D. Zero - Overview Caries Process and The New Model For Management of Caries

Overview Caries Process and the
New Model for Management of Caries

| Domenick Zero, DDS, MS, Andrea
Ferreira Z, DDS, MSD, PhD
05/29/2012
1
Overview Caries Process
and the New Models for
Management of Caries
Domenick Zero, DDS, MS
Andrea Ferreira Zandona, DDS, MSD, PhD
Indiana University School of Dentistry
Department of Preventive and Community Dentistry
Oral Health Research Institute
05/29/2012
OUTLINE
Caries Theories/Working Hypotheses
Dental Caries Process
Etiologic Factors
Site-specific
Dynamic Disease Process
Personalized Approach Caries Management
Where we are
Where we need to go
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Simple Truths About Dental Caries
People like to eat and our diets are largely influenced by
what food is presented to us (opportunistic)
Food manufacturers exploit our biology (preference for
sweets and grazing)
Government plays a only minor role in modifying the food
choices
Attempts at behavior modification by health care professions
has not had a major impact (but we should keep trying)
SUBSTRATE
MICRO-
ORGANISMS
HOST
&
TEETH
Bacteria and humans have co-evolved over millions of
years and its hard to change this relationship overnight
Non-specific chemotheraputic approaches are not effective
and may even be deleterious
Targeted approaches at specific organisms have not as yet
been proven to be effective
Genes plays some role, but probably not a major role
given the localized nature of the disease process
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Chemoparasitic Theory
Caries is brought about by acid dissolution of the
mineral phase of the teeth, the acid being produced by
metabolism of dietary carbohydrates by oral bacteria.
In a secondary step the organic phase of enamel and
dentin is broken down.
W.D. Miller (1890)
We have had a scientific basis understanding
the caries process for over 120 years
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Dental Caries Working Hypotheses
Infectious and transmittable disease caused by
Streptococcus mutans (Losche, 1976) Medical Model
Dietary carbohydrate-modified infectious disease
(Bowen & Birkhed, 1986)
Ecological shift in dental plaque resulting in a
pathogenic microflora (Marsh, 2003)
Biopsychosocial disease model (Reisine and Litt,1993)
Genetic basis for increase risk of dental caries
(Hassell & Harris, 1995)
Are we preventing or controlling dental
caries based on any of these hypotheses?
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2
Ecological Plaque Hypothesis
Marsh (2006)
05/29/2012
Working Hypothesis:
Dental caries is primarily the consequence of
physiological adaptation by (endogenous)
plaque bacteria to a low pH environment.
Zero DT. Adaptations in dental plaque. In: "Cariology for the Nineties".
Bowen W.H. and Tabak, L., eds. University of Rochester Press,
Rochester, pp. 333-350, 1993.
Zero DT. Dental Caries Process. Dent Clin North Am 43:635-664, 1999
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Low pH Adjacent
to Tooth Surface
Diet Saliva
Plaque
Characteristics
Adaptation
Selection
Zero (1993)
increased acid tolerance
increased acid production
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Updated Scheme
Zero, Arthur & Zandona, unpublished
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Key Features of Dental Caries
Multifactorial etiology
Site-specific disease
Time-dependent dynamic disease
process modified by protective factors
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Main Etiological Factors
Tooth location and morphology
Dental biofilm microorganisms with acidogenic and
aciduric properties
Frequent dietary exposure to fermentable
carbohydrates
Salivary flow rate and composition
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3
Types of Caries
Approximal Caries
Caries Adjacent to a Restoration
(Secondary Caries)
Root Surface Caries
Smooth Surface Caries
Occlusal Caries
(pit and fissure caries)
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Dental plaque (biofilm) microorganisms with
acidogenic and aciduric properties
carbohydrates
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Microorganisms Associated with
Dental Caries in Humans
Streptococcus mutans
Streptococcus sobrinus
Lactobacillus species
Actinomyces species
non-mutans streptococci
Other species yeasts, Bifidobacterium,
Propionibacterium, Atopobium
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197 bacterial different species/
phylotypes detected using 16S
rRNA gene cloning, of which
50% were not cultivable
10% of the subjects with
dental caries did not have
detectable levels of S. mutans
Bacterial species other than
S. mutans, likely play important
roles in caries progression
Aas et al (2008)
S
p
a
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H
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e
i
t
y
Kolenbrander et al. (2002)
Dental Biofilm Diversity
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Caries-Associated Virulence Traits
Biofilm formation - adherence and colonization
Acid producing ability mainly lactic acid from fermentable
carbohydrates
Aciduric potential - ability to survive and continue to produce
acid at a low pH
Formation and utilization of storage polysaccharides
Formation of insoluble extracellular glucans
S. mutans has all of these traits; however, many other
species found in the dental biofilm also have them
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carbohydrates
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4
Vipeholm Study
Gustafsson et al. (1954)
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Conclusions Based on the Vipeholm Study
The amount of sugar eaten is not as important as the
form in which it is eaten.
Sticky sugar products which tend to be retained on
teeth have a greater caries potential than sugar
consumed in a liquid form.
The more frequent sugar is consumed the greater the
risk.
Sugar consumed between meals has much greater
caries potential than when consumed during a meal.
Gustafsson et al. (1954)
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Stephan Curve
4.5
5.0
5.5
6.0
6.5
7.0
0 10 20 30 40 50 60
Time, minutes
P
l
a
q
u
e

p
H
Critical pH
10% Sucrose Rinse
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8
A
M
b
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e
a
k
f
a
s
t
1
0
A
M

c
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f
f
e
e

b
r
e
a
k
1
2

N
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h
3
P
M

s
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a
c
k
6
P
M
d
i
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r
8
P
M
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o
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t
i
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s
s
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a
c
k
i
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g
1
0
P
M
B
e
d
t
i
m
e
2
4

h
o
u
r
s
time of day
m
i
n
e
r
a
l

c
o
n
t
e
n
tnet
loss
Hypothetical Change in Tooth Mineral
Content Over a 24 hour Period
Zero (1999)
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Is sucrose
the arch criminal
of dental caries
? ?
Newbrun (1969)
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Cariogenic Properties of Sucrose
Highly soluble in oral fluids
Freely diffusible in dental plaque
Readily metabolized by plaque bacteria
Serves in the formation of insoluble extracellular
glucan (mutan) in the presence of the enzyme
glucosyltransferase from S. mutans
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5
Role of Extracellular Polymers
Bacterial adherence and
colonization
Structural matrix for
plaque
Reserve carbohydrate
source
Protective function
Modify diffusion
properties of plaque
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carbohydrates
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Salivary Tooth Protective Mechanisms
Mechanical cleansing action
Dilution and buffering of plaque acids
Buffering systems - Carbonic acid-bicarbonate, phosphate, proteins
Ammonia and urea
Small peptides (sialin)
Anti-solubility Factors
Calcium, phosphate, fluoride
Statherins, histatins, proline-rich proteins
Acquired pellicle
Remineralization and repair of enamel
Calcium, phosphate, fluoride
Organic matter
Antimicrobial properties
Secretory IgA, non-immunological aggregating macromolecules,
lysozyme, lactoferrin, peroxidase/myeloperoxidase
Mandel (1989)
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4.5
5.0
5.5
6.0
6.5
7.0
0 10 20 30 40 50 60
Time, minutes
P
l
a
q
u
e

p
H
Critical pH
10% Sucrose Rinse
Stephan Curve in Patient With Salivary
Gland Hypofunction
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8
A
M
b
r
e
a
k
f
a
s
t
1
0
A
M

c
o
f
f
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b
r
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a
k
1
2

N
o
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c
h
3
P
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s
n
a
c
k
6
P
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8
P
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o
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u
o
u
s
s
n
a
c
k
i
n
g
1
0
P
M
B
e
d
t
i
m
e
2
4

h
o
u
r
s
time of day
m
i
n
e
r
a
l

c
o
n
t
e
n
tnet
loss
Hypothetical Change in Tooth Mineral
Content Over a 24 hour Period
modified from Zero (1999)
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6
Site-specific Disease Process
Dental caries is a highl y localized and complex process
which occurs in areas of stagnation where plaque can
accumulate undisturbed. Each tooth site represents a
unique environment that influences plaque composition,
metabolic status and thickness, as well as access by
dietary substrates, saliva and anticaries agents.
(Zero DT. Dental Caries Process. Dent Clin North Am 43:635-664, 1999.)
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Site-specific Biological and Behavioral
Modifying Factors
Pre-eruptive and post-eruptive fluoride exposure
Oral hygiene practices
Plaque removal, fluoride use
Dental biofilm
Composition, metabolic state, thickness, diffusion properties, degree of
saturation with respect to tooth mineral
Saliva flow rate and composition
Proximity to salivary gland orifices, salivary film thickness and velocity
Acquired pellicle
Composition and thickness
Eating and drinking pattern
Oral physiology affecting clearance pattern
Cariogenic foods and beverages
Fluoride
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Site Specific Plaque Biofilm Factors
Composition
Diffusion properties
Metabolic state
Thickness
CHO
H
+
H
+
DENTIN
ENAMEL
Degree of saturation
with respect to
tooth mineral
Ca PO
4
F
F
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Site Specific Salivary Factors
Proximity to salivary
gland orifices
Salivary film thickness
Salivary film velocity
CHO H
+
ENAMEL
DENTIN
Pellicle composition
and thickness
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8H
+
+ Ca
10
(PO
4
)
6
OH
2 F
-
Dynamic Nature of Dental Caries
6(HPO
4
)
- -
+ 10Ca
++
+ 2H
2
O
demineralization
Undersaturated
conditions in oral fluids
remineralization
Supersaturated
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7
Carious Lesion Development (hypothetical)
(modified from Zero DT. Dental Clinics of North America, 1999)
0 1 2 3 4
time after eruption (years)
m
i
n
e
r
a
l

c
o
n
t
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n
t
1
Posteruptive
maturation
arrested lesion
cavitation
clinically detectable lesion
(white spot)
Fluoride works here
Fluoride works here too
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White Spot Lesion
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Demineralization Progression
5 m
4 hours
12 hours
8 hours
16 hours
Microchannels Mineral dissolution
Ando et al. (2003) 6
th
Indiana Conference
Surface
layer
reforming
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White Spot Surface Layer
The caries process is initially driven by an interaction
between the biofilm and the tooth surface
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Surface Zone
Body of Lesion
Dark Zone
Translucent Zone
Normal Enamel (Silverstone et al., 1981)
(Larsen &
Pearce, 1992)
Non-cavitated (Subsurface) Lesion / White Spot
Acquired Pellicle
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Factors Affecting Remineralization
Tooth
enamel or dentin, surface involved, extent of demineralization
Acquired Pellicle
composition, thickness
Dental Bioflim
thickness, diffusion properties, Ca, PO
4
and F content, pH
Saliva
flow rate, composition (proteins, Ca, PO
4
and F content)
Diet
indirect effects on plaque metabolism (acid production), and
direct effects by introducing reparative factors such as the
calcium and phosphate from dairy products
Zero DT. Application of clinical models in remineralization research.
J Clin Dent 10 (Spec Iss):74-85,1999.
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8
Surface Zone
Body of Lesion
Dark Zone
Translucent Zone
Normal Enamel
Acquired Pellicle
Non-cavitated (Subsurface) Lesion / White Spot
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Changes in Our Understanding of
Dental Caries
Moved from the concept that caries is a treatable
disease to caries is a totally controllable disease
Lesions progress more slowly and cavitate later in
the post-fluoride era
Caries is a dynamic process that can be arrested or
reversed at an early stage
Has the way we manage caries changed, or are we stuck?
And if so, what do we need to do to get unstuck?
05/29/2012
Premise
Our current system for treating dental caries in most
countries is too expensive and not very effective,
because it doesnt appropriately manage the disease
process.
We need a whole new approach with new tools to make
additional significant improvements in oral health.
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Simple Truths About Our Current System
of Managing Dental Caries in the US
Dentists will not change the way they are managing dental
caries without external drivers
New technology (tools) that dentists perceive will improve
their practice
New financial incentives or disincentives
New regulatory/legal environment
Standard of Care driven by evidence based dentistry
Law suits
The few Cariologists in US dental schools have only limited
impact on changing the way graduating dentists manage
dental caries
The major impactor on practice behavior is what is taught
in the clinic, mainly by part-time faculty and what patients
and third party payers are willing to pay for.
05/29/2012
8H
+
+ Ca
10
(PO
4
)
6
OH
2
6(HPO
4
)
- -
+ 10Ca
++
+ 2H
2
O
demineralization
Historical Understanding of Dental Caries
Very good for dentists
Our profession is heavily biased towards
our successes and not our failures
Dental Caries (Cavity) Restoration Larger Restoration
Endodontics or Extraction Prosthodontics
Maybe not the best for patients
05/29/2012
8H
+
+ Ca
10
(PO
4
)
6
OH
2 F
-
Modern Understanding of Dental Caries
6(HPO
4
)
- -
+ 10Ca
++
+ 2H
2
O
demineralization
Undersaturated
remineralization
Supersaturated
The early stages of dental caries can be prevented, reversed or
arrested, primary through the elimination or modification of
etiological factors (dietary, microbial) and/or by enhancing
protective factors (fluoride, sealants and salivary stimulation).
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9
(Early) Lesion Detection
& Assessment
Risk Assessment
Preventive Intervention
(prevent, reverse, arrest)
Restorative Intervention
(only when absolutely necessary)
Oral Health
Outcome
Diagnosis & Prognosis
risk/benefit
cost/benefit
patient preferences
Modern Management of Dental Caries
Zero et al. Dent Clin N Amer 2011;55(1):29-46.
05/29/2012
(Early) Lesion Detection
& Assessment
Risk Assessment
Preventive Intervention
(prevent, reverse, arrest)
Restorative Intervention
(only when absolutely necessary)
Oral Health
Outcome
Diagnosis & Prognosis
risk/benefit
cost/benefit
patient preferences
Modern Management of Dental Caries
We currently evaluate these components as independent processes
and not as one system that impacts the long-term health of patients.
Bader JD, Shugars DA. Variations in dentists' clinical decisions. J Public Health Dent 1995;55:181-188.
BLACK BOX
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PrimaryPreventionatthePatientLevel
SecondaryPrevention TertiaryPrevention(Care)
Caries Risk Assessment at the Patient Level
No
Disease
ICDAS0
Initial
Lesion
ICDAS1
Initial
Lesion
ICDAS2
Moderate
Lesion
ICDAS3
Moderate
Lesion
ICDAS4
Extensive
Lesion
ICDAS5
Extensive
Lesion
ICDAS6
Staging
ofLesion
Severity
DIAGNOSIS
Caries Lesion Activity Assessment
Caries Risk Assessment at the Tooth Surface Level
Radiographs and Other Diagnostic Aids
Additional
Information
thatInforms
Diagnosis
No
Treatment
Remineralize Arrest Sealant Minimal
Surgical
Traditional
Surgical
Endodontic
Treatment
Extraction
Zero et al. Dent Clin N Amer 2011;55(1):29-46.
Personalized Caries Management
05/29/2012
Interactions Between Caries Risk
Assessment and Caries Diagnosis
Caries Diagnosis should inform Caries Risk Assessment
Based on careful examination of the oral cavity, patients with
the presence of detectable caries active lesions are at a
minimum at moderate caries risk.
Patients without the presence of clinically detectable caries
active lesions may be at moderate or high risk depending on
recent changes in their risk factors/indicators.
Caries Risk Status should inform Caries Diagnosis and
Treatment Decisions by helping to:
determine if incipient lesions are active.
determine the appropriate level of preventive intervention.
determine if operative care is indicated (or not), especially for
questionable lesions.
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IUSD Smile-on Caries Management E-learning Course
START
05/29/2012
Problem Definition
The Institute of Medicines (IOM) review of evidence-
based health care found that, despite benefits from
rapid growth in medical research and increasing
expenditures for health care in the United States,
far too much time is spent on health care activities
that do not improve health, and not enough time is
spent on healthcare activities that will.
Olson, Aisner, McGinnis (2007)
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10
Preventive Treatment Planning
Fluoride (highly effective in all forms)
Water fluoridation
Professionally applied
Home delivery
Sealants (highly effective if applied correctly)
Salivary stimulation
Chewing gum
Diet modification
Behavioral
Protective food additives
Antimicrobial
Non-specific
Targeted
Non- fluoride remineralizing strategies
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What This Conference Should Be About Is
How Can We Get Dentistry Unstuck
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GOAL FOR THE DENTAL PROFESSION
Dental caries never progresses beyond the ICDAS code 3
stage for patients who are routinely seeking dental care.
What is needed to achieve this goal:
High accurate technology-based diagnostic tools
To detect and stage lesion severity
To determine caries lesion activity status
Caries Risk Assessment at the patient level
Practitioner friendly electronic aids
Caries Risk Assessment at the tooth surface level
Point-of-care diagnosis test to determine biofilm pathogenicity
Algorithm-based computer clinical decision support systems that
factor in all components of the diagnosis process.
New interventions strategies that target the main etiological factor
dietomicrobial interaction
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Human progress is neither automatic nor inevitable.
Rev. Dr. Martin Luther King Jr.
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Systems Approach To Oral Health Management
Fontana & Zero. Bridging the Gap in Caries Management Between Research and Practice
Through Education: The Indiana University Experience. J Dent Educ 2007;71:579-591.
T
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Professional
Organizations
05/29/2012

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