Transcript Etiology, Epidemiology, and Prevention of Dental Disease in Children

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Discipline : “ Preventive Dentistry”
Programme of lectures: – 7 lectures + 7 lectures
u Textbooks for self-study are:
- Norman O. Harris, Primary Preventive Dentistry,
6th Ed. (2004); 7th ed.(2009)
- Hardy Limeback , Comprehensive Preventive
Dentistry, 2012
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Exam : after 7 semester - in January 2015. Exam
consists : 1 written question from the syllabus and
test ( multiple choice), all in one day.
Etiology and pathogenesis of
dental caries.
Prof.d-r R.Kabaktchieva- 2014
 The
-
three general disease categories of
focus in dentistry are :
dental decay,
periodontal disease,
oral cancer.
Dentistry
in the past has been
treatment oriented,but we are
witnessing an interest prevention.

It is obviously better to prevent
the disease in the first place,
than treat it once it has happened.
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The goals of preventive dentistry are
to avoid disease altogether.
Maintaining a disease-free state
can result from primary prevention.
 When lifestyle changes are made early on,
the risk for developing dental disease are minimized.

Lifestyle changes
u – less carbohydrates
u – better oral hygiene
u – improved nutrition
u – better education
 Secondary
prevention (reverse, arrest incipient caries) and
early intervention (MID &“Preventive Resins”)
can be used to reverse the initiation of disease.
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An outcome of good health can still be achieved,
when incipient enamel lesions are reversed before
cavities form.
MID- minimal intervention dentistry
!
 Far
too often though, dentists spend most
of their time treating dental disease
in an endless cycle of repeat restorations,
which leads…… to tooth loss.
The goal of primary prevention
is never to have had
any kind of dental disease.
Dental decay (dental caries): global patterns
Fig. Global prevalence of caries from World War II to present.
The relative decline in caries, was represented by DMFT (decayed, missing, filled
teeth)
Are also shown other factors that have contributed to the decline in caries
worldwide (labeled a to j)
Comprehensive Preventive Dentistry- H. Limeback

Тhe prevalence of caries has changed over the
decades.

In every developed country, there has been
a steady decline in dental decay.

Experts believe, that it was primarily
the introduction of fluoride therapies after the
1960s that had a huge impact on dental decay rates.
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To know how to prevent ,
need to know disease,
its etiology and pathogenesis
Etiology and Pathogenesis of Dental Caries
In dealing with disease,
“prevention is better than a cure.”
Definition

Dental caries is a dietary
carbohydrate-modified
bacterial infectious disease
with saliva as a critical
regulator.

It is the most common
chronic infectious disease of
childhood
Contemporary definition :

Tooth decay is localized progressive disease,
whose character consists in the destruction of tooth
structures mainly under the influence of metabolic products
of the oral microflora;

Each level of decomposition is clinically differentiated.
Kidd
Caries process takes place in the biofilm on the
tooth surface .
Carious lesion is the result of carious process
developing between the microbial biofilm and tooth
structure
The metabolic activity of the
microorganisms in the biofilm is invisible
to the clinician,
but carious lesion that is a result of this
activity is clinically apparent.
Caries Factors
Must have a tooth, plaque
bacteria, fermentable
carbohydrate, saliva, and
enough time in order for a
carious lesion to develop .
Caries results when all of the
factors that contribute to caries
overlap. (red color, center).
diagram
The classic Venne
diagram of caries.
Several factors influencing
each component, ( see the
diagram,) affect the rate and
severity of the caries.
This is a convenient analogy to understand and is an
offshoot of the classic Venn diagram ( first introduced by Keyes (1962).
The role of microorganisms
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Caries is an infectious disease that is
actually transmissible,
usually when the mother infected with
S. mutans, infects her infant when the
child’s first teeth appear in the oral
cavity (Kulkarni et al. 1989).
 Dental caries does not occur in a sterile
mouth. (no mouth can ever be made sterile)
The conditions in the oral cavity are ideal for
the growth of bacteria that metabolize sugar to
acids.
The oral cavity is generally a warm place, at
body temperature (37°C) encouraging the growth
of bacteria.
Non-specific Plaque Hypothesis
Microorganisms in dental caries first
observed by van Leeuwenhoek in 1683
W.D. Miller – University of Berlin 1890 –
considered all bacteria in mouth were
potentially cariogenic – hence, non-specific plaque
theory
Acid production by bacteria considered
responsible for breakdown of tooth
Specific Plaque Hypothesis
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1924 – Clarke isolated a streptococcus
species from a cavity in a child
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The bacteria underwent some changes
as the culture aged – Clarke named it
Streptococcus mutans for “mutation”
Mutans streptococci
– Keyes “rediscovered” S. mutans
 He demonstrated that:
 1960
– specific microorganisms were responsible for caries
– caries was transmissible
 Later,
the responsible bacteria were found to
comprise seven distinct species – only mutans and
sobrinus are associated with caries in humans
Characteristics of MS
 Ecological
niche: human oral cavity
 “Intentionally designed … to be a cariogenic
organism” (Coykendall 1976)
 Cariogenic
properties
– ability to produce acid (acidogenicity)
– ability to withstand acid conditions (aciduricity)
– ability to adhere to teeth
Characteristics of MS
Metabolism yields:
– acids, primarily lactic, from a variety of sugars
– extracellular polyglucose, called glucan, which
creates irreversible attachment (from sucrose
metabolism only)
 MS is responsible for initiation of caries
 MS is a necessary, but not solely sufficient, factor for
dental caries

Acquisition of MS by Infants

MS colonize oral cavity after eruption of teeth –
require hard, non-desquamating surface;

Some believe in “window of infectivity “ that relievs
on virgin tooth surfaces for initial colonization;

Second “window may open” when permanent
dentition erupts
Acquisition of MS by Infants

MS is poor competitor for colonization – once
stable biofilm is in place, ability for MS to
colonize is reduced

Infants who acquire sanguis early have less MS
mitis
Birth
1
sanguis
8
mutans
11
19
26
33 mos.
Transmission of MS
Vertical transmission
 Source is usually mother
 Fidelity is >70%
 Transmission may occur at
birth, but MS reside in low
numbers in reservoirs such
as tonsils or dorsum of
tongue

Other Microorganisms
 Lactobacilli
sp.
– found in large numbers in some children
– considered opportunistic, not initiators
– numbers in cavity increase after DEJ
invaded
– lactobacilli are good indicators of total
carbohydrate intake
Etiology - Diet
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Hopewood House (Australia) 1947 – 52 determine
– diets devoid of sugar and white flour- extremely
low dental caries prevalence

Vipeholm (Sweden) 1945 – 52 determined
– effects of frequency of sugar consumption
– effects of consistency (retentiveness) of sugar
– sugar at meals vs. in between meals
Lessons from Vipeholm (Sweden)
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Sugar consumption at meals – slight increase in caries;
Sugar between meals – marked increase in caries;
Sugar in sticky candies – greatest caries activity;
Caries activity differs among individuals
Caries activity declines with withdrawal of sugar-rich
foods
The role of dietary sugars
Not all sugars are cariogenic.
The more common dietary sugars are presented.
The cariogenic potential of carbohydrates are presented too.
The sugars with the most
cariogenicity are sucrose
and glucose (red).
Other carbohydrates
(maltose, lactose, fructose,
and starch) are less
cariogenic.
The sugar alcohols, such as
sorbitol and mannitol, are
the least cariogenic (yellow)
Xylitol has even been
shown to be anticariogenic
(green).
 The
disaccharide sucrose and the
monosaccharide glucose ( a component of sucrose),
are most cariogenic.
 Frequent
ingestion, can cause severe damage
to the tooth.

There is no question that carbohydrates are
the main etiological reason for the development of caries.

One of the strategies in prevention of caries is to limit
access to the more cariogenic sugars and substitute them
with the anti-cariogentic ones.

Not only does their conversion to acid result in
enamel dissolution, but they also encourage the growth
of more virulent cariogenic bacteria.
Sucrose
 Glucose
+ fructose
extracellular polyglucose,
glucan, (from sucrose metabolism only)
creates irreversible attachment
metabolized by plaque bacteria
glucan
+
fructan
Glucan
 Water
soluble
 Extracellular “glue”
 Enables adhesion to tooth
– reduced susceptibility to mechanical
disruption
 Inhibits
diffusion properties of plaque
– reduces buffering capacity of saliva
– inhibits transport of acid away from tooth
Role of Other Sugars



Fructose and glucose are as effective as sucrose in
their ability to cause a pH drop;
Fructose is nearly equal to sucrose in cariogenicity;
Raw starch causes only a small drop in plaque pH
Role of Refined Starch
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Soluble starch and refined
starch can be broken down by
salivary amylase into sugars
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These refined carbohydrates
cause a variable pH drop that
may be as large as that caused
by sucrose
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The supragingival bacteria are
dominated with streptococci
and lactobacilli that can lower the
plaque pH and induce decalcifications
white spot lesions.
Figure shows an illustration of dental plaque at
the gingival margin.
1) The enamel (e) has plaque biofilm (b) growing at the border of the
nflamed gingival (g).
2) Same plaque at closer look. There is a ‘white spot’ lesion (w) developing at
he margin of the gingiva, and brown calculus (c) developing in the sulcus
ttached to the tooth.
3) Close-up view of plaque. Biofilm bacteria, which
onsists of several species of bacteria (cocci, rods, motile spirochetes),
organic material (salivary proteins) and organic matter secreted by the
acteria (yellow-stained)

The plaque that is responsible for caries is generally
located supragingivally and is acidogenic.
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People who consume sugars frequently in their diet
increase the levels of streptococci and lactobacilli
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The two bacteria species thought to be responsible for
caries.

These bacteria continue to thrive as the pH drops.

If the plaque is not removed, eventually, the enamel
starts to decalcify and an incipient ‘white spot’ lesion
ensues.
Figure .The enamel white spot lesion at the mesial contact zone of the
first maxillary right molar .
These white-spot lesions are sometimes filled by dentists
but can be remineralized.
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Marsh (1994) was able to show,
that feeding of bacteria a meal of glucose
can encourage the growth of cariogenic bacteria
when the pH is allowed to drop .
Repeated glucose rinses encourages SM and LB growth when plaque acid is not
controlled
Fluoride at high concentrations inhibits SM , but not LB !!!
Xylitol had inhibitory properties for both cariogenic and periodontal bacteria.
The demineralization–remineralization
balance in caries
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The plaque thickness dominated by cariogenic bacteria, can
effectively keep the saliva from reaching the enamel surface.
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In addition, the more plaque there is, the more acid is produced.
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These acids have a longer time to penetrate into the enamel under
thick biofilm - This allows the tooth to demineralize!!!!
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If the saliva reaches the acids they are washed away and
neutralized by the salivary buffers - This allows the tooth to
remineralize.

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The cycle repeats itself over and over
with every sweet snack and meal
containing fermentable sugars
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Caries occurs when the frequency of
sugar exposure during the day is high.
The repeated cycle of ‘sugar attacks.’
The pH of dental plaque in
response to glucose has been
studied using the classic
Stephan curve
The diagram illustrates the plaque pH response curves
that have been obtained from patients with different
risks for caries.
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A high-risk individual, when
given a glucose rinse , will
experience a dramatic drop in
the plaque pH well below the
critical pH of 5.5.
 The area under the pH-time curve
(AUC)representing the time spend at
pH lower than the critical pH.
The AUC for a high risk
individual will be very large.
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The recovery to neutral pH in
the high risk individual will be
slow.
AUC is a better measure of total
caries risk.
 The
person with a high risk for caries snacks
frequently during the day,
and the total AUCs clearly are excessive
and will not allow remineralization to occur.
 If
that daily trend continues, the person will
experience dental decay.

For a moderate risk
individual (yellow), the
initial pH drop may only
be a little lower than the
critical pH, and the AUC
will be much less.
For a caries-resistant person
(green),the initial pH drop of
that person’s plaque may
not even reach the critical pH,
and the recovery will be very
quick.

The person with moderate caries risk might have three
meals and one snack of moderate cariogenic potential
on a daily basis,
and the AUCs below the critical pH might result in a net
loss of mineral.

At this stage, remineralization
strategies might work.
Тhe person at low risk may not snack
at all and has three meals of low
cariogenicity spread apart during the
day.
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Researchers have determined that:
it is not only the frequency of ingestion that is
important, but it is also
the type of fermentable carbohydrate that is
ingested.
Kleinberg et al. (1982) determined
that increasing glucose concentrations
results in lower pH drops
1.0% Glucose
50% Glucose
1.0% Glucose
8.0
7.0
6.0
0
20
40
60
80
100
Etiology – Host Factors
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Tooth factors
– quality of enamel
– presence/depth of pits and fissures
– hypoplasia
– fluoride exposure
Saliva
– pH
– flow rate
– buffering capacity
– antimicrobial components
Saliva
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“Is to teeth what blood is to cells of the body”
Composition
– supersaturated with Ca, P
– bicarbonate – principal buffer
– proteins, immunologic/antibacterial components
– fluoride
– viscosity depends on gland, nervous control of
secretion
pH normally around 7.0; varies from ~5.5-8.0
The main components of saliva and their function
Classification
of component
Ingredient
Function
Inorganic
Water (99%)
Inorganic, organic
Carbonate,
phosphate, protein
Buffers acid
Organic
Amylase, lipase,
protease,
pyrophosphatase,
lysozyme
Antibacterial
Organic
Mucins
Lubricant, calcium binding
Organic
IgA
Antibacterial
The role of saliva
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Saliva contains antibacterial proteins,
electrolytes for remineralization and
the essential nutrients for bacteria to grow.
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The host provides the dietary carbohydrates
that are easily converted to energy and acids by
the bacteria that leads to dissolution of dental
hard tissues.
The role of saliva
 Because of its buffering capacity and ability to
neutralize acids,
a simple intervention such as stimulating the saliva
with chewing gum can arrest white spot lesions
and prevent cavities from forming (Stookey 2008).
Saliva
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Flow rate Increased by:
– gustatory stimulants (sugar-free candy)
– masticatory stimulants (s-f chewing gum)
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reduced by:
– medications (antihistamines, antiasthmatics,
others)
– disease (degenerative, metaplastic)
– dehydration
– radiation
– age
2. Pathogenesis of dental caries
Mechanism of development of dental
caries
Sequence of the mechanism for the development of
dental caries
1.
Degradation
of inorganic
matter in
enamel
Acid
demineraliz
ation of
enamel
Demineraliz
ation
by chelators
2.
Degradation
of organic
matter
Acid
digestion of
organic
matter
Proteolytic
degradation
of organic
matter
Mechanism of acid demineralization
Carbohydra
tes from
food
Plaque’s
microorg
anisms
Release of calcium
and phosphate ions
Dissolution of
enamel crystals
acids
Narrow intercrystal
spaces of the
enamel surface
dissociati
on
hydrogen
ions
Dissolution in the presence of chelators
Carboxylic acids
Lactates
Amino -Acids
Bonding the
calcium at the
enamel surface
and extraction
Citrates
Development of caries in the
presence of inhibitors
pyrophosp
hates
diphosphates
calcium
fluoride
fluorapatite
=
hinder
dissolution
Mechanism of degradation of organic matter
acid soluble
acid insoluble
Degradation in acid
medium
proteolytic enzymes
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interventions aim
to modify the steps in the repeat
demineralization and
remineralization cycles.
1.

Neutralize the plaque acids:
This can be done by adding base
or adding buffers such as sodium
bicarbonate (baking soda) to the
saliva to boost its ability to neutralize
acids.
2. Improve hygiene:

With bacterial levels low, less acid is
produced.

Plaque layers don’t have a chance to grow
thick;

Saliva can penetrate better to the
enamel surface through thin layers of plaque.
3. Introduce antimicrobials:
 Since caries is a disease caused by
bacteria, simply eliminating the
bacteria or controlling their growth
will reduce the caries incidence.
 Chlorhexidine, xylitol, ozone,
even experimental antibodies, have
been used to control bacterial growth.
4. Stimulate saliva:
 Saliva contains numerous components that fight tooth decay
 buffers,
remineralizing minerals,
antimicrobial enzymes, antibodies.
5. Topical fluorides:

Fluoride added to the remineralizing
incipient lesion increases the enamel crystals’
resistance to dissolution by plaque acids.
6. Remineralizing strategies:
Remineralization can be
promoted with the use of calciumphosphate complexes such
and ACP-CPP.
end