How does epidemiology help
in the understanding of
oral diseases?
Introduction
In general, epidemiology is the
study of how often diseases occur in
different groups of people and why
they occur (Coggon et al., 1997).
Other rather similar definition states
that epidemiology is the scientific
study of the frequency, distribution
and determinants of health and
disease in human populations. Oral
epidemiology, hence, is that branch
of the discipline that studies oral
health and diseases (Community
Dental Health Services, 2004).
The information gained from
epidemiological studies not only
provides better understanding of a
particular disease but may also be
applied in planning and evaluating
strategies to prevention and
treatment. It provides a guide to the
management of patient in whom
disease has already developed.
Clinicians may not actually carry out
the epidemiological surveys but their
clinical practice is influenced by
epidemiological information. For
example, clinicians may require
information regarding the prognosis
of the disease or the best treatment
option for a particular age group with
a specific condition. This would
definitely require an understanding of
the natural history of the disease and
the way in which it may be modified
by specific factors for a particular
case. As such, epidemiological
studies serve two main targets,
population health practices and
clinical practices. This is made
possible as the central concern of
epidemiological studies is with
causation and the relationships
between various exposures or
interventions and their outcomes. All
decisions that health professionals
make about disease and its treatment
involve assumptions about cause and
effect relationships (Community
Dental Health Services, 2004).
This paper is organised in the
following way: The first section will
briefly illustrate some basic concepts
in the application of epidemiological
studies with regards to aetiology and
the use of conceptual framework to
explain diseases. It is imperative to
have some understanding about
these basic concepts in order to
APDF Newsletter July to August
appreciate how epidemiology helps
in the understanding of oral diseases.
The second section will focus on how
epidemiological studies assists
clinicians in understanding oral
diseases. Examples of its application
in three aspects of dentistry;
cariology, periodontology and oral
cancer, will also be briefly illustrated
as examples to assist in
understanding the subject. It should
be bear in mind that it is not the
intention of this paper to provide an
i n - d e p t h a p p r a i s a l o f
epidemiological methodology but to
explain how data derived from
epidemiological studies have
contributed in the following aspects:
- determination of risk factors in
oral diseases,
- global distribution of
oral diseases, and
- pattern and progression of
oral diseases.
Basic concepts in the
application of epidemiological
studies.
Aetiology and conceptual
framework
Probably the two most
fundamental questions asked by any
clinicians are, what causes a
particular disease and what is the
probability (risks) that an individual
develops a given disease or
experience changes in health status.
It is imperative to appreciate that the
recognition of risk factors requires a
good understanding of the
aetiological factor. Understanding
the aetiology or aetiologies of
diseases also forms the basis of
prevention. Applied to periodontal
diseases, for example, experimental
gingivitis studies have shown that the
accumulation of dental plaque
biofilms challenges the body defence
mechanisms by eliciting an
inflammatory process and this will
persist as long as the dental plaque is
present (Albandar, 2002). The same
is also true in the study of cariology,
where the experimental human study
by von der Fehr et al., (1970), which
looked at the effect of sucrose
solution rinse with abstinence from
oral hygiene, showed that sugar is not
an absolute aetiologic factor but is a
Author: Kei Joe LEONG
risk factor (modifying risk factor)
while the aetiologic factor lies in the
dental plaque (Axelsson, 2000).
With regards to contributing
further information about aetiology,
epidemiological studies may be
broadly divided into three groups;
descriptive, analytic, and
experimental. In descriptive studies
the frequency of occurrence of
disease in different communities or in
different subgroups within a
community is described. Analytic
studies are designed to test
hypotheses about the influences that
determine why some populations, or
certain individuals within a
population, are affected by a disease
while others are not. Experimental
studies test such hypotheses by
showing whether or not altering
exposure to a suspected cause may
change the frequency of a disease
(Barker et al., 1998).
Identification of a potential
causal factor alone is not sufficient to
estimate its role during the process
that eventually leads to an outcome.
These study designs may not be able
to reproduce real life processes. In
the real life situation, both biological
and non-biological variables have a
role that eventually leads to the
outcome of a disease. This inter-
relationship between biological and
non-biological variables is highly
complex (Holst et al., 2001). In
attempting to relate all these factors
together, a conceptual framework
would be required. A conceptual
framework is a model used to
d e s c r i b e t h e i n t e r- r e l a t i o n s h i p s
between possible risk factors
(biological and non-biological) on an
outcome of a disease. It provides
guidance for statistical analysis and
aids the interpretation of their results
in the light of social and biological
knowledge (Victora et al., 1997). In
the field of cariology, for example,
Holst et al. (2001) suggested the
following framework for explaining
caries in a wider scale (Figure 1).
This framework includes variables
from social structure, social context,
individual level and biological level.
17
 Social Structure Social Context
Political
culture
Social
environment
Health
policy
Home,
School,
Work
Economic
conditons
Figure 1. An approach to a framework for explaining caries in
populations (Holst et al., 2001)
A s m e n t i o n e d e a r l i e r,
epidemiology attempts to identify
factors or determinants whose
eliminations would prevent or reduce
the morbidity rate. Traditionally, this
is achieved through a combination of
inductive and deductive conclusions
to discover the related causes of a
disease (Scheutz and Poulsen, 1999).
The basis of inductive understanding
of scientific knowledge is that all
scientific knowledge can be derived
from observation. Generalisation is
made on the basis of finite number of
observations of a particular event.
For example, if A1 is followed by B1,
A2 is followed by B2, An is followed
by Bn, then it could be reasoned that
A is always followed by B. The
problem arising from this universal
statement (conclusion) is that these
observations merely show a series of
events and not causal relationship.
Nevertheless, base on these universal
statements or principles, we should
be able to construct a frame of
reference from these principles and
assumptions to deduce (the deductive
approach) some of the implications
on which to base our explanation and
predictions (Scheutz and Poulsen,
1999). Deductive approach in the
development of a theory is based on a
selection of variables to be tested,
determining the methods of
registration and measurement, and
interpreting the data collected
(Scheutz and Poulsen, 1999). This
logical approach can be summarised
in the following flowchart (Figure 2):
Scheutz and Poulsen (1999),
however, proposed a more pragmatic
approach in the identification of
related causes of disease. The
authors stated that a factor is a cause
of disease when changes in a factor
inevitably lead to changes in
morbidity. They further claimed that
APDF Newsletter July to August
Individual Level Biological Level
Psychologic
reactions
Brain
Health
behaviour
Oral
ecology
Caries
Material
factors
Conceptual model
Changes in morbidity
after intervention
Are the statistical
associations causal?
Conceptual model
Figure 3: Identification of causes based on a conception model
(Scheutz and Poulsen, 1999).
describing disease as multifactorial is
meaningless and that belief in a
specific factor as the one and only
cause is unproductive and pointless.
For example, it is not sufficient and
not straightforward to quote,
“…sugar causes caries”. Many other
factors would need to be taken into
consideration including; the type of
sugar, method and frequency of its
consumption must all be specified.
Likewise, not everyone with the same
sugar consumption will develop
caries. Therefore, we should be
actually looking at what other
components operate together to
cause caries. This concept, where
many factors act together to cause a
disease is known as “causal web”. In
the example described above, the
possible components are; amount of
plaque, buffering capacity of saliva,
characteristic of the enamel,
microbial flora, genetic factors and
fluoride. This pragmatic approach of
producing a conceptual model in
epidemiological studies could be
illustrated using the following
diagram (Figure 3).
Empirical data obtained through
observation
Induction
Conceptual model
Deduction
Explanation and prediction
Figure 2: Flowchart showing the
application of the induction and
deduction approach in
epidemiological studies.
Empirical data
Calculation of statistical
associations in the model’s
causal web after adjusting
for confounders
Application of epidemiology in
understanding oral diseases
Determination of risk factors in
oral diseases
Risk generally refers to the
probability of an event happening.
From a medical perspective, the term
“risk factors” is used to indicate the
likelihood that an individual or a
group of population who are exposed
to certain factors (risk factors) will
subsequently develop a particular
disease. Therefore one of the uses of
identifying risk factors is to predict the
occurrence of disease. Although risk
factor does not necessarily cause
disease, the knowledge of risk can be
used in the diagnostic process, since
the presence of a risk factor increases
the prevalence of disease. This is
particularly true if the factor is strong
and predominant as individuals who
are not exposed to it is unlikely to
develop the disease. Apart from
prediction and diagnosis,
identification of risk factors also aids
in prevention of diseases (Fletcher et
al., 1996).
Epidemiological approach in
periodontology is rather similar to
18
that of cariology as it also includes
both biological and non-biological
variables in determining the risk
factors for periodontal disease. It is
acknowledged from previous studies
in animals and humans that
periodontitis is preceded by
gingivitis. Epidemiological studies
have shown that, although the
prevalence of gingivitis is high among
children and adolescents, only a
subset of individuals and a limited
percentage of sites in these
individuals will experience severe loss
of periodontal tissues. Consequently,
periodontal disease activity is not
linearly continuous but there exist
certain risk factors that affect its
p r e d i c t a b i l i t y ( A l b a n d a r, 2 0 0 2 ) .
Hyman and Reid (2003) quoted that
epidemiological studies in the field of
periodontology have investigated
potential demographic and lifestyle
risk factors for periodontal diseases.
A g e , g e n d e r, t o b a c c o u s e , a n d
diabetes mellitus have been
consistently identified as important
potential risk factors for destructive
periodontitis. They also reported
studies that identified additional risk
factors such as, osteoporosis,
plaque, gingivitis, angina, allergy,
d e n t a l v i s i t s , c o r o n a l d e c a y,
education, income, family history of
edentulism, and non-white
racial/ethnic group (Hyman and Reid,
2003).
Following identification of risk
factors, Albandar and Rams (2002)
commented that in the assessment of
causation between periodontal
diseases and their suspected
aetiologic risk factors, it is extremely
valuable to demonstrate consistency
of the relationships in multiple,
representative population samples.
Furthermore, if various researchers
investigated various populations
produced similar conclusions on the
distributions of periodontal diseases
and/or their associations with
putative risk factors, then one can be
more confident of the existence of the
causal relationship (Albandar and
Rams, 2002). This, however, does
not necessarily mean that
inconsistency in reports of risk factors
of oral diseases from different
populations will be of no value.
Inconsistency in global
epidemiological reports of risk
factors of oral diseases may actually
be caused by some unknown or
unidentified risk factors and this will
usually prompt further exploration.
Data obtained from global
epidemiological studies of oral
cancers have revealed that risk
APDF Newsletter July to August
factors are geographically
determined. The specific risk factors
in different geographical area has
been identified; tobacco and/or
alcohol in western and southern
Europe and southern Africa, betel
quid in south-central Asia and
Melanesia, and the high rates of lip
cancer in Australia/New Zealand has
been attributed to solar radiation
(Scully and Bedi, 2000). Betel-quid
chewing, with or without the
inclusions of tobacco, has long been
identified as a major risk factor in
oral cancer for the older Asian
population. The inclusion of tobacco
in the quid is shown to increase the
risk significantly (Llewellyn et al.,
2001).
Global distribution of oral
diseases
The global distribution of certain
oral diseases provides a better
understanding of the diseases in
terms of knowing which particular
part of world (specific population) is
more at risk of certain oral disease.
This, eventually, has great implication
in prevention and management of the
oral disease. Data from global
epidemiological studies in
periodontology clearly showed a less
pronounced relationship between
dental plaque and the severe form of
periodontitis. It is also
acknowledged that the severe forms
of periodontitis affect only a sub set
of population groups globally, even
though plaque-induced gingivitis and
slight to moderate forms of
periodontitis are widespread within
the same population (Albandar and
Rams, 2002). The report by Albandar
and Rams (2002) also showed that
only a relatively small subset of the
populations in the United States of
America, Central and South America,
Europe, Africa and Asia/Oceania
exhibit this severe forms of
periodontal attachment loss with
deep periodontal pocket formation.
Moreover, these studies showed that
there is a significant interaction
between genetic factors and other
environmental and demographic
factors, including a possible
modifying effect of smoking, and
variability in the occurrence of certain
genotypes in different race-ethnicity
groups. The most significant gene
aberrations studied so far are those
thought to be associated with altered
host immune response to infection
including interleukin-1 (IL-1) gene,
vitamin D recptor gene and fMLP
receptor gene. Genetic variation in
cytokine expression is used as a
possible marker for aggressive
periodontitis. For example, the IL-1 is
a potent stimulator of bone resorption
and hyperproduction of this cytokine
following infection by periodontal
pathogens is believed to be one of the
mechanisms of periodontal tissue
destruction. Although the potential
use of IL-1 polymorphisms as a
marker for severe periodontitis may
not be straight forward due to
conflicting results in different studies
of population, it has been shown that
African American and Caucasian
American families with IL-1 genotype
positive are at a higher risk for
aggressive periodontitis irrespective
of race or smoking status (Albandar
and Rams, 2002).
Likewise, widespread
application of epidemiological
studies in the field of oral cancer has
provided valuable information
concerning distribution of the
disease, its incidence and
prevalence, aetiological factors,
survival rates and genetic
predispo sitio n (Scully and B edi,
2000). Reports of estimates of the
worldwide incidence of 25 major
cancers in 1990 states that oral
cancer is the 12th most common
cancer in the world and the 8th most
frequent cancer in men. Oral cancer
in men mainly occurs in western and
southern Europe, south Asia,
Melanesia, southern Africa and
Australia/New Zealand whereas oral
cancer in women is prevalent in
south-central Asia, Melanesia and
Australia/New Zealand. Genetic
predisposition in oral cancer was also
noted to be geographically
determined. The molecular changes
found to be associated with oral
carcinomas in western countries (UK,
USA, Australia), particularly P53
mutations, are infrequent in the east
(India, south-east Asia), where the
involvement of RAS oncogenes,
including mutation, loss of
heterozygosity (H-RAS) and
amplification (K- and N-RAS) are
common. Genetic differences in the
ability to metabolise pro-carcinogens
and carcinogens or the ability to
repair DNA damage may also exists
between different ethnic groups.
Pattern and progression of oral
diseases
Epidemiological studies of
dental caries showed that caries
appears to be distributed in a
characteristic manner within the oral
cavity. Findings showed certain
symmetry between the maxillary and
mandibular arches. Furthermore,
19

Figure 4. Percentages of different dental conditions on each tooth caused
by caries in both upper and lower arches for adults.
Diagram reprinted from Pitts et al. (2003).
there is also evidence to suggest that
there is bilaterality in the occurrence
of dental caries (Axelsson, 2000).
The degree of bilaterality in both
arches is best illustrated in the
following diagram (Figure 4), which is
based on the data available from the
National Surveys of Adults’ Dental
Health in the United Kingdom 1998.
Figure 4 shows two examples from the
data with regards to the percentages
of different conditions caused by
caries on each tooth in both right and
left side of the upper and lower
arches for adults aged 55 years or
more and in all dentate adults (Pitts et
al., 2003). Although the degree of
symmetry between the upper and
lower arches is not very obvious, the
pattern of distribution of these
conditions appears to be remarkably
symmetrical on both right and left
sides on each arch. The clinical
implication of this bilaterality
according to Axelsson (2000) is that,
if a lesion is detected on a particular
tooth surface, the risk of a lesion
developing on the contralateral
similar surface is greater than on any
other surfaces on the same side of the
mouth.
Apart from providing data
regarding pattern of distribution of
oral diseases, epidemiological data
could also contribute to the
understanding of patterns of progress
of certain oral diseases. One such
oral disease that has been
investigated for its pattern of
APDF Newsletter July to August
progression through epidemiological
studies is caries in children under the
age of 6 years, often called early
childhood caries. We l l - d e f i n e d
caries patterns would enhance the
ability of an analysis to identify
associations between suspected risk
factors and early childhood caries as
each risk factor may have an
association that is temporally critical
to the cariogenic process (Psoter et
al., 2003). Furthermore,
understanding the pattern of diseases
may help the clinician to plan
accordingly as to when to intervene to
prevent the progression of diseases.
Using a method known as
multidimensional scaling, Psoter et
al. (2003) used data collected from
previous epidemiological studies,
5171 children aged 5-59 months
(1994-1995), to propose patterns of
caries in the primary dentition of
preschool children. A conceptional
map was drawn to illustrate these
patterns (Figure 5).
With regards to periodontal
diseases, Albandar and Rams (2002)
stated in their overview of global
epidemiology of periodontal diseases
that, while gingivitis parallels with the
level of oral hygiene in a population,
it is by itself a poor predictor of
subsequent periodontal disease
activity. Regardless of this, young
subjects with overt gingival
inflammation more frequently exhibit
periodontal attachment loss than
adolescents without gingival
inflammation. Furthermore,
gingivitis always appears to precede
the development of periodontitis, as
there is no data around the world that
indicate the onset of periodontitis
occurs without gingival inflammation.
Conclusion
Epidemiological data does not
merely provide information about
frequency of occurrence of disease in
different population. Some of the
concepts applied in the process of
d e t e r m i n a t i o n o f a e t i o l o g y, r i s k
factors and conceptual frameworks to
e x p l a i n i n t e r- r e l a t i o n s h i p o f t h e
factors have been illustrated. A brief
account of how epidemiological
studies may help in the understanding
of oral diseases has also been
discussed. The three main aspects of
application of epidemiological
studies discussed in this paper are,
determination of risk factors in oral
diseases, global distribution of oral
diseases and pattern and progression
of oral diseases. The list of these
aspects may not be complete as there
could well be other aspects where
epidemiological studies may be
applied in the study of oral diseases.
Understanding the inter-relationship
and role of biological and non-
biological factors of diseases
provides the clinicians an insight on
the extent of their part, as to what can
and cannot be change in prevention
of diseases and also in patient
management. Furthermore, due to
the limitation of clinical data on its
own, epidemiological data would be
needed to test it objectively.
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20
 Figure 5. Conceptional map of caries patterns in the primary dentition
derived from multidimensional scaling in children 5-59 months of age.
Diagram reprinted from Psoter et al. (2003).

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