Present and Future Approaches

for the Control of Caries

Kenneth J. Anusavice, Ph.D., D.M.D.
Abstract: This article summarizes current and potential future approaches for the management of caries. Current surveys suggest
that traditional “drill, fill, and bill” dentistry is still widely practiced in the United States in spite of considerable evidence that
supports a minimally invasive treatment approach. Because there is a wide variability in treatment decisions on when and how to
prevent new lesions, on how to arrest the progression of existing lesions, and on when and how to place initial and replacement
restorations, the findings from some studies differ significantly from the results of other studies. While fluoride treatments are
known to prevent a percentage of new lesions, they do not have the ability to prevent all caries lesions. Modern management of
caries entails treating patients according to risk and monitoring early lesions in tooth surfaces that are not cavitated. Although we
know that the dmfs score for children is a powerful predictor of caries increment in permanent teeth of these children a few years
later, this score is rarely used in private practice as a measure of risk or as a measure of treatment success. Although these modern
methods for caries management offer great promise for controlling the disease, they may take decades to apply in a standardized
way so that the variability in treatment is reduced. However, during the next two decades, an alternative approach to caries
prevention such as replacement therapy and a caries vaccine may become available as a more consistent method of controlling
this disease.
Dr. Anusavice is Associate Dean for Research and Chair of the Department of Dental Biomaterials at the University of Florida
College of Dentistry. Direct correspondence to him at Department of Dental Biomaterials, University of Florida, College of
Dentistry, P.O. Box 100446, Gainesville, FL 32610-0446; 352-392-4351 phone; 352-392-7808 fax; kanusavice@dental.ufl.edu.
Key words: caries, restorative dentistry, dental materials, fluoride, prevention, dental sealants, caries vaccine

A
lthough we have known for many years that
caries is an infectious disease, the manage-
ment of early and late stages of the disease
are still treated identically on state and regional den-
tal board exams and in dental practices, and treat-
ment decisions for caries management vary consid-
erably among practicing dentists.1-9 Early lesions
provide evidence of caries activity, which can be ar-
rested and the tooth surfaces remineralized through
appropriate treatment. However, because some cli-
nicians are not confident of their ability to detect early
lesions, to arrest the disease, and to remineralize dem-
ineralized enamel, restorations are often placed in-
dependent of the radiographic depth of the lesion.
Other clinicians practice minimally invasive dentistry
and monitor early lesions after initial treatment to
ensure that the caries activity is arrested and that the
enamel can be remineralized.10-18 Thus, there is con-
siderable variability in caries detection, caries activ-
ity assessment, caries risk assessment, the best treat-
ment options for high-risk patients, decisions on
when and how to treat teeth with carious lesions, and
the best method for monitoring disease.
A shift in emphasis appears to have occurred
in dental schools toward assessment of caries risk,
modern management of the disease, and delayed res-
toration until the probability of cavitation has in-
creased to a critical threshold level. Based on survey
responses from forty-two of fifty-five dental schools
on the threshold required for surgical intervention,
Yorty and Brown19 reported that only 30 percent of
responding schools allowed teeth to be restored to
satisfy clinical requirements and competencies when
radiographs indicated evidence of enamel lesions. At
70 percent of the responding schools, restorations
were not indicated until the lesions were classified
either as being in the outer third of dentin (D1) (55
percent), the middle third of dentin (D2) (10 percent),
or the inner third of dentin (D3) (5 percent). Also, 81
percent of the forty-two respondents reported hav-
ing a formal caries risk training program for
predoctoral dental students. Thirty-six percent of
thirty-nine schools have caries risk assessment re-
quirements for graduation, and 38 percent of the
schools require caries risk assessment for clinical
competencies. Multiple new or active caries lesions
were given as the most commonly used criterion for
classification of a patient at high risk.
However, a 2001 survey of requirements on
state and regional board exams indicates that estab-
lished clinicians responsible for dental board exami-
nations still allow enamel lesions to be restored.1 Ap-
proximately 72 percent of the states allowed teeth
with lesions either in the outer half of enamel (E1)
or inner half of enamel (E2) lesion to be restored.
About 37 percent of these states allowed teeth with

538 Journal of Dental Education ■ Volume 69, Number 5

an E1 lesion to be restored. Only twelve of the forty-
six states (26 percent) covered by these boards did
not allow teeth with E1 or E2 lesions to be surgi-
cally treated.
Premature surgical intervention and placement
of restorations may lead to overtreatment and the
earlier introduction of the restoration life cycle, which
may result in larger and larger subsequent replace-
ment restorations and shorter associated survival
times. However, as restorations increase in size and
cusp replacements are involved in high caries-risk
patients, none of the current restorative materials are
entirely satisfactory for long-term durability.20 For
restorations with fewer than four surfaces, second-
ary caries is likely to lead to replacement decisions,
while for four-surface situations, fractures are more
likely to occur.21
Future methods of caries lesion detection and
measurements of therapeutic outcomes used to pre-
vent or control the disease will employ to a greater
extent improved diagnostic devices that can accu-
rately detect early lesions, “hidden” occlusal lesions,
and provide 3D images of the demineralized regions.
During the transition period, better diagnostic devices
and methods will be introduced to enhance the sen-
sitivity and specificity of caries detection and lesion
depth estimation. In addition, some clinicians advo-
cate the use of air abrasion to confirm the suspected
presence of carious lesions in pit or fissure areas.22 It
is clear that concepts of minimal intervention den-
tistry are becoming more widely accepted.15
This improved imaging capability will provide
greater support to promote the principles of mini-
mally invasive dentistry including caries risk assess-
ment, monitoring of noncavitated carious tooth sur-
faces, remineralization therapy, and use of “smart”
preventive and restorative materials that will improve
our ability to monitor disease activity and the out-
comes of preservative therapies.
In addition to the use of conventional physical
and chemotherapeutic methods of caries manage-
ment, future prevention methods may also include
replacement therapy (probiotics) and/or vaccines. For
caries-active individuals, acidogenic and acid-toler-
ant gram-positive bacteria such as mutans strepto-
cocci and lactobacilli abound relative to acid-sensi-
tive species associated with sound enamel. One of
the replacement therapy options entails the applica-
tion of a genetically engineered “effector strain” of
S. mutans that will replace the cariogenic or “wild
strain” to prevent or arrest caries and to promote
optimal remineralization of tooth surfaces that have
May 2005 ■ Journal of Dental Education
been demineralized but that have not become cavi-
tated.23-26 Another approach is based on a genetic
modification of two plaque streptococci to create
organisms that produce ammonia from urea and argi-
nine. These organisms will reside in dental plaque,
and the ammonia produced from salivary and dietary
substrates will prevent the colonization of cariogenic
bacteria and ensure internal pH homeostasis.27
This review summarizes the principles, ben-
efits, and drawbacks of four caries management ap-
proaches likely to coexist in the near future to sup-
port our societal need to either prevent this infectious
disease or to significantly reduce its activity level
and the potential costly consequences of disease
progression.
Physical/Mechanical and
Chemotherapeutic
Approaches to Caries
Management
Caries is a disease caused by a group of oral
streptococcal micro-organisms, comprised primarily
of S. mutans, that occurs in three phases: 1) initial
interaction with the tooth surface mediated by
adhesins; 2) accumulation of the bacteria in a biofilm
and the production of glucose and glucans by the
bacterial enzyme glucosyl transferase; and 3) the
formation of lactic acid.
Three current methods of caries management
include traditional prevention (prophylaxis and fluo-
ride) and early surgical intervention; traditional pre-
vention and minimal intervention; and risk assess-
ment, prevention assessment, variable recall periods
based on risk, lesion monitoring, and delayed inter-
vention. The main steps involved in the third method
are shown schematically in Figure 1.
Recent evidence suggests that only 40.9 per-
cent of proximal surfaces of permanent teeth and 28.3
percent of primary teeth with lesions in the outer half
of dentin are not cavitated.28 This means that teeth with
such lesions can be monitored rather than restored until
the lesion has progressed well into dentin.
Early detection of carious lesions and assess-
ment of disease activity provide a greater opportu-
nity to limit the extent of demineralization associ-
ated with the disease process. Bjørndal and
Thylstrup29 demonstrated through histological analy-
ses that the size of a caries lesion along the
539

Lesion
Detection
and
Severity
Assessment
Monitoring
Risk Assessment
and Treatment
Disease
Control
Figure 1. Management plan for treatment of caries as an infectious disease
dentinoenamel junction (DEJ) is controlled by the
size of the outer enamel lesion (Figure 2). The chance
to prevent further enamel demineralization and po-
tentially to remineralize the affected enamel struc-
ture can markedly limit the size of restorations placed
(if needed) and, more importantly, it may eliminate
the need for a restoration altogether.
The minimally invasive dentistry approach is
based on assessment of caries risk and control of
caries as an infectious disease process. Thus, deci-
sions to restore are delayed until it is clear that tooth
surfaces are cavitated or are likely to become cavi-
Figure 2. The size of a carious lesion along the DEJ (smaller vertical bar) is related to the size of outer enamel lesion
(larger vertical bar).
540
tated despite all practical preventive
and remineralization efforts.
According to the study of
Pitts and Rimmer, 28 lesions in
enamel should not be restored since
only 10.5 percent of permanent
teeth are likely to be cavitated when
proximal lesions are in the inner
half of enamel (Figure 3). Thus, a
classification of lesion severity is
important since decisions on when
to restore can be made on a more
standardized basis. One common
classification system consists of E0
(no lesion), E1 (lesion within the
outer half of enamel), E2 (inner half
of enamel), D1 (outer third of den-
tin), D2 (middle third of dentin), and
D3 (inner third of dentin). Radio-
graphs of the same tooth with no lesion (E0), an E2
lesion, and a D1 lesion are shown in Figure 4.
The primary public health measures are the use
of topical fluoride agents and fluoridated water. Tra-
ditional physical/mechanical methods of caries pre-
vention in the United States include oral hygiene pro-
cedures (tooth brushing, flossing, and professional
tooth debridement). Fluoride-containing and triclosan-
containing toothpastes provide chemotherapeutic ben-
efits as well. However, professionally prescribed che-
motherapeutic agents are often applied to further
reduce the caries risk of susceptible individuals.
Journal of Dental Education ■ Volume 69, Number 5
 100
95.5
100
Primary Teeth
Percent Cavitation

80 Permanent Teeth

60
40.9
40 28.3

20 10.5
2 0 2.9
0
Outer 1⁄2 Inner 1⁄2 Outer 1⁄2 Inner ⁄2
1

Enamel Enamel Dentin Dentin

Lesion Severity

Figure 3. Percent cavitation of proximal surfaces of primary and permanent teeth as a function of lesion severity

Chemotherapeutic agents such as

those containing fluorine and
chlorhexidine may also be prescribed
and applied at home, in the office, or in
both places. These include fluoride var-
nish, fluoride gel, chlorhexidine, and
fluoride-releasing restoratives.
Chlorhexidine varnish is also available
in some countries.
Figure 4. Radiographs of E0, E2, and D1 lesions

Fluoride Toothpaste
Marinho et al.30 performed a search of the
Cochrane Oral Health Group’s Trials Register (2000)
plus several other databases on randomized or quasi-
randomized controlled trials with blind outcome as-
sessment to analyze comparative caries prevention
data for fluoride toothpaste with placebo in children
up to sixteen years during at least one year. The
pooled DMFS (decayed, missing, and filled tooth
surfaces) prevented fraction was 24 percent
(p<0.0001), indicating that 1.6 children need to brush
with a fluoride toothpaste (rather than a nonfluoride
toothpaste) over three years to prevent one DMFS in
populations with an annual caries increment of 2.6
DMFS. In populations with an annual caries incre-
ment of 1.1 DMFS, 3.7 children will need to use a
fluoride toothpaste for three years to avoid one
DMFS. They concluded that the benefits of fluoride
toothpaste are firmly established.

May 2005 ■ Journal of Dental Education 541

 However, daily toothbrushing by children with
a fluoridated toothpaste alone is unlikely to prevent
all new caries lesions. Saporito et al.31 reported that
twice daily toothbrushing with toothpaste contain-
ing 0.243 percent NaF or 0.76 percent sodium
monofluorophosphate toothpastes by U.S. and Puerto
Rican children in the third, fourth, and fifth grades
resulted in caries increments (DFS: decayed and
filled tooth surfaces) of 1.68 and 1.70, respectively,
after one year and 3.56 and 3.56, respectively, after
two years.
For adults, the use of a 0.243 percent NaF tooth-
paste containing 0.3 percent triclosan resulted in a
12.2 percent reduction in caries increment (DFS) after
one year and a 16.6 percent reduction after two
years.32 The reduction at two years was significantly
greater than that associated with a comparable tooth-
paste without triclosan. Triclosan (a diphenyl ether
[bis-phenyl] derivative, known as either 2,4,4’-
trichloro-2’-hydroxydiphenyl ether or 5-Chloro-2-
[2,4-dichlorophenoxy] phenol) is a broad-spectrum
antibacterial agent with bacteriostatic activity against
a wide range of both gram-negative and gram-posi-
tive bacteria. Although some studies suggest the safety
of triclosan in toothpastes,33,34 this topic has been the
center of considerable debate, and further investiga-
tion is needed to resolve these uncertainties.
Fluoridated Water
The CDC in 2001 issued recommendations re-
garding the use of fluoride to prevent and control
dental caries.35 Based on studies that suggest frequent
exposure to small amounts of daily fluoride will ef-
fectively reduce the risk for dental caries in all age
groups, the CDC work group recommended that all
dentate individuals drink water with an optimal fluo-
ride concentration and brush their teeth twice daily
with fluoride toothpaste. However, the group empha-
sized that additional fluoride measures might be
needed for persons at high risk for dental caries and
that controlled (measured) use of supplementary fluo-
ride modalities is particularly appropriate during
anterior tooth enamel development (age <6 years).
For caries prevention regimens to be as effec-
tive as possible, transfer of research evidence to the
practicing dental team is crucially important. Based
on a survey of 498 U.S. dental hygienists in 2000,
Forrest et al.36 reported that more than 40 percent of
the hygienists did not recognize remineralization as
the most important mechanism of action of fluoride,
and fewer than 50 percent of the survey respondents
542
recognized that dental caries is a chronic infectious
disease. An analysis of four factors related to knowl-
edge and practice showed that younger graduates,
recent graduates, and members of the American Den-
tal Hygiene Association were more knowledgeable
about the effectiveness of caries preventive proce-
dures for children (p<0.01). Although a majority of
respondents knew that adults benefited from fluo-
ride and that root caries was an emerging problem,
this knowledge was not consistent with treatment
provided in their dental practices (p=.02). Less than
35 percent of the hygienists reported that they pro-
vide fluoride to adults of any age or that they waited
until the disease was present before fluoride is ap-
plied. A 1-min application of an APF gel or foam
was most often provided to children and adults who
were given fluoride treatments. The respondents gen-
erally overrated the effectiveness of flossing and
toothbrushing while underrating the effectiveness of
fluorides.
Fluoride Mouthrinses, Toothpaste,
and Gel
Marinho et al.37 reviewed the literature for ran-
domized or quasi-randomized controlled trials with
blind outcome assessment, comparing fluoride
mouthrinse with placebo or no treatment in children
up to sixteen years during at least one year. The main
outcome was caries increment measured by the
change in decayed, missing, and filled tooth surfaces
(D[M]FS). Based on the results of thirty-four stud-
ies, they concluded that fluoride rinses led to a pre-
vented fraction of 26 percent (23 to 30 percent). Thus,
in populations of children with a caries increment of
0.25 DFS per year, sixteen children will need to use
a mouthrinse to avoid one DFS. In populations hav-
ing a caries increment of 2.14 DFS, two children
would need to rinse to avoid one DFS.
Twetman et al.38 systematically reviewed and
evaluated the scientific literature between 1966 and
April 2003 on the caries preventive effect of fluo-
ride toothpastes in various age groups, with special
emphasis on fluoride concentration and supervised
versus nonsupervised toothbrushing. This systematic
search of electronic databases was conducted with
the inclusion criteria of a randomized or controlled
clinical trial, at least two years follow-up, and caries
increment in the permanent dentition (DMFS/T) or
primary dentition (DMFS/T) as an endpoint. The re-
sults of this review suggest 1) strong evidence for
Journal of Dental Education ■ Volume 69, Number 5
the caries preventive effect of daily use of fluoride
toothpaste compared with placebo in the young per-
manent dentition (prevented fraction of 24.9 percent);
2) a superior preventive effect of toothpastes con-
taining 1,500 ppm F compared with standard tooth-
pastes containing 1,000 ppm F in the young perma-
nent dentition (prevented fraction of 9.7 percent); and
3) higher caries reductions in studies with supervised
toothbrushing compared with nonsupervised (pre-
vented fraction of 23.3 percent). Evidence to sup-
port the effect of fluoride toothpaste in the primary
dentition was incomplete. This study supported the
effectiveness of daily toothbrushing with fluoridated
toothpastes for caries prevention, although long-term
studies are still lacking for adults.
Based on a systematic review of seventy-four
studies by Marinho et al.,39 the pooled prevented frac-
tion was 24 percent (21-28 percent). This indicates
that 1.6 children would need to brush their teeth with
a fluoridated toothpaste to prevent one DFS in popu-
lations with a caries increment of 2.6 DFS per year.
If the population caries increment was 1.1 D(M)FS
per year, 3.7 children would need to use a fluoride
toothpaste to avoid one D(M)FS.
Marinho et al.40 performed a systematic review
of twenty-three randomized or quasi-randomized
controlled trials with blind outcome assessment, com-
paring fluoride gel with placebo or no treatment in
children up to sixteen years during at least one year.
The main outcome was caries increment measured
by the change in decayed, missing, and filled tooth
surfaces (D[M]FS). They found a prevented fraction
of 28 percent (19-37 percent). The prevented frac-
tion (PF) was, on average, 19 percent higher than
that in the nonplacebo controlled trials. Based on a
comparison with fourteen placebo-controlled trials,
a reduction of 21 percent should occur in D(M)FS,
indicating that two individuals would have to be
treated in a population with a caries increment of 2.2
D(M)FS per year or twenty-four would need to be
treated in a population with a caries increment of 0.2
D(M)FS per year.
Professionally Applied Fluoride
Supplemented with Fluoride from
Toothpaste
Splieth et al.41 raised the question of whether
traditional caries prevention programs that target
specific groups are still effective. Given the caries
decline of approximately 80 percent in children re-
May 2005 ■ Journal of Dental Education
siding in Western Europe and other industrialized
countries, they emphasized the need to identify the
optimal method to control future caries prevention.
Regular fluoride application in a dental office plus
the use of a fluoride toothpaste has achieved signifi-
cant caries reductions over the past two decades.
However, these therapies have caused a skewed dis-
tribution of high-risk individuals. These investiga-
tors suggest that topical fluoride applications at a fre-
quency of six or more times per year combined with
effective plaque removal can successfully prevent
caries in high caries-risk groups. They further con-
clude that oral health promotion programs that are
only educational in nature and do not include fluo-
ride treatment may not be effective. Furthermore,
preventive measures performed at home or in a pri-
vate practice are associated with minimal compliance
in high-risk groups. Thus, they suggest that outreach-
ing programs that ensure more consistent control over
caries management will be more effective.
Marinho et al.39 concluded that topical fluorides
(mouthrinses, gels, or varnishes) used in addition to
fluoride toothpaste achieved a modest caries reduc-
tion (10 percent prevented fraction, p=0.01) com-
pared to toothpaste alone. The combined use of fluo-
ride gel and a fluoride mouthrinse resulted in a
prevented fraction of 23 percent (p=0.02).
Zimmer et al.42 conducted a randomized con-
trolled clinical trial on high-risk children who re-
ceived professional tooth cleaning and an applica-
tion of 0.1 percent NaF fluoride varnish four times
per year and concluded that “it might not be possible
to prevent caries in high-risk children by means of
the described program.”
Fluoride Varnish
Based on another systematic review, Bader et
al.43 assessed the strength of the evidence for the ef-
ficacy of professional caries preventive methods for
high caries-risk individuals and the efficacy of pro-
fessional treatment regimens to arrest or reverse
noncavitated carious lesions. A search of 1,435 ar-
ticles resulted in twenty-two studies that evaluated
the prevention of carious lesions in caries-active or
high-risk individuals. Overall, the strength of the
evidence was “fair” for fluoride varnishes and “in-
sufficient” for all other methods. For seven other
studies related to the management of noncavitated
carious lesions, the strength of evidence for efficacy
was “insufficient” for all treatment methods. These
results suggest that our previous data on the efficacy
543
 of the methods are inadequate to permit definitive
recommendations to be made for individual patients
with specific caries risk levels.
Mejare et al.44 also performed a systematic re-
view and reported that resin sealants produced a rela-
tive caries reduction of 33 percent over a period of
at least two years in permanent first molars of chil-
dren up to age fourteen. They concluded that there is
limited evidence to prove that fissure sealing of first
permanent molars with resin-based materials has a
caries-preventive effect and that the evidence is in-
complete for permanent second molars, premolars,
and primary molars and for glass ionomer cements
used as sealants.
A Cochrane Review of sealants in the perma-
nent teeth of five to ten year old children by Ahovuo-
Saloranta et al.45 revealed caries reductions ranging
from 86 percent at twelve months to 57 percent at
forty-eight to fifty-four months. The authors recom-
mended sealing occlusal surfaces of permanent mo-
lars with resin-based sealants to prevent caries al-
though they recommend that the caries prevalence
level of both individuals and the population should
be taken into account.
Petersson et al.46 evaluated the caries-preven-
tive effect of professional fluoride varnish treatments
based on a systematic search of the literature for ar-
ticles published between 1966 and August 2003. Of
302 identified papers, twenty-four reports were in-
cluded from randomized and controlled clinical tri-
als comparing fluoride varnish with placebo, no ac-
tive treatment, or other fluoride preventive regimens
with at least two years’ duration. The results suggest
limited evidence for the caries preventive effect of
topical fluoride varnish applied to permanent teeth.
The average prevented fraction was 30 percent (0-
69 percent) compared with untreated controls. In-
conclusive evidence was reported for fluoride var-
nish application to primary teeth and to posterior adult
teeth.
Marinho et al.47 conducted an evidence-based
review of randomized or quasi-randomized con-
trolled trials with blind outcome assessment for the
use of fluoride varnish in children up to sixteen years
during at least one year. They reported a prevented
fraction (DFS) of 46 percent (30 to 63 percent) based
on seven selected studies. This review suggests a
substantial caries-inhibiting effect of fluoride varnish
in both the permanent and the deciduous dentitions
based largely on trials with no treatment controls.
544
Antibacterial and Antimicrobial
and Bactericidal Agents
Twetman48 examined recent evidence on the
use of antibacterial agents to prevent and control
caries and concluded that there is limited evidence
for the effectiveness of chlorhexidine (CHX) gels,
rinses, and toothpaste in preventing caries in the per-
manent teeth of children and adolescents. Twenty-
two of the interventions in controlled clinical trials
from 1995 to May 2003 were related to CHX-con-
taining varnishes. According to the ranking system
of the Swedish Council on Technology Assessment
in Health Care, the evidence for an anticaries effect
of CHX varnishes was inconclusive for caries-ac-
tive schoolchildren and adolescents with regular fluo-
ride exposure. A preventive effect of CHX varnishes
on fissure caries was demonstrated in four out of five
studies, when compared with no treatment in chil-
dren with low fluoride exposure. The evidence for
arresting root caries in dry-mouth patients and frail
elderly subjects was also inconclusive.
Van Rijkom et al.49 performed a meta analysis
and reported a 46 percent prevented caries fraction
for individuals treated with chlorhexidine. Multiple
regression analysis revealed no significant difference
among the prevented fractions as a function of ap-
plication method, application frequency, caries risk,
fluoride regimen, and tooth surface. The prevented
fraction of chlorhexidine (46 percent) appears to be
comparable to that associated with the use of fluo-
ride varnish (Figure 5), and it tends to be more
effective than fluoride gels, rinses, and fluoride-
containing toothpaste.
One of the most controversial issues regarding
caries prevention using bactericidal or antibacterial
agents is whether chlorhexidine can be combined
with fluoride in either a gel or solution form. Some
evidence suggests that the positively charged chlor-
hexidine ion and the negatively charged fluoride ion
do not necessarily negate the action of each other.
Katz50 reported that individuals who were irradiated
for head and neck cancer and who received a com-
bined treatment of four topical applications of 1.0
percent sodium fluoride-1.0 percent chlorhexidine
digluconate gel plus daily rinses with an 0.05 per-
cent sodium fluoride-0.2 percent chlorhexidine
solution had no new lesions in the subsequent six- to
ten-month period. This treatment also resulted in
remineralization of existing incipient lesions. The
chlorhexidine-fluoride rinses alone also prevented
Journal of Dental Education ■ Volume 69, Number 5
 80
Prevented Fraction (%)
60
40
24
21
20
0
FG TP
Figure 5. Prevented fraction (∆
∆DMFS) for various prevention methods
FG=fluoride gel; TP=fluoride-containing toothpaste; FR=fluoride rinse; V1=fluoride varnish for primary teeth; V=all fluoride
varnish applications; V2=fluoride varnish for permanent teeth; CHX=all chlorhexidine applications; SEAL=pit and fissure
sealant
radiation caries but did not permit remineralization
to occur. The four topical applications with a fluo-
ride gel and daily rinses with an 0.05 percent sodium
fluoride solution were inadequate to prevent radia-
tion caries.
Ogaard et al.51 conducted a randomized pro-
spective clinical study with 220 patients scheduled
for fixed orthodontic therapy to test the hypothesis
that application of Cervitec: antimicrobial varnish,
which contained 1 percent chlorhexidine plus 1 per-
cent thymol (Ivoclar Vivadent, Schaan,
Liechtenstein) in combination with Fluor Protector
(Ivoclar Vivadent, Schaan, Liechtenstein), a varnish
containing 5 percent difluorosilane (Group 1) was
significantly more effective in reducing white spot
lesions on the facial surfaces than application of the
fluoride varnish alone (Group 2). The antimicrobial
varnish significantly reduced the number of mutans
streptococci in plaque during the first forty-eight
weeks of treatment. This result was not associated
with significantly fewer white spot lesions on the
facial surfaces compared with the group receiving
only the fluoride varnish application. However, the
May 2005 ■ Journal of Dental Education
71
46 46
40
33
26
FR V1 V V2 CHX SEAL
combination of the antimicrobial and fluoride var-
nishes more effectively reduced the caries increment
for the maxillary incisors. The investigators specu-
lated that this was partly caused by an inhibiting ef-
fect of the antimicrobial varnish in an area with low
oral clearance of fluorine ions and partly by an in-
hibiting effect of the varnish on mutans streptococci
(ms).
Tenovuo et al.52 demonstrated that if mothers
with ms levels higher than 105 CFU/mL were given
1 percent chlorhexidine-0.2 percent sodium fluoride
gel treatments twice a year for three years (Group 1),
the primary teeth of their children (from age one to
four years) would have less colonization by ms and
they would have fewer lesions than the children of
mothers with high ms counts (>105 CFU/mL) who
did not receive the combined gel treatment (Control
Group 2). In the total study population of 151 chil-
dren, 16 percent, 42 percent, and 54 percent of the
children were colonized by ms by the ages of two,
three, and four years, respectively. Most children
were colonized only by S. mutans, but two had both
S. mutans and S. sobrinus, and two had only S.
545
 sobrinus. Twenty-eight percent of the ms-positive
children developed caries by the age of four years,
whereas 14.8 percent of the children with dental car-
ies did not have any detectable ms in their plaque
samples. The colonization by ms and the caries inci-
dence were highest in the children of Control Group
1 and lower in the children of mothers in experimen-
tal Group 1 and in Control Group 2 (ms counts of
<105 CFU/mL and no gel treatments). The results of
this study suggest that the reduction of maternal sali-
vary ms at the time of tooth emergence may delay,
or even prevent, the colonization of ms in the
children’s primary teeth with a corresponding de-
crease in caries incidence, even in a population with
an already low prevalence of dental caries.
Ullsfoss et al.53 investigated the effect of two
daily rinses with 2.2 mM chlorhexidine and one daily
rinse with 11.9 mM NaF in an in vivo human caries
model using plaque-retaining bands on premolar
teeth scheduled for extraction. A total of twenty-eight
teeth were fitted with the bands for four weeks. The
tooth surfaces were analyzed by microradiography
after the teeth were extracted. The combination of
chlorhexidine and flouride rinses resulted in a slightly
greater loss of enamel mineral compared with that
observed in “sound” enamel and clearly less than that
associated with flouride rinses alone. Both total
plaque bacteria and S. mutans were reduced by
chlorhexidine rinses.
Xylitol
There appears to be some benefit for caries
prevention by using xylitol as a sugar substitute in
toothpaste, chewing gum, and other products used or
consumed intraorally. Mäkinen et al.54 reported a sig-
nificant reduction in caries increment for children who
were given a xylitol-containing chewing gum for up
to five times per day. Isokangas et al.55 have shown
that regular maternal use of xylitol chewing gum by
195 mothers with high salivary ms levels resulted in a
statistically significant reduction in ms colonization
in their children’s teeth at the age of two compared
with the teeth of children whose mothers received fluo-
ride or chlorhexidine varnish treatment. At the age of
five, the dentinal caries (DMFS) in the xylitol group
was reduced by about 70 percent compared with that
in the fluoride or chlorhexidine groups. The authors
concluded that the maternal use of xylitol chewing
gum can prevent dental caries in children by prevent-
ing the transmission of mutans streptococci from
mother to child. However, based on a systematic re-
546
view of eighteen articles that met the criteria suggested
by the Swedish Council on Technology in Health Care,
Lingstrom et al.56 concluded that the evidence for the
use of sorbitol or xylitol in chewing gum was incon-
clusive and they recommended more well-designed,
randomized clinical trials with adequate control groups
and acceptable compliance.
Ozone Technology
The ability of ozone gas (O3) to kill bacteria,
fungi, and viruses is well known.57,58 However, al-
though useful bactericidal action against a variety of
human pathogens has been reported for ozone con-
centrations between 0.3 to 0.9 ppm, these bacteri-
cidal ozone concentrations are close to the limit per-
mitted for human exposure.58 Few well-controlled
studies have been performed to investigate the bac-
tericidal effect of various doses of ozone gas on oral
microorganisms. Oizumi et al.59 reported that an
ozone generator using 20 mg/h of ozone was required
to disinfect dentures that contained Streptococcus
mutans (strain IID 973), Staphylococcus aureus
(strain 209-P), and Candida albicans (strain LAM
14322).
The evidence to support the use of ozone gas
to prevent caries and to enhance remineralization of
demineralized enamel is limited. In vitro and in vivo
reports support the potential to arrest caries and to
possibly remineralize demineralized tooth struc-
ture.60-62 Rickard et al.63 performed a systematic as-
sessment of the scientific literature to assess whether
ozone is effective in arresting or reversing the pro-
gression of dental caries. Three trials were included,
with a combined total of 432 randomized lesions (137
participants). Individual studies revealed inconsis-
tent effects of ozone on management of caries le-
sions as a function of different measures of caries
progression or regression. Few studies of secondary
outcomes have been performed, and only one trial
has reported an absence of adverse events. Because
of the high risk of bias in the available studies and
the lack of consistent results between different out-
come measures, the authors conclude that there is
no reliable evidence to support the application of
ozone gas to the surface of decayed teeth to arrest or
reverse the demineralization process. They concluded
that more evidence of appropriate rigor and quality
is required before ozone can be accepted for primary
dental care or as an alternative to current methods
for the management and treatment of dental caries.
Journal of Dental Education ■ Volume 69, Number 5
 against known bacterial pathogens. Recent progress
Summary of Current is particularly evident in the application of avirulent
Streptococcus mutans to control dental caries, alpha
Treatment Methods hemolytic streptococci to reduce otitis media recur-
rences, and Streptococcus salivarius to prevent strep-
Clearly, systematic reviews of the literature do
tococcal pharyngitis.69
not produce conclusive support on the best methods
Replacement therapy involves the use of a
for preventing new caries lesions or preventing the
harmless effector strain that is permanently colonized
propagation of existing lesions. There is even far less
in the host’s microflora. This effector strain is de-
evidence to support the use of any therapeutic regi-
signed to prevent the colonization or outgrowth of a
mens to prevent or control secondary caries although
particular pathogen.
some evidence exists to support the assumption that
Many reports have described both positive and
secondary caries behaves like primary caries.64,65
negative bacterial interactions in which a specific
However, we must apply the “best knowledge” avail-
indigenous microorganism promotes or blocks the
able to control or prevent the disease in this popula-
presence of a pathogen. To prevent an infection us-
tion of individuals at risk for the disease. In the ab-
ing replacement therapy (recently referred to as
sence of a comprehensive body of conclusive clinical
probiotic therapy), a natural or genetically modified
results, modern caries management must be based
effector strain is used to intentionally colonize the
on the principles of disease management. These in-
sites in susceptible host tissues that are normally
clude accurate lesion detection, classification of le-
colonized by a pathogen. If the effector strain is bet-
sion severity, assessment of caries risk, matching of
ter adapted than the pathogen, colonization or out-
treatment to the risk level, monitoring for evidence
growth of the pathogen will be prevented by block-
of remineralization or further demineralization, and
ing the attachment sites, by competing for essential
assigning recall intervals according to treatment out-
nutrients, or via other mechanisms. As long as the
comes and current risk levels.
effector strain persists as a resident of the indigenous
A remaining concern regarding the multiple use
flora, the host is protected potentially for an unlim-
of fluoride regimens is the risk for fluorosis. Because
ited period of time.
of limited data on the cumulative ingestion of fluo-
S. mutans strain BCS3-L1 is a genetically
ride from drinking water, fluoride-containing tooth-
modified effector strain designed for use in replace-
paste, and other sources, the prevalence of fluorosis
ment therapy to prevent dental caries.23 To be an ef-
should be monitored to ensure that children are not
fective effector strain, BCS3-L1 must satisfy four
being overdosed with fluoride used for caries treat-
prerequisites:
ment.66
1. It must have a significantly reduced pathogenic
potential to promote caries.70
Replacement Therapy 2. It must persistently colonize the S. mutans sites,
Among indigenous oral microorganisms are thereby preventing colonization by disease-caus-
those bacteria that have a significant pathogenic po- ing strains whenever the host comes into con-
tential for the host. Caries-promoting bacteria include tact with them.
S. mutans and lactobacilli. Although S. mutans has 3. It must aggressively displace indigenous strains
an affinity for attachment to tooth surfaces, Lacto- of S. mutans and allow previously infected sub-
bacillus casei and Lactobacillus fermenti have a low jects to be treated with replacement therapy.
affinity for oral surfaces, suggesting that their asso- 4. It must be safe and not make the host suscep-
tible to other disease conditions.
ciation with carious lesions may be related to me-
Regarding its pathogenicity, lactate dehydro-
chanical adherence.67 Scientists have investigated
genase (LDH) deficiency can be used as the approach
numerous mechanisms to intervene in these bacte-
for reducing acidogenicity in the construction of the
rial interactions. Ingestion of probiotic bacteria, par-
BCS3-L1 strain.70 Cloning the structural gene encod-
ticularly lactobacilli,68 is commonly practiced to pro-
ing the S. mutans LDH provided the basis for pro-
mote well-balanced intestinal microflora. As bacterial
ducing LDH-deficient clones,71,72 suggesting that
resistance to antimicrobial agents has increased, so
LDH-deficiency was a lethal mutation in most S.
too has research into colonization of human tissues
mutans strains. However, at high sugar concentra-
with specific effector strains capable of competing
tions, the levels of activity of these enzymes are ap-

May 2005 ■ Journal of Dental Education 547

 parently insufficient to compensate for the absence
of LDH. A supplemental alcohol dehydrogenase
(ADH) activity can complement the LDH deficiency
when expressed in the temperature sensitive LDH
mutant.73
Recombinant DNA technology was used to de-
lete the gene encoding lactate dehydrogenase in BCS3-
L1 making it unable to produce lactic acid.24 This ef-
fector strain was also designed to produce elevated
amounts of a novel peptide antibiotic called mutacin
1140 that gives it a strong selective advantage over
most other strains of S. mutans. This effector strain
has shown no measurable LDH activity, and it induces
a tenfold elevated level of ADH activity relative to its
JH1140 parent. Fermentation end-product analysis
revealed that BCS3-L1 made no detectable lactic
acid.23 As predicted from earlier work,74 most of the
metabolized carbon was converted to the neutral end-
products, ethanol and acetoin.
Under various cultivation conditions, includ-
ing growth on a variety of sugars and polyols, such
as sucrose, fructose, lactose, mannitol, and sorbitol,
BCS3-L1 yielded final pH values that were 0.4 to
1.2 pH units higher than those of its parent, JH1140.
The reduced acidogenic potential of BCS3-L1 re-
sulted in a greatly decreased cariogenic potential as
shown in several animal models.23 BCS3-L1 was sig-
nificantly less cariogenic than JH1140 in both gno-
tobiotic- and conventional-rodent models. It colo-
nized the teeth of conventional rats as well as JH1140
in both aggressive-displacement and preemptive-
colonization models. No gross or microscopic ab-
normalities of major organs were associated with oral
colonization of rats with BCS3-L1 for a period of
six months.23 The results of these studies provided
strong evidence that an LDH-deficient S. mutans
strain such as BCS3-L1 has significantly reduced
pathogenic potential, and thus satisfies the first pre-
requisite for use as an effector strain in replacement
therapy for dental caries.
Transmission of mutans streptococci within the
human population has been extensively studied. Most
studies support the idea that this organism is usually
transmitted from mother (primary caretaker) to child
within a several year period following the onset of
tooth eruption.75-79 Other studies75-83 have demon-
strated the difficulty of maintaining laboratory strains
of mutans streptococci in the mouths of humans, es-
pecially when they already had an indigenous strain
of this organism.
From a standpoint of replacement therapy for
caries prevention, implantation of an effector strain
548
would best be achieved in children immediately af-
ter tooth eruption and before the acquisition of a car-
ies-inducing strain. To prevent overcolonization by
wild-type strains when the host comes in contact with
them, an effector strain should have some signifi-
cant selective advantage to colonization. This would
also enable subjects who have already been infected
with a caries-inducing strain of S. mutans to be treated
by replacement therapy. Mutacin 1140 is capable of
killing virtually all other strains of mutans strepto-
cocci against which it was tested.84
To serve as an effector strain for the preven-
tion of dental caries, BCS3-L1 must be genetically
stable. Sufficient mutacin 1140 has not been puri-
fied to directly test its toxicity. However, the proto-
type lantibiotic, nisin, is known to have extremely
low toxicity,85,86 and has been developed and used
for decades as a food preservative that is generally
recognized as safe.
It is conceivable that mutacin production by
BCS3-L1 and the fermentation products resulting
from LDH deficiency could alter plaque ecology and
produce another microorganism with pathogenic
potential. The mutacin 1140 producing strain of S.
mutans eliminated mutacin-sensitive indigenous
strains of S. mutans but had no effect on indigenous
S. oralis strains that were equally sensitive to mutacin
killing in vitro.25 These results indicate that S. mutans
has a physically distinct habitat that is separated from
the S. oralis habitat by a distance sufficient for dilu-
tion to reduce the concentration of mutacin below
its minimal inhibitory concentration. A similar ex-
planation could account for the failure to observe
qualitative or quantitative changes in the plaque of
rats following long-term infection with an LDH de-
ficient mutant, even though the mutant’s metabolic
end-products are certain to be different from those
of the wild-type strain.74
A final aspect of replacement therapy safety is
the requirement for controlled spread of the effector
strain within the population. Mutacin 1140 up-pro-
duction clearly provides a selective advantage to
BCS3-L1 colonization. However, the minimum in-
fectious dose has not been determined for this strain
or any S. mutans strain in humans. Wives and chil-
dren of the two subjects infected with the mutacin
up-producing S. mutans strain were not colonized
when tested fourteen years after the initial infection
regimen (J.D. Hillman, personal communication).
Obviously, further studies with larger populations
need to be performed to measure the potential for
horizontal transmission. It is expected that, like wild-
Journal of Dental Education ■ Volume 69, Number 5
type strains of S. mutans, vertical transmission of
BCS3-L1 from mother to child will occur at a high
frequency. The reduced pathogenic potential of the
BCS3-L1 probiotic strain, its proven colonization
potential, and its genetic stability support its poten-
tial use as an effector strain for replacement therapy
to prevent dental caries in human populations at risk
for this disease. The main advantages of this replace-
ment therapy include the lifelong protection provided
by a single application, the negligible risk for unto-
ward results, and the lack of a need for patient edu-
cation and compliance that are required for conven-
tional oral hygiene regimens.
A clinical trial began early in 2005 to test the
effectiveness of replacement therapy. Thus, it is too
early to determine the potential of this treatment
method to prevent new caries lesions and to arrest
existing lesions without any significant side effects.
Genetically Engineered, Alkali-
Producing Streptococci
The pH of plaque fluid is a key environmental
factor affecting the physiology, ecology, and patho-
genicity of the oral biofilms colonizing the hard tis-
sues of the human mouth. Much attention has been
focused on controlling organic acids produced
through the metabolism of carbohydrates by patho-
genic oral bacteria. Oral bacteria can be genetically
modified to produce alkali environments, which may
be beneficial in preventing or arresting the caries
process. Recent evidence suggests that alkali gen-
eration may play a major role in pH homeostasis in
oral biofilms and it may moderate initiation and pro-
gression of dental caries. In a brief review, Burne
and Marquis27 have described a process of alkali gen-
eration resulting from ammonia produced from argi-
nine and urea. This process is associated with a ge-
netically altered strain of streptococci interacting with
components of dental plaque. No data are yet avail-
able from randomized, controlled clinical trials to
support the application of this potential therapy.
Caries Vaccine
This section describes methods by which mu-
cosal host defenses can be induced by immunization
to interfere with the colonization of mutans strepto-
cocci. Anticaries vaccines operate on the principle
of reducing the population of the indigenous bacte-
ria that are associated with the caries disease pro-
cess. The two-step process of vaccine development
May 2005 ■ Journal of Dental Education
involves identification of specific antigens of mutans
streptococci against which protective immune re-
sponses can be induced, and the application of an
immunization treatment method that will sustain
adequate levels of salivary antibodies. Key antigens
include streptococcal surface proteins that control
attachment to tooth surfaces and glucosyltransferases
that produce adhesive glucans from sucrose.87 Oral
application of specific antibodies against selected
antigens of mutans streptococci (passive immuniza-
tion) has produced promising results.
The feasibility of immunizing experimental
animals with protein antigens obtained from Strep-
tococcus mutans against oral colonization by mutans
streptococci has been demonstrated in several stud-
ies. Immunization is induced by IgA antibodies that
can inhibit mechanisms of streptococcal accumula-
tion on tooth surfaces depending on the choice of
vaccine antigen. Mucosal immunization is designed
to induce high levels of salivary antibodies that can
be sustained for extended periods and to ensure so-
called “immune memory.”88 Human studies have
shown that passively applied salivary antibodies to
mutans streptococci can suppress recolonization by
mutans streptococci. However, validation of vaccine
effectiveness will depend on the performance of can-
didate vaccines in clinical trials.88,89
Some methods of mucosal vaccine antigen de-
livery have resulted in inhibition of dental caries as-
sociated with S. mutans infection. Although passive
administration of antibodies to virulence antigens of
S. mutans has shown some promise, the caries-pro-
tective benefits of active immunization using caries
vaccines must be proven in pediatric clinical trials.90
For a caries vaccine to be accepted by the den-
tal profession, many questions need to be answered.
One of the most important questions is: what will be
the long-term effect of altering the indigenous oral
microflora? Also, can the highest caries activity level
of infection caused by the pathogen, Streptococcus
mutans, be inactivated immunologically? Which en-
try pathways of S. mutans into the dental biofilm can
be controlled by immunization? Can an immune re-
sponse be induced by virulence factors associated
with S. mutans? How safe are caries vaccines rela-
tive to other caries prevention regimens? Will the
profession adopt vaccination as a caries prevention
mechanism given the greatly reduced caries preva-
lence over the past several decades?
Considerable evidence exists to confirm Strep-
tococcus mutans as the primary caries-inducing
microorganism, and a cell-surface protein antigen,
549
 and glucosyltransferases and glucan binding proteins
as major colonization factors.91-95 It is believed that
mucosal induction of salivary IgA antibody to
glucosyltransferases inhibits the attachment to and
accumulation of S. mutans on hard tissue. A nasal
spray vaccine produces a better mucosal IgA response
compared with oral and tonsilar administration. Hu-
man trials should focus initially on Phase I trials on
pre-adolescents and later on Phase I, II, and III trials
on infants prior to tooth eruption.
Adherence of S. mutans bacteria to tooth tis-
sues is a prerequisite for colonization. Other evidence
supports the need for vaccines or other therapies to
inhibit specific virulence factors to prevent caries.
Active and passive immunization processes have
been developed for immunotherapy against dental
caries. Significant caries inhibition effects have been
shown in experimental mice, rats, and monkeys,
which have been immunized subcutaneously, orally,96
or intranasally97 with these antigens. However, only
a few studies have examined the efficacy of dental
caries vaccines in humans. Recently, local passive
immunization using murine monoclonal antibodies,
transgenic plant antibodies, egg-yolk antibodies, and
bovine milk antibodies to antigens of mutans strep-
tococci have been applied to control bacterial colo-
nization and dental caries in humans. Such immuni-
zation is believed to be a safer approach for
controlling dental caries than active immunization.98
Russell et al.99 and Wu and Russell100 focused
on the saliva-binding region where certain residues
appear to be important in attachment to the salivary
pellicle on the tooth surface. Antibodies against this
part of the molecule can exert an anti-adherence func-
tion. Antibodies against antigen I-II are effective anti-
adherence antibodies. There is no evidence that an-
tigen I-II has cardiovascular cross reactivity.
Recently, investigators have shifted their fo-
cus toward mucosal vaccines that employ the im-
munogenicity of cholera toxin and its B subunit us-
ing rat and monkey models or toward the
saliva-binding region in the rat model that is geneti-
cally coupled to the nontoxic components of antigen
I-II. However, no longitudinal clinical data from in-
fancy onward are available to demonstrate a corre-
lation between antibodies to antigen I-II and a de-
crease in the concentration of S. mutans colonies.101
In this regard, many obstacles remain for vaccine
development to be successful including the high costs
required and the lack of prioritization of caries vac-
cines in the last Institute of Medicine report. Other
uncertainties include the number of contacts that will
550
be required with a primary provider, the overall deliv-
ery cost, the benefits versus risks of active and pas-
sive immunity approaches, the role of industry, and
acceptance by the dental profession and the public.
Conclusion
Any method of caries management must deal
with one or more of the three main stages of the dis-
ease process: 1) the initial interaction of bacterial cells
with the tooth that is mediated by adhesins; 2) the
colonization and growth of cariogenic bacteria in a
biofilm; and 3) the production of glucose and gly-
cans by glucosyl transferase, a bacterial enzyme,
which affects the production of lactic acid that ini-
tiates the demineralization process. Chemical agents
are designed to disrupt cell metabolism and to kill
all disease-producing cells or a significant percentage
of the cells. This therapy is designed either to prevent
the disease process or to cause a reduction in disease-
related manifestations.
In general, replacement therapy employs a care-
fully constructed effector strain that provides a num-
ber of advantages over conventional prevention strat-
egies and oral vaccines. In the case of dental caries,
a single colonization regimen that leads to persistent
colonization by the effector strain should provide life-
long protection. In the event that the effector strain
does not persist indefinitely in some subjects, reap-
plication can be performed as the need arises with-
out significant added concern for safety or effective-
ness. One of the greatest advantages of replacement
therapy and caries vaccination is that there is mini-
mal need for patient compliance relative to caries
prevention although oral hygiene measures to pre-
vent periodontal disease will still be required.
The development of a vaccine useful against
caries infection faces an even greater challenge be-
cause of the elimination of one of the commensal
oral microorganisms. Before any vaccine is brought
to market, the long-term consequences of disturbing
the commensal microflora of the oral cavity that has
evolved over many centuries must be determined.
The current resurgence of various infectious
diseases indicates that traditional and antibacterial-
based therapies alone will not suffice. The contin-
ued study of bacterial interactions as they occur in
vivo will inevitably lead to the identification of natu-
rally occurring effector strains for the replacement
therapy of various infections. If ultimately success-
ful, the use of genetic engineering to tailor an effec-
Journal of Dental Education ■ Volume 69, Number 5
tor strain for replacement therapy of dental caries
will encourage similar efforts to prevent other infec-
tious diseases.
However, until such time as these alternative
therapies are proven to be safe and effective for hu-
mans, conventional caries prevention methods pri-
marily based on applications of fluoride must be used.
Of the currently available methods, treatment regi-
mens should be designed according to caries risk lev-
els. Conscientious use of conventional prevention
methods (brushing, flossing, topical fluoride, con-
trolled sugar consumption, etc.) is sufficient in most
cases to maintain the S. mutans level below its mini-
mal pathogenic concentration. The fact that dental
caries remains as one of the most common infec-
tious diseases afflicting humans is a clear indication
that a truly effective prevention strategy cannot rely
on patient compliance.
For low-risk patients, minimal fluoride expo-
sure is indicated. If fluoride treatment is indicated
because of inadequate water fluoride content or
the presence of other major risk factors, a low-dose,
high-frequency application is recommended. For
moderate-risk and high-risk patients, antibacterial or
bactericidal agents should be considered for those
individuals with high levels of S. mutans (>106 CFU/
mL saliva). However, for modern management of
caries as an infectious disease to be successful, car-
ies risk must be assessed periodically and lesion se-
verity must be monitored to track the activity status
of the disease and to adjust the treatment, if neces-
sary, should the risk level of the patient decrease or
increase significantly during the active treatment
method.9,102
Acknowledgments
This article was supported in part by NIH/
NIDCR Grant No. DE13412.
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