Discipline : Preventive Dentistry

Programme of lectures: 7 lectures + 7 lectures

Textbooks for

self-study are:

- Norman O. Harris, Primary Preventive Dentistry,

6th Ed. (2004); 7th ed.(2009)
- Hardy Limeback , Comprehensive Preventive
Dentistry, 2012
th
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.

 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
less carbohydrates
better oral hygiene
improved nutrition
better education

 Secondary

prevention (reverse, arrest incipient caries) and

early intervention (MID &Preventive Resins)
can be used to reverse the initiation of disease.

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

he 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.

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.

Dental caries is a dietary

carbohydrate-modified
Definition
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

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.

diagram

(red color, center).

The classic Venne

diagram of 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

 Caries

is an infectious disease that is

actually transmissible,
usually when the mother infected with
S. mutans, infects her infant when the
childs 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 (37C) 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

1924 Clarke isolated a streptococcus

species from a cavity in a child

The bacteria underwent some changes

as the culture aged Clarke named it
Specific
Plaque Hypothesis
Streptococcus
mutans for mutation

Mutans streptococci
1960

Keyes rediscovered S. mutans

He demonstrated that:
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

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
Characteristics
of
MS
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

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

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
Sugar consumption
at meals (Sweden)
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

 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

Soluble starch and refined

starch can be broken down by
salivary amylase into sugars

These refined carbohydrates

cause a variable pH drop that
may be as large as that caused
by sucrose

 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 inflamed
ingival (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.

People who consume sugars frequently in their diet increase the levels of
streptococci and lactobacilli

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.

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 demineralizationremineralization
balance in caries

The plaque thickness dominated by cariogenic bacteria, can

effectively keep the saliva from reaching the enamel surface.

In addition, the more plaque there is, the more acid is produced.

These acids have a longer time to penetrate into the enamel under
thick biofilm - This allows the tooth to demineralize!!!!

If the saliva reaches the acids they are washed away and neutralized
by the salivary buffers - This allows the tooth to remineralize.

The cycle repeats itself over and over

with every sweet snack and meal
containing fermentable sugars

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.

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 recovery to neutral pH in
the high risk individual will be
slow.

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.

 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
persons plaque may
not even reach the critical pH, and

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.

 he

person at low risk may not snack

at all and has three meals of low
cariogenicity spread apart during the
day.
This allow remineralization to occur.

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

20

40

60

80

100

Etiology Host Factors

Tooth factors
quality of enamel
presence/depth of pits and fissures
hypoplasia
fluoride exposure
Saliva
pH
flow rate
buffering capacity
antimicrobial components

Saliva

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

Saliva contains antibacterial proteins,

electrolytes for remineralization and
the essential nutrients for bacteria to grow.

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

Flow rate Increased by:

gustatory stimulants (sugar-free candy)
masticatory stimulants (s-f chewing gum)

reduced by:

medications (antihistamines, antiasthmatics, others)

disease (degenerative, metaplastic)
dehydration
radiation
age

2. Pathogenesis of dental caries

Mechanism of development of dental
caries

Mechanism of acid demineralization

Development of caries in the

presence of inhibitors

Preventive

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 dont 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