Epidemiology and

Prevention of Dental Caries

Dr Mrs Juliana O Taiwo
Associate Professor of Community Dentistry
Department of Periodontology and
Community Dentistry
 Epidemiology is the study of the distribution,
determinants and frequency of disease or
health conditions in human populations.
 Disease frequency involves the measurement

of the existence or occurrence of diseases,

disability and deaths and summing them as
rates or ratios. This is necessary before any
investigations of the patterns of disease
occurrence in a population can be done.
 The measure of frequency of disease,
disability or death are summarized as
incidence rate and prevalence rate.
 Distribution of disease: This answers the

question of Who, where and when. This

involves the distribution pattern by place,
person and time. These may involve,
comparing different populations, groups,
with in a population or both at different
times.
 Determinants of Disease: This is achieved
after collecting information on the first two. A
hypothesis is propounded and tested to
identify causes and risk factors.
 In epidemiology mortality, morbidity,

disability natality, medical needs(i.e health

services and other health related
events),presence, absence and distribution of
environmental factors, presence, absence of
distribution of
 disease or attributes of disease are all
measured.
 I will therefore discuss epidemiology of

dental caries according to its distribution,

determinants and frequency.
 Dental caries is defined as the

demineralization of dental hard tissues

(enamel, dentine and cementum)
 of the erupted tooth, as a result of acid
produced by certain oral bacteria, notably
streptococcus mutants, lactobacillus
acidophilus and Actinomyces , during the
metabolism of dietary sugar notably sucrose.
 Dental caries is the most prevalent disease of

the oral cavity, leading to serious economic

and social consequences.
Fig. 1
 Various epidemiological survey showed a
marked decrease of caries prevalence in the
developed or industrialized countries .Fig 2
Whilst in developing countries there is an
increase .( Denloye et al)
 In spite of significant improvement in the oral
health of Americans, dental caries still affects
a majority of school children.
 The decline in prevalence of caries in the
developed countries is demonstrated in the
following studies.
Fig. 2
(a) Kumar et al (New York) 1998
(b) Evans et al (United Kingdom mean DMFT was
2.55 1998
(c) Obry-Musset A M (France)
 Age and Dental Caries
Research has demonstrated that the
incidence and prevalence of dental caries is
highest in children and the elderly and least
in adults.
 WHO Global Oral data bank for Europe
demonstrate caries prevalence of 22.2 to 30.2
in the elderly. Refer to table 1
 Socio economic status and caries
In developed or industrialized countries
people of low socioeconomic status have a
higher caries experience than people of high
socio economic status . In developing countries
it is the reverse . However most recent data
demonstrates an increasing trend among
children in the villages.( Denloye et al )
 In a review of data from 1941 – 1978 on
socio economic status and caries 33 reported
a higher caries experience in the lower social
classes whilst five reported no difference and
2 reported reduced prevalence. (Carmichael
1980)
 Also studies have shown that people in the

lower socioeconomic group have a higher (D)

decay and (M) missing factor in their DMFT.
 whilst people of higher socioeconomic
group have a higher F (filled) factor in their
DMFT. Note, this is an indication of unmet
need in the lower socio economic group.
 In developing countries even though caries

experience is low some of these countries

which have shown a change in life style
and diet to that of developed countries
have demonstrated an increase in caries
experience. e.g. Sri - lanka.
 Although the prevalence of dental caries is
low in developing countries recent studies
have shown an increasing trend in dental
caries and the consumption of sugar a
causative factor in the initiation and progress
of caries (Henshaw and Adenubi 1975, Sardo
Infirri and Barmas 1978, and of recent
Denloye et al).
 Also children of high socio economic group
have a higher prevalence of caries than
children from the lower socio economic
group Of recent we are beginning to see
more caries in children from rural
communities (Denloye et al)
Fig. 3
 • ETIOLOGY OF CARIES
Dental Caries is an infectious multifactoral disease.
Different factors are involved in the initiation and
progress of caries.Fig3
Four main factors are involved:
a) The Host
b) Supragingival plague micro organism
c) Diet (Substrate)
d) Time
 Fig. 4

Diet
Supragingival Substrate
plague
micro organism

Time
Host

We shall look at these factors individually

Host Factors; these include:
a) Morphology of the tooth (the fissure
patterns, the shape etc.)
b) The ability of the enamel to remineralise
c) Fluoride distribution in the enamel
d) Age
e) Saliva: - Saliva is very important subject in
the etiology of dental caries.
f) Arrangement of the teeth
 MORPHOLOGY OF THE TOOTH

Susceptibility of different areas of the enamel of the

same tooth to a standard acid attack in vitro, vary. Some
areas in the same tooth are more susceptible than
others.

• The Shape of the tooth, the size of the fissures play an

important role in the process of caries

•Shallow fissures are easy to clean and are less prone to

caries process whilst deep and narrow fissures are
difficult to clean and are more susceptible to caries
Fig. 5

Shallow fissures Deep fissures

•FLOURIDE DISTRIBUTION
Research has shown that the fluoride concentration in the
enamel falls steeply from the occlusal surface towards the
dentino-enamel junction and there is an inverse relationship
between the F content of surface enamel and caries
experience. i.e. people with high flouride content in their
enamel have lower caries experience.
SALIVA
•Saliva is very important in the initiation and progress of
dental caries.
•Saliva is a fluid secreted by the salivary glands.
•The amount of saliva secreted daily is between
0.5-1.0L.
•Saliva has almost the same composition as blood plasma.
•Secretion of saliva is stimulated
a) Psychologically -This is well developed in
animals e.g dog.
b) Chemically -Salt, sweet and sour taste
c) Biologically -Wound in oral cavity increase
salivary flow.
d) Mechanically -Mastication
Functions of Saliva
e) Lubrication f) Pellicle formation
f) Ion reservoir g) Digestion
g) Buffering capacity h) Taste
h) Cleansing of food debris i) Water balance
i) Antimicrobial: J) Agglutination
(antibacterial factors e.g lysozymes, (immunological- immunoglobulin A
lactoferin, lactoperoxidase) and Salivary immuglobulin A)
Other factors affecting the secreation of saliva is fear and sleep
•Salivary proteins are considered as aglutinins.
They agglutinate strep mutans etc.

•Hydrogen is an important ion in the inorganic component of

saliva

•Calcium is another important ion in the inorganic component

of saliva. It exist in both ionized and non-ionized form.

•Based on its content 2types of saliva composition can be

identified
a) Low flow rate which contains magnesium and phosphate
b) High flow rate which contains proteins, sodium and
bicarbonate.
•Fluoride is present in both and this depends mostly on
external introduction
•Low flow rate is not satisfactory because it has a poor
buffering capacity
•Fast and high flow rate has a good buffering capacity
•We can also identify unstimulated and stimulated saliva

• Protective characteristic
a) Salivary flow rate
b) Buffering capacity
c) Antibacterial
d) Immunocological
•Salivary gland hypo function
a) Hyposecreation of saliva
b) Xerostomia ( dry mouth )
• There is enough evidence that salivary flow rate is
related to caries experience.
• There is an inverse relationship between salivary flow
rate and caries.
Buffering capacity of saliva
• Of great importance is the buffering capacity of saliva
in the prevention of caries. Nearly everybody,s normal
oral flora contains microorganisms which are capable
of metabolising fermentatable carbohydrates leading
to the production of a variety of acidic by products.
• People have to digest food containing fermentable
carbohydrates to meet their nutrient energy requirements
and therefore the production of acids in the oral cavity
of an individual is inevitable, reducing the pH of plague.
• However the plague pH goes from acid to normal
(resting level) within a few minutes and this depend on
saliva.
• This is due primarily to the carbonate and phosphate, pH
buffering agents in saliva.
• This process is in equilibrium i.e. an equilibrium exist
within the dental plague whereby the pH of the plague
decrease when the host ingest food and then returns to
resting level after some time.
SUPRAGINVIVAL PLAGUE MICROORGANISM

•There is enough evidence showing that micro-organism in

supragingival plague are responsible for dental caries.
•Much evidence have identified streptococcus mutans(MS)
as the major pathogens of dental caries. The following are
some of the evidence implicating streptococcus mutans(MS)
a) Ms are frequently isolated from cavitated caries lesions
b) Ms induce caries formation in animals fed a sucrose rich
diet.
c) Ms are highly acidogenic and aciduric (Loesche 1986)
d) Ms are able to produce surface antigens VII and water
soluble glucan which promote bacteria adhesion to the
tooth surface and to other bacteria. (Hamada and Slade
1980).
• A systematic literature review by Tanzer et al (2001)
confirms a central role of Ms in the innitiation of
dental caries on enamel and root surfaces.
• However some studies (Stephan 1940) demonstrated a
pH drop in the absence of mutans streptococcus but in
the presence of other mixed bacteria.
• Contemporary well designed studies confirmed that
the level of MS is not necessarily high in caries
associated biofilms especially in the microflora
associated with non-cavitated stages of the caries
lesion formation (Van Houte et al 1991,Sansone et al
1993).
• Van Ruyven et al (2000) detected other bacteria rather
than the above mutans streptococcus and Actinomyces
from dental biofilms covering white spot lessions.
•These include lactobicilli, Bifidobacterium, non-mutans
streptococci, propion bacterium
It was found that these other bacteria exist in initial lesions
whilst the population of MS is greater in cavitated lesions.
•It was therefore proposed that the other bacteria including
non-mutans streptococci and Actinomyces are more closely
involved in the innitiation of caries.
•This process of dental caries is said to be an example of
AMPHIBIOSIS refering to dynamic adaptation that occurs
in response to changing enviromental conditions between
two dissimilar organisms living together. Under normal
condition microorganism live in a symbiotic relationship
but this may change under changing conditions with
mutualism becoming parasitism.
•This dynamism adaptation is the basic principle of
endogenous disease process including dental caries. This is
congruent (appropriate ) with the ecological caries
hypothesis.
•From this fact it is now known that the innitial colonizers
of newly cleaned tooth surface are
a) Strep Sanguinis b) Strep oralis c) Strep mitis I
d) Actinomyces ) Strep mutans comprise only 2% of the
innitial population of Streptococcus.
•As the microflora ages the composition shifts from
Streptococcus dorminant to Actinomyces dorminant. (Van
palestein helderman 1981, Sasone et al 1993, Van Houte et
al 1996).
• It was concluded that at the different stages of the carious
lesion the composition of the bacteria involved changes.
•Reasons proposed for the changes in the composition of
population of bacteria is referred to as microbial acid-
induced adaptation and subsequent acid induced
selection of low pH.
•This means that the non-mutan streps and the other
bacteria are involved in the initiation of the caries process
producing acid and lowering the pH. But at a low pH below
5.5 they are inactivated and eliminated gradually as the pH
falls further. These bacteria only play a role in destabilizing
the homeostasis of the plague by facilitating a shift of
demineralization/remineralization balance from net mineral
gain to net mineral loss resulting in the ACIDOGENIC
STAGE.
•Once the acid environment has been established mutans
streptococcus (MS) and other aciduric bacteria take over;
increasing and promoting lesion development.
At the advancing front of dentin caries, lactobacilli
prevotellae and Bifidobacterium are more prevalent
( Becker et al 2002, Mazourani et al 2009).
• In cavitated lesion the population of MS is 30%
suggesting that MS is associated with cavitated lesions
MS are encountered less frequently at advancing front of
dentin caries lesion.
•MS, lactobicilli and Bifidobacterium are more
acidogenic and aciduric.
•The critical pH for demineralisation of enamel to occur
is pH 5.5.
•Non- mutan streptococci and Actinomyces can have a
variety of glycosidases which can liberate sugars and
amino acids from glycoproteins such as mucin in saliva
(e.g. sialidases)
• Under severely acidic conditions M.S and lactobacilli
are more competitive. E.g. under rapid exposure to pH4
as observed in mature plague non-Mutans streptococci
and Actinomyces loose their viability.
• in summary the following microorganisms are involved
in the caries process.
a) Mutans streptococci
b) Non-mutans streptococci (strep mitis, strep oralis,
strep saguinis). c) Lactobicilli d)Bifido
bacterium
e) Propion bacterium f) Actinomyces (e.g. naeslunelii,
• Non-mutans streptococci, Bifidobacterium,
Actinomyces, prevotellae, propionbacterium are found
more at the innitial stage of caries process.
•When an acidic environment is established, ACIDURIC
STAGE, acid induced selection by acid impairment and
growth competition eliminate them leading to a shift in
the composition of the microflora to mutans
streptococcus (MS) and lactobacilli which are
ACIDURIC BACTERIA.
• mutans streptococcus and lactobacilli are found in
advance lesions i.e cavitated lesion.
Fig. 6

Caries-associated Bacteria in the Caries Process

DIET (SUBSTRATE)
Diet can affect the tooth in two ways, 1st while the tooth is
developing, i.e before eruption and Secondly while the tooth
has erupted in the mouth.
• the relationship of diet to the tooth during the pre-eruptive
phase is nutritional while once the tooth has erupted into the
oral cavity the relationship to diet is environmental rather
than nutritional.
Pre-eruptive Effect
• vitamin A, Vitamin C and Vitamin D deficiencies as well
as deficiencies and inbalance ratios of calcium and
phosphorus cause characteristic malformations in
histolologic structure of the developing tooth.
•Inadequate amounts of Vitamin D, calcium and
phosphorus result in imperfect calcification of the
mineralizing enamel matrix and dentin matrix, Although
only vitamin D deficiency during development is
believed to result in an increase susceptibility of the
tooth to caries in human populations. The others have
been proved to result in an increased caries
susceptibility of the tooth in animals.

•Note that calcium also has an environmental effect. It

plays an important role in the
remineralization/demineralization process of the tooth.
•There is enough evidence confirming the role of non fermen
table sugar in the initiation and progress of caries. e.g.
Human observational studies, human interventional studies,
animal experiments, plague pH studies and laboratory
experiments,
• C.O.M.A (Committee on Medical Aspect of Food) report.
Concentration of free sugar is an important factor. This is
demonstrated by the dose response curve for sugar and
caries. At levels of sugar consumption below
10kg/person/year the incidence of caries is acceptably low
whilst at levels beyond 15kg the incidence increase more
rapidly.( fig.7)
Fig. 7 Dose response curve of Sugar and caries
• The Consistency is very important. Sticky thick sugary
food encourage the progress of caries.

•The Frequency is very important. The rate at which sugary

food is taken is proportional to the incidence of caries
(e.g. Vipeholm )
• Other additives can influence the process of caries. Some
foods and elements and vitamins are known to have a
deterrent effect on the process of caries e.g. inorganic
phosphate, organic phosphate, phytate, calcium.

•Some other elements like selenium can accelerate the

process of caries.
Fig 9.
Time
Time is very important in the prevention of dental caries as
an etiological factor. It takes 3yrs for a white spot lesion to
cavitate .So with good screening and surveillance dental
caries can be prevented.

PREVENTION OF DENTAL CARIES

• Prevention of dental caries will involve methods directed
at the various etiologic factors
a) this will involve methods directed at increasing host
resistance to caries.
b) This will involve methods directed at controlling
plague microorganism involved in caries process
c) This will involve control of dietary factors.
d) Time is an important factor in the prevention of dental
caries. It is important to identify the white spot lesions
early and treat them.

Methods directed at increasing the resistance of the host

(tooth)
1) Flouridation
a) Systemic intake of flouride
i. Water fouridation (community and school water flouridation)
ii. Intake of flouride supplements (flouride drops, tablets, milk,
fruit juice)
iii. Flouride salt
b) Topical application of fluoride
i. Fluoride solution e.g. NaF solutions
ii. Fluoride gels e.g. NaF gels
iii.Fluoride mouth rinses
iv. fluoride vanishes e.g. Duraphat
v. Fluoride tooth paste

2) Control of factors that will disturb or affect the flow and

function of saliva
3) Immunization of the host.
 FLUORIDE IN THE PREVENTION OF DENTAL CARIES
• Fluoride is a big topic and can not be even completely
treated even in 4 lectures. I will therefore give you a
summary of this.
• The effect of fluoride on the tooth was first discovered
by Dr. Mckay in Colorado Springs
• Dr. H Trendley Dean in his research proved that there is
an inverse relationship between endemic flour osis and
caries.
No. of caries Experience

Fluoride concentration in water

and caries Experience

F: Content of Water
Fig. 10
•He proved that at 1ppM F in drinking water, there is
maximal reduction in caries experience without mottling
of the teeth or in some places there may be sporadic
instances of the mildest form of flourosis.
•1ppM means 1 part of fluoride to every million part of
water which is equivalent to 1mg F: per litre of water.
(health Education Authority Britain 1989)bn
•The concentration of fluoride in community water
fluoridation ranges from 1.8ppm in tropical countries to
1.2ppm in temperate or cold countries (U.S, Europe)
whilst for school water fluoridation the concentration of
F is 4.5 to 5 times higher than community water suply.
(4.5ppM )
• water fluoridation is defined as the upward adjustment
of F concentration of the community central water supply
to an optimum level of 1ppm for the purpose of
•Mechanism by which fluoride prevents caries
a) Pre-eruptive effect
i. Affects morphology of the tooth.
ii.Affects the mineral crystals of the tooth converting calcium
hydroxyl phosphate (ca10 (p04 )6F2) to calcium fluroapatite
( ca10(po4 )6F2
b) Post Eruptive Effect of fluoride
i. Fluoride in the presence of dilute acid reduces enamel
dissolution.
ii.Fluoride accelerates remineralization of the early carious
lesions
iii.Acid soluble fluoride (F-)exerts inhibitary action on further
acid production by plague micro-organisms.
iv.Fluoride reduces or prevents colonisation of the tooth surface.
v.Fluoride interferes with the uptake of glucose across the cell
membrane and disrupts glycolysis
Topical Fluoridation
Fluoride toothpaste has contributed greatly to the reduction
in caries prevalence in the world. Fig6.
• In the presence of acid the uptake of fluoride by the tooth
is greater.
•In the clinic acidulated phosphate fluoride (APF) 1.23% is
often used. It is marketed in to form of gel or solution
•Ensuring proper nutrition especially the necessary
vitamins and elements and proteins etc. will develop the
resistance of the tooth to caries.
•Immunization of the host. With the new knowledge on
microbiology of caries , it is obvious that the argument of
non- specificity of mutans streptococcus is substaintiated.
The studies on caries vacine has been at a stand still at the
animal experiment stage.
Fig. 11
 CONTROL OF CARIES MICROORGANISM

This can be grouped into mechanical control and chemical

control and introduction of competitors
A. Mechanical control
i. Fissure sealants
ii. Maintaining stringent oral hygiene

B. Chemical plague bacteria control

i. Chlorhexidine
C. Introduction of competitors
i. Probiotics
ii.Prebiotics.
FISSURE SEALANTS
Definition: Fissure sealants are fluid resin materials, which
polymerise in situ, and are used to occlude pits and fissures
principally found on the occlusal surfaces of premolar and
molar teeth for the purpose of preventing dental caries on
the occlusal surfaces of these teeth.
•We have already discussed how the morphology of the
tooth encourages the process of caries and the host
susceptible areas of the surface are the pits and fissures
(50% of the caries in chidren are in pits and fissures)
•Also it has been demonstrated that fluorides are least
effective on the pits and fissures. Fi7, Fig8.
•Fissure sealants therefore are the solution to caries in pits
and fissures.
Fig. 13
Composition: - Fissure sealants are products of bisphenol and
glycidyl methacrylate (BIS GMA) resin, filled with 50% silica.
Some fissure sealants are fluoride releasing glass ionomer
cement
Types of Fissure sealant
i. 1st generation fissure sealants. These are ULTRA-VIOLENT
LIGHT CURED
ii.2nd generation fissure sealants: These are autopolymerise
sealants
iii. 3rd generation fissure sealants: These are visible light
cured.
iv.4th generation fissure sealants :These contain flourides.
• The 4th generation fissure sealants also known as F- releasing
sealants include glass ionomer cements which are either
conventional glass ionomer cements or silver cerment
cement. They are known to have the best retention rate.
 METHOD OF APPLICATION OF FISSURE SEALANTS
•Method of application vary according to the material from
which it is made.
•Fissure sealants which are resin based
i. 1st the teeth to be treated is isolated and cleaned with
pumice and water on a bristle brush.
ii. The tooth is washed of all traces of pumice
iii.Etch solution or gel containing 30-50% phosphoric acid
is applied to the surface of the tooth on a small sponge
or pledget of cotton wool or special brush for 30sec but
for primary teeth for 120 sec.
iv.The fissure is dredged with a fine probe for a few
seconds
v. the phosphoric acid is washed off for 30sec.
vi. The enamel is thoroughly dried.
vii. The fissure, sealant is then applied and light cured.
•If an autopolymerise agent is used then the components
are mixed and allowed to flow into the fissure and over the
sorrounding enamel by capillary action.
• For glass ionomer based sealants the method of
application is different.
 METHOD OF APPLICATION OF GLASS IONOMER
CEMENT SEALANT
i. Isolation and drying but without cleaning with
pumice.
ii. The enamel surface is conditioned with
POLYACRYLIC ACID for 30seconds.
iii.The pit or the fissure is dredged with a fine probe
iv.The conditioned surface is washed, dried and
isolated.
v. The cement is mixed and beads of sealants are
transferred onto the tooth with a probe. The probe is
used to fill the whole depth of the fissure with the
sealant.
i. A cling film or articulating wax is used to cover the
fissure sealant on the tooth to prevent it from dehydration
ii. Once the sealant has set a round bur is used to remove
the excess cement.
iii.Finally a thin layer of light curing agent is applied over
the cement and light cured.
• In the prevention of dental caries all strategies primary
prevention, secondary prevention and high risk strategies
will be involved
• Secondary prevention and high risk strategies will
involve identification of the people who have the early
stages of the disease (secondary prevention strategy) and
people who are at high risk of developing caries.
 Examples of some contemporary

A. Adjustment of contributing factors to dental caries

i. Reduction of the amount of frequency of sucrose

intake.
ii. Access to F-
iii. increase of saliva buffering function and flow rate
and ph.
iv. Increasing the mineral suplly through supplements
e.g. (a) casein phosphopeptides (cpp)
(b) amophous calcium phosphate complex (ACP)
•Normal demineralization needs to be addressed in
order to regain oral balance. This is done by
EXTERNAL REMINERALIZATION and INTERNAL
REMINERALIZATION .
•External remineralization relies on an increase of saliva
flow through fluid intake, use of dental chewing gum,
efficient oral hygeine, diet adjustment and the use of
dentifrice containing CPP/ACP (18.8mg) and fluoride.
•Remineralization depends on presence of water, a
pH76.5 and the availability of minerals such as calcium,
phosphate and strotium.