect could be confirmed even

after thermocycling; when placed on acid-

etched surfaces, the resin adhered firmly to the

enamel with no evidence of demineralization

or enlargement of previously demineralized

areas underneath the sealants (see Table

1).109

A similar (but indeed different) approach

aimed at placing a physical barrier between

(carious) enamel and potentially cariogenic

biofilms. This concept has been retransmit-

ted from occlusal surfaces, where fissure

sealing has been performed successfully for

decades. Application of a thin layer of sealant

onto acid-etched artificial lesions has been

described as successfully improving the

resistance of subsurface lesions against

cariogenic challenge.110,111 Indeed, this was

not astonishing when regarding the already

known protective effects of fissure sealants;

a further concept has used an adhesive

patch as a barrier to block microorganisms

and their respective acids. This adhesive

patch also proved to be resistant against

acidic attacks.105

With “orthodontic” sealants, similar results

could be observed. Light-cured sealant treat-

ment after orthodontic appliance placement

significantly reduced or even prevented enam-

el demineralization.112,113 In another study,

demineralization in the sealant group was

reduced significantly, and teeth treated with

fluoride varnish exhibited 30% less demineral-

ization than the control teeth. Usually, sealants

are applied after acid etching, and removal of

surface coating after completion of orthodon-

tic therapy will leave resin tags in formerly

etched enamel; these areas have been shown

to be caries resistant as well.114 Therefore, par-

ticularly in patients who exhibit poor compli-

ance with oral hygiene and home fluoride use,

sealing has been recommended.115

In vivo studies proving the concept of resin infiltrationA recent SEM study on in vivo sealed (Clinpro

Sealant, 3M ESPE; with and without a pre-

ceding bonding) natural subsurface lesions

demonstrated an irregular resin network with

twisted and curved tags, while with the sound

enamel areas a regular etching pattern was

observed. Resin tag lengths were consider-

ably short and ranged from 4.2 to 5.5 µm. No

increased penetration depths could be

observed after the additional use of a low-

viscosity adhesive bonding agent (Single




Kielbassa et a l

Bond, 3M ESPE). No further pretreatment of

enamel was performed, and acid etching of

the surface zone was done with a phosphor-

ic acid gel.116 Penetration depths of the

sealant were somewhat higher in another

study using the same design; however, pre-

treatment with a bonding agent resulted in

decreased tag lengths.117 Nevertheless, in

both studies, a physical barrier was formed,

with protective function against exposure of

acids from bacterial origin, and cutting off

possibly remaining bacteria (within an

advanced lesion) from a nutritional supply of

fermentable carbohydrates.14

This was corroborated in a clinical study

on sealed (Gluma One Bond, Heraeus

Kulzer; or Concise Sealant, 3M ESPE; 18

months, 72 patients) proximal early active

lesions. As validated by subtraction radiogra-

phy, 43.5% of the sealed proximal lesions

had progressed during the 18-month study,

while 84.1% of the untreated controls (floss-

ing) showed increased demineralization

depths,118 thus indicating a reduced (and not

an arrested) progression rate for the proce-

dure. Interestingly, deeper test lesions

showed lower progression rates (33.0%)

when compared to untreated control sites,

thus reemphasizing the results already

known from fissure sealants119 to some

extent. From these observations, it might be

speculated whether lesion arrest over longer

periods after infiltration is due to reduced

microorganism viability or physical barrier

against acids from bacterial origin.120

A second clinical study on sealed (Concise

Sealant; 2 years, 50 patients) proximal sur-

faces17 (no data could be combined with the

latter trial,118 due to the diversity between the

studies) revealed that only 7% to 8% of the

sealed lesions showed progression, com-

pared to a 12% rate in the control group (flu-

oride varnish).17 This study did not use sub-

traction radiography for evaluation; thus, the

evaluated values are best compared to the

individual visual assessment values of the

study mentioned above; here, the correspon-

ding values were 9.7% for sealed lesions and

26.4% for the control group.118 In total, these

results show a tendency that would be com-

parable with the outcomes of a recent study

on occlusal fissure sealing; here, caries pro-

gression was highest in the control group,

and this was followed by the fluoride varnish

and the sealing group as well.121 However,

more clinical studies are clearly warranted.

Orthodontic treatment with fixed appli-

ances has been associated with white spot

lesions that often occur in otherwise well-

treated cases. The overall prevalence among

orthodontic patients is comparably high (up

to 44%),122 depending on the methods used

to assess and score decalcification, the pres-

ence of decalcification before treatment, and

the use of fluoride supplements during treat-

ment. A recent study revealed that the used

sealant (UltraSeal XT Plus, Ultradent) suc-

ceeded in preventing enamel from deminer-

alization. Unsealed teeth had a 3.8 times

greater number of white spot lesions than did

the teeth with sealants.123 However, it is inter-

esting to note that the sealant failed to protect

the entire enamel surface in 2 patients, obvi-

ously because of a failure of the sealant to

completely bond to the enamel surface,123

thus indicating that a thorough control of the

technique seems mandatory. Up to now, stud-

ies on infiltrant or sealant retention on (proxi-

mal) smooth surfaces with incipient lesions

are lacking. Nonetheless, a recent clinical

study on (proximal) adhesive patches showed

promising results since lesion progress was

predominantly arrested and remained stable

over a 2-year period, even after loss of the

patch. This indicated the postive effects of the

underlying bonding material.124

Advantages of the resin infiltrationconceptCaries-related clinical decision making

remains a centerpiece of clinical dentistry.

However, most dentistry still is re-dentistry

(with continued restorative procedures nec-

essary within the life span of the patient), and

the traditional core skills, along with the man-

ual dexterity and technical competence, have

less to offer to oral health than many clini-

cians have been accustomed to think. From

the foregoing review, it seems clear that the

resin infiltration technique bears several

advantages. These include:

• Mechanical stabilization of demineralized

enamel




Kielbassa et a l

• Preservation of sound hard substance

(protection of both the same and the adja-

cent tooth)

• Permanent occlusion of superficial micro-

pores and cavities

• Obturation of porous, deeply demineral-

ized areas

• Arrest of lesion progress

• Minimized risk of secondary caries

• Delay of restorative intervention for longer

periods

• No risk of postoperative sensitivity and

pulpal inflammation

• Reduced risk of gingivitis and periodontitis

• Improved esthetic outcome when used as

a “masking” resin on demineralized labial

surfaces (white spot lesions, ie, with ortho-

dontic patients)

• High patient acceptance

Figs 7a to 7h Preoperative view (a) revealing proximal caries at the mesial aspect of the maxillary lateral incisor. Rubber dam is neces-sary with the resin infiltration technique. After a sectional impression, SEM (b) revealed the cavitation present on the mesial surface.(c) Conditioning of the surface with hydrochloric acid (120 seconds; protection of neighboring tooth with metal matrix) was followed byexcessive drying (using alcohol and air blast). (d) Application of experimental resin infiltrant (2 times, with surplus) was followed by photo-polymerization (40 seconds). (e) Removal of polymerized surplus with a polishing strip. (f) Postoperative view. (g) Clinical situation 4 weeksafter treatment (with recovered papilla). (h) SEM of resin-infiltrated surface after sectional impression (4 weeks after treatment) revealingsubstantial flattening of lesion area.

a b c

g h

d e f




Kielbassa et a l

Therefore, regarding the impact on the

clinical decision process, a longitudinal clini-

cal risk assessment to discriminate between

progressive and remineralized lesions should

be established. Within the concept of minimal

intervention dentistry,7 the infiltration

approach seems suitable in case of early

treatment decision needs; at the same time,

even for later stages of the caries process

(in case remineralization with fluorides is not

considered a viable approach) this concept

should be an alternative to any type of cavity

preparation (see Figs 6 and 7), thus at least

postponing (if not avoiding) sacrifice of sound

structures. For protection reasons, and to

ensure dryness, use of rubber dam is recom-

mended with the resin infiltration technique.

Finally, resin infiltrants can be combined with

conventional resin restorations in case of

more complex treatment situations (Fig 8),4,18

and this should help to preserve dental hard

tissues.

CONCLUSIONS

With regard to the implications for practice,

resin infiltrants and some (un)filled resins obvi-

ously have a favorable penetration potential in

subsurface enamel lesions. In view of the

results presented in the current review, the

resin infiltration technique is a promising

microinvasive approach to preserve (deminer-

alized) enamel. With the use of adequate

materials with a sufficient resistance to

mechanical and chemical degradation, and

with a careful application technique, lesion

arrest seems achievable on a supervised

basis, thus closing the gap between oral hy-

giene and minimally invasive dentistry, and

providing a wait-and-see position to both the

clinician and the patient.

When reflecting on the implications for

research, the number of clinical trials was

found to be small. Therefore, more high-quality

research is needed to evaluate to what extent

there is a difference in the effectiveness of infil-

trated lesions and sites to be preserved by oral

hygiene/fluoride programs; the carry-over

effect of fluoride applications cannot be totally

ruled out, and randomized controlled trials with

a parallel group design seem mandatory.

Moreover, there is need to study the reasons for

lesion progress, in vitro and in vivo; mechanical,

chemical, and biologic behavior of materials

used as infiltrants, with variations of application

procedures (repeated application after different

time intervals, possible needs for reinfiltration

regimens within preventive-oriented recalls),

are considered fields of major interest.

ACKNOWLEDGMENTS

The authors are indebted to Dr Christian Hartwig for the

drawing of Fig 2 (reproduced with permission of S.Karger AG,

Basel, Switzerland). The assistance of Mrs Helga Grundt

(Department of Operative Dentistry and Periodontology,

CharitéCentrum 3, Berlin, Germany) with the scanning elec-

tron micrographs is greatly appreciated. Charité-

Universitätsmedizin Berlin holds US (US10/432,271) and

European (EP06021966.4) patent applications for an infiltra-

tion technique for dental caries lesions in which 2 of the

authors are appointed as inventors. Development of a resin

infiltrant has been furthered by a collaboration between

Charité, Berlin, and DMG, Hamburg, Germany,. SInce March

2009,a resin infiltrant called Icon has been marketed by DMG.

Figs 8a to 8c (a) Preoperative view of a 22-year-old patient after orthodontic therapy, with gross caries lesions and frank cavities onlabial surfaces. (b) Finished restorations (microfilled composite resin; 1 week after treatment) of cavitations; demineralized areas (of allteeth) were etched and resin infiltrated. (c) Postoperative view, 13 months after treatment.

a b c




Kielbassa et a l

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