Dental caries: An updated medical model

of risk assessment
V. Kim Kutsch, DMD
Oral BioTech, Albany, Ore
Dental caries is a transmissible, complex biofilm disease that creates prolonged periods of low pH in the mouth, resulting in
a net mineral loss from the teeth. Historically, the disease model for dental caries consisted of mutans streptococci and
Lactobacillus species, and the dental profession focused on restoring the lesions/damage from the disease by using a surgical
model. The current recommendation is to implement a risk-assessment-based medical model called CAMBRA (caries
management by risk assessment) to diagnose and treat dental caries. Unfortunately, many of the suggestions of CAMBRA
have been overly complicated and confusing for clinicians. The risk of caries, however, is usually related to just a few common
factors, and these factors result in common patterns of disease. This article examines the biofilm model of dental caries,
identifies the common disease patterns, and discusses their targeted therapeutic strategies to make CAMBRA more easily
adaptable for the privately practicing professional. (J Prosthet Dent 2014;111:280-285)

Dental caries is a transmissible bio-
film dysfunction of the teeth marked by
prolonged periods of low pH, which
results in a net mineral loss.1 Histori-
cally, the disease model for dental
caries consisted of mutans streptococ-
ci and Lactobacillus species.2 However,
more recent scientific evidence indicates
that the disease is more complex than
this model suggests and that it has
traits in common with other biofilm
diseases.
Biofilm research using DNA se-
quencing identification of bacteria has
identified some 40 bacterial species
to date as having a role in dental caries,
and that list continues to grow.
In recent independent studies, Bifido-
bacterium species, Scardovia wiggsiae,
Slackia exigua, and Propionibacterium acid-
ifaciens have been implicated.3-5 Next-
generation sequencing technologies
promise to add to these species as the
biofilm model of dental caries becomes
better understood. Dental caries also
has potential systemic effects.6 Studies
from randomly collected coronary pla-
que specimens during surgery indicate
that when found in the mouth, the
most common oral bacteria found in
the coronary plaque is also Streptococcus
mutans.6 The authors concluded that S
mutans was responsible for most bac-
terial endocarditis and that by com-
parison, the presence of periodontal
pathogens was negligible. S mutans is
also able to invade endothelial cells
directly by means of its cnm (collagen-
binding protein) gene.7 Further studies
have also implicated caries-causing
bacteria in impaired cognitive func-
tion, ulcerative colitis, and accelerated
plaque growth after angioplasty.8-10
Dental caries also has apparent hered-
itary characteristics and genetic associ-
ations.11,12 Early studies found that
individuals with the G20A poly-
morphism for beta-defensin-1, a sali-
vary bacteriolytic enzyme, had 5 times
the decayed, missing, and filled teeth
(DMFT) scores seen in those with
other variations of this gene.11 Heredi-
tary associations with the TAS2R38
taste-bud gene increase the risk for
dental caries.12 A recent genome-wide-
association study indicated multiple
gene site associations with an increased
risk for caries, the strongest of which
was LYZL2 (lysozyme-like 2), which en-
codes another bacteriolytic enzyme.13
The data from this study also indi-
cated 5 distinct patterns of decay
geographically in the mouth, with the
LYZL2 gene being associated with
carious lesions only in the mandibular
incisors.13 Additional genetic associa-
tions have been attributed to a muta-
tion in matrix metalloproteinase 13
(MMP13) and the HLA antigen allele
HLA-DQ2.14,15 Regardless of how
complex the biofilm disease model be-
comes, however, dental caries still
means prolonged periods of low pH,
resulting in a net mineral loss from the
teeth. With the continued development
of next-generation sequencing technol-
ogies, examining the biofilm and its
metabolic outcome differently will be
possible. Nyvad et al16 have explored
the novel idea of viewing the biofilm as
a single organism, as first proposed by
Buchen.17 Biofilm is a collection of
distinct and separate organisms, but it
behaves collectively as one superor-
ganism. As such, it is less important to
identify which specific bacterial species
are present. Instead, the authors pro-
posed a metagenomic study to identify
which genes were present in the biofilm
in total. The genes that are active pro-
duce the proteins resulting in metabolic
output from the biofilm. In the case of
dental caries, the concern is that acid

This study was presented to the American Academy of Restorative Dentistry, Chicago, Ill, February 2013.

Chief Executive Officer, Oral BioTech; Private practice, Albany, Ore.

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April 2014
output creates prolonged periods of
low pH. Future dental caries biofilm
research, therefore, should not be
focused on specific bacteria but on the
function and output of the biofilm.16
CARIES RISK ASSESSMENT
As the scientific evidence has grown,
the dental profession has progressed
from an intuitive model of medicine
(educated guess; drill and fill lesions) to
an empirical model (probabilistic
model based on systematic reviews of
randomized controlled trials; fluoride
and nonfluoride anticaries therapies).
Continued growth in the evidence base
will lead the profession into a future of
precision medicine, in which the cause
of a disease is known and can be
measured and targeted for therapy.18
Results to date have been mixed
regarding the sensitivity and specificity
of various caries risk assessment (CRA)
tools. Pediatricians who identified pla-
que on the maxillary central incisors (a
caries risk factor) in children during
well-care visits had a 55% sensitivity
and an 80% specificity.19 Another study
examined the caries risk assessment
tool (CAT) of the American Academy of
Pediatric Dentistry, independently of
socioeconomic status, and compared
the results with mutans streptococcal
cultures. The CAT had a high sensitivity
of 100% and a low specificity of 2.9%,
whereas the mutans streptococcal cul-
ture alone resulted in an 86.5% sensi-
tivity and a 93.4% specificity. The
mutans streptococcal culture alone
outperformed the CAT.20 A study
examining the Cariogram risk assess-
ment tool over a 2-year period in
school-age children found both a high
sensitivity (83%) and a high specificity
(85%), and a strong correlation was
found between caries risk profiles and
caries incidence after 2 years.21 A 6-year
retrospective analysis of the CAMBRA
(caries management by risk assess-
ment) CRA form reported a higher
incidence of cavitated lesions among
those assessed as being at extreme risk
compared with those diagnosed as
being at low risk initially.22 Finally,
Kutsch
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a systematic review of 4 CRA tools
concluded that the evidence for the
validity of existing systems for CRA
is limited and that valid and reli-
able methods for CRA are urgently
needed.23
CAMBRA is the next attempt to
explain the underlying risks and causes
of dental caries in an individual.24
Identifying the risks allows for individ-
ualized, targeted therapy. There are
known and validated common risk
factors for dental caries, as well as
disease indicators.22 The same 6-year
retrospective study examined 12 954
individuals, and the odds ratios (ORs)
of these factors and indicators have
been established and validated.22 The
disease indicators include visible cavi-
tation or radiographic radiolucencies
penetrating to dentin (OR, 8.21), active
white spot lesions (OR, 2.77), and a
history of a restored cavity in the pre-
vious 3 years (OR, 1.46). Risk factors
include noticeable plaque buildup on
the teeth (OR, 2.55), frequent snacking
(OR, 1.77), hyposalivation (OR, 1.27),
exposed roots (OR, 1.19), deep pits
and fissures (OR, 1.80), and recrea-
tional drug use (OR, 1.95). These new
data have added to the factors and
changed the picture for dental caries,
but this change has simplified the
situation for those in clinical practice.
By identifying pattern recognition for
common clinical causes of dental
caries, the new factors include bacteria
(either too much bacterial load or high
acid output of the biofilm); diet (either
excessive sugar consumption or snack-
ing too frequently); saliva (either
hyposalivation or poor buffering ca-
pacity); and genetics (multiple possible
associative genes).
CAMBRA is a simple process, con-
sisting of 3 separate steps: assessment,
diagnosis, and prescription. CRA is
performed with a standardized CRA
form. CRA forms are available from the
American Dental Association, the Cali-
fornia Dental Association Foundation,
the American Academy of Pediatric
Dentistry, and other organizations.
Assessment consists of identifying
known risk factors for an individual
281
patient and noting any disease in-
dicators. Various biometrics have been
used in clinical practice for dental
caries, but most have involved culturing
saliva to measure mutans streptococcal
and Lactobacillus levels. A current bio-
metric uses the adenosine triphosphate
(ATP) bioluminescence of a dental
biofilm specimen, which correlates with
overall bacterial load and the func-
tioning/metabolic output of the bio-
film.25,26 High ATP presence indicates
either high bacterial load or high
metabolic output.27
One of the challenges of imple-
menting CAMBRA in clinical practice
stems from the lack of time available to
perform this task, as it is usually
assigned to an already burdened hy-
giene appointment. A recent CRA form
developed for clinical practice ad-
dresses this issue beginning with 3
motivational interview questions, fol-
lowed by the self-reporting of risk fac-
tors by the patient (Fig. 1). This can be
accomplished in the reception area
before a dental hygiene visit. The dental
professional can then identify disease
indicators and discuss the risk factors
with the patient.2
The caries diagnosis is made by
examining all of the patient data: the
CRA form, oral examination, radio-
graphs, history, and any biometrics (if
used). The American Dental Associa-
tion Council on Scientific Affairs pub-
lished definitions for the various risk
categories for children and adults in a
special supplement to the Journal of the
American Dental Association in 2006.28
Once the caries diagnosis is deter-
mined, the next step is to design ther-
apeutic strategies for the patient,
specifically targeting individual risks.
Prescriptive strategies can be orga-
nized into 3 categories: reparative stra-
tegies, therapeutic materials, and
behavioral changes. Reparative strate-
gies are well developed by the dental
profession and include remineralization
and restoration. The best scientific evi-
dence for remineralization is with fluo-
ride, although most of the compelling
scientific evidence is from studies
on children, and the results are
282 Volume 111 Issue 4

1 Caries risk assessment form adapted for clinical practice.

extrapolated to all age groups.29,30
Whereas fluoridated water has been
found to reduce the overall decay rate
in populations, the best form of pro-
fessionally applied fluoride is fluoride
varnish.31,32 Patient-applied fluoride is
best in the form of a 0.05% fluoride
rinse or a 5000-ppm fluoride gel. For
patients with a high risk of caries, the
recommendation for fluoride varnish is
every 3 months; more frequent appli-
cation does not add benefit.
Current remineralization research
also involves several forms of cal-
cium phosphate, including nanoparticle

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April 2014
hydroxyapatite.33,34 Although more re-
search is indicated, it has been found that
the nanoparticle hydroxyapatite is bio-
mimetic for the natural building blocks of
enamel and reduces biofilm formation.35
Restoration of active cavitated lesions is
required. The clinician may elect to stage
the treatment of lesions in the patient with
a high risk of caries, first restoring all le-
sions with an intermediate material such
as glass ionomer cement while working
with the patient to modify the biofilm and
behaviors. Patients at high risk or extreme
risk (such as, because of hyposalivation)
may develop new lesions within 1 year,36
so it is appropriate to stage their restor-
ative care.
Therapeutic strategies include an-
timicrobial, metabolic, pH, and
potentially probiotic categories. Anti-
microbial strategies typically include the
use of povidone-iodine, chlorhexidine,
or sodium hypochlorite rinse. Biofilms
are resistant to change, and it may take
2 or more years of using these rinses to
modify the biofilm and reduce the pa-
tient’s caries risk.36 Whereas it is
appropriate to use an antimicrobial
agent for a patient with a high biofilm
load, patients that lack a high biofilm
load but have other risk factors may not
benefit from an antimicrobial strategy.
One potential metabolic strategy for
the biofilm is xylitol. Xylitol has
been found to potentiate even small
amounts of fluoride, so it might be
beneficial to combine xylitol with fluo-
ride strategies.37 However, there is
conflicting evidence for xylitol; a recent
study in adults found that long-term
daily use of xylitol mints alone did not
decrease the caries outcome in those at
high risk.38 This multisite study perhaps
indicates that a 1-dimensional treat-
ment of xylitol in patients with high
caries risk may not be effective given the
complex biofilm nature of the caries
disease. Conversely, numerous studies
have found that xylitol is an effective
anticaries agent.39-41 Recently, a study
has indicated that xylitol seems to
have an anticaries effect on root
surface lesions in caries-active adults.42
Xylitol may be effective when applied in
a combined approach with other
Kutsch
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strategies targeted to the patient’s spe-
cific risk factors but may be ineffective
as a solo strategy. In addition, pH
modification may reverse both the se-
lection pressure and therefore the
output of the biofilm, with the added
benefit that it also drives remineraliza-
tion.1 For patients with inadequate
saliva, neutralization strategies supple-
ment the protective role of the saliva.
Probiotics deserve mention. A pro-
biotic is a therapeutic agent that con-
sists of living microorganisms, primarily
bacteria; that is safe for human con-
sumption; and that when ingested has
beneficial effects beyond just nutrition.
The strategy is to influence the makeup
of the biofilm by consuming less-
pathogenic organisms. Probiotics have
been used with great success in treating
conditions such as diarrhea and Crohn
disease.43 In dental caries, the probiotic
must be able to adhere to and integrate
into the biofilm, compete with and
antagonize cariogens, and have low-
acid-production metabolism. Although
additional research is indicated, pro-
biotics offer a potential additional
strategy for the future.44
Behavioral issues include strategies to
alter behavior and also to account for
risks that cannot be modified. Some be-
haviors are theoretically modifiable and
some are not. Diet and home care both
play significant roles in dental caries.
Excessive plaque buildup or bacterial
load, accompanied by infrequent
disruption, leads to site-specific demin-
eralization of the teeth. Home care in-
structions such as daily brushing and
flossing continue to be important. Di-
etary issues tend to stem from excessive
sugar intake or from snacking too
frequently. Both of these behaviors
should be modifiable, but human
behavioral change is not easy, nor is it
linear.45,46 In a recent clinical trial in pa-
tients improving their oral hygiene be-
haviors, some improved during the term,
some stayed the same, and some
improved and then relapsed.47 Motiva-
tional interview and wellness coaching
principles can help patients manage their
own behavioral changes, but realistically
these changes take time and consistent
283
reinforcement.48,49 A recent study also
provides some discouraging results; it
found that it is easier to change patients’
alcohol intake than it is to change their
sugar consumption.50
Nonmodifiable issues typically involve
medication-induced hyposalivation, ag-
ing, reduced cognitive or physical func-
tion, and special needs. Hyposalivation is
a significant risk factor for dental caries
and most often relates to medication
use.51 The more medications involved,
the greater the risk and severity of
hyposalivation.
Designing an appropriate and
effective treatment strategy for an indi-
vidual patient is straightforward. The
causes drive the treatment strategies.
The patient in Figure 2 is at high risk for
dental caries, as is the patient in
Figure 3. However, the risk factors
associated with these 2 patients are
significantly different and require a
targeted approach for their treatment
to be successful. If the patient has a
bacterial issue (see Fig. 2), it should be
addressed with antimicrobials, pH
modification, and home care in-
structions. For the patient with a di-
etary issue, the strategy should focus on
modifying their sugar consumption or
snacking habits. The patient with
hyposalivation (see Fig. 3) will likely
benefit from maintaining hydration
levels and from pH neutralization ma-
terials, both of which support a healthy
oral environment. The patient with a
genetic risk for dental caries will be
harder to diagnose but will benefit from
minimizing acid exposure during the
day and maintaining good health. For
the clinician, it is important to have an
appreciation and understanding of the
complexity of the dental caries biofilm
disease model. But perhaps more
importantly, being able to identify the
common disease patterns and associ-
ated therapies presented in this article
should make CAMBRA more easily
adaptable in clinical practice.
SUMMARY
Dental caries is a complex biofilm
disease with many associated risk
284
2 Patient with high caries risk with bacterial load and home
care risk factors.
3 Patient with high caries risk with medication-induced
xerostomia.
factors and disease indicators. The
dental profession has historically
treated the disease by focusing on
restoring cavitated lesions. CAMBRA,
an emerging philosophy, also includes
identifying specific risk factors and dis-
ease indicators for an individual patient
and designing targeted therapies to
address those risks. CAMBRA provides
the next step toward precision medicine
and the more effective treatment of
dental caries in clinical practice.
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Corresponding author:
Dr V. Kim Kutsch
2200 14th Street SE
Albany, OR 97322
E-mail: kimkutsch@aol.com
Copyright ª 2014 by the Editorial Council for
The Journal of Prosthetic Dentistry.