Conmiwiity Dent Oral Epidemiol 1997: 25: 5-12 Copyright © Munksgaard 1997

I'ritited in Denmark . Aii rigllts reserved

Communify Dentistry
and Oral Epidemiology
ISSN 0301-5661

O. Fejerskov
Concepts of dental caries and their Department of Dental Pathology, Operative
Dentistry and Endodontics, Royal Dentai Coilege,
Faculty of Health Sciences, University of Aarhus,

consequences for understanding Denmark

the disease
O, Fejerskov: Concepts of dental caries and their consequences for understanding
the disease. Community Dent Oral Epidemiol 1997; 25: 5-12. © Munksgaard, 1997

Abstract - The way in which we conceptually consider dental caries determines

our choice of preventive and treatment strategy. In this paper the definition of
dental caries is discussed and the related problems concerning causality are ad-
dressed. Dental caries reflects symptoms of ongoing and past disease - not the
disease itself. As such, it is important to reeord early stages of signs ofthe disease,
i.e. non-cavitated stages of lesion development. The dynamic nature of the pro-
cesses leading to net loss of mineral (hence a lesion) is emphasized, and appreciat-
ing that caries is ubiquitous in populations around the world and initiation and
progression of lesions continues lifelong leads to the logical conclusion that we
Key words: cariogenic microfiora: dental piaque,
can control dental caries through a variety of measures - but not truly prevent diet: oral hygiene: tooth susceptibility
the disease. We can prevent cavities by controlling the patho-physiological events
O. Fejerskov, Department of Dentai Pathoiogy,
which may result in a net loss of mineral. The relative role of dental plaque in Operative Dentistry and Endodontics, Royal
earies control is discussed in relation to the role of the many determinants which Dentai College, Faculty of Health Sciences,
influence the likelihood for lesion development. It is concluded that several para- Venneiyst Boulevard, DK-8000 Aarhus C,
Denmark
digms about the nature of dental caries should be reconsidered to provide the
most cost-effective dental services. Accepted for publication 12 August 1996

Several observations made over the past
10 years have in my opinion neeessitat-
ed this workshop. The decline in dental
caries, which Brst became interna-
tionally accepted about 15 years ago
(1), was for very long thought to be an
excellent example of the dental profes-
sion's success in caries prevention. At a
certain point the enthusiasm led to an
over-reaction with statements such as
".. we are seeing the end of a disease
that has plagued mankind throughout
history" (NIDR Researeh Digest 1988
(2)). When such a statement comes
from an authoritative institution like
NIDR, it is understandable that it has
immense implications for attitudes
towards dentistry as a whole.
Ever since the dental profession be-
eame established as an independent
medical entity, most of its time has been
spent on the relief of pain cau,sed by
dental caries. Moreover, the often in-
adequate dental restorations made
when treating dental caries resulted
over time in the need for replacements
and thus further tooth damage ~ all too
often resulting in the ultimate loss of
teeth. Thus, the major reason for re-
movable and fixed prosthodontics, and
in recent years the variety of implants,
indirectly reflects the result of the
disease dental caries.
Naturally, many have tried to explain
the reason for the decline in dental ear-
ies, but it is noteworthy that the expla-
nations often reflect the profession's dif-
(iculty in understanding the nature of
the disease. Thus, a few factors are
often claimed to be almost entirely re-
sponsible. Examples are changes in
sugar consumption or the widespread
use of fluorides, but as 1 will come back
to later, neither of these factors alone
or in combination has been scientiflc-
ally documented to be able to explain
the changes. The rather simple concepts
of earies etiology and pathogenesis de-
veloped during the middle of this centu-
ry still predominate without any ap-
parent appreciation of the exponential
growth in scientific knowledge during
recent decades, indicating the need for
reconsideration. It eould, of course, be
argued that the extensive scientific ac-
tivity within the very many fields related
to dental caries have had limited clinical
relevance. To me, it seems more likely
that it is a reflection of the fact that
with increased sophistication in the re-
search tools available within the dif-
ferent disciplines such as microbiology,
immunology, electron microscopy, mo-
lecular biology, etc, the scientists are
often trying to relate their detailed and
isolated observations to past clinical
 FEJERSKOV
data and concepts about the diseases
which may not be relevant or updated.
We also have to appreciate that, for
example, the many different so-called
"necessary causes" which have been
suggested concerning caries are primar-
ily derived from in vitro and animal
models, where tight control of con-
founding factors can be accomplished.
The human mouth is not, however, ade-
quately simulated by such models, be-
cause the ecology of the oral cavity is
subjected to widely diverse and variable
experiences within and among individ-
uals.
Finally, it is not uncommon in the lit-
erature within thefieldof oral epidemi-
ology and community dentistry to see
discussions where authors interpret
their data by quoting "known estab-
lished facts" often derived from numer-
ous reviews without the necessary re-
flection as to whether these data - onee
very interesting but derived from stud-
ies based on the scientific premises pre-
vailing at the time - are scientifically
valid for today's discussions.
When, for example, epidemiologists
and public health dentists are not aware
of, or do not understand, the wealth of
new information derived from research
within the basic scienees related to den-
tal caries, it is not surprising that we are
seeing so little development in preven-
tive dentistry. Moreover, we experience
an apparent eontroversy at meetings
and in the literature; a controversy re-
flecting the faet that people are using
the same terminology, but their con-
cepts about the phenomena they are re-
porting upon are in fact very different,
A good example is the continued con-
troversy regarding the notion of cause
and effect. ROTHMAN (3) assumed the
notion of cause and effect and proceed-
ed to distinguish among types of causes,
primary and secondary, neeessary and
sufficient, etc. However, it is apparent
that when related to the earies process,
such an exercise requires that people
agree on specific definitions and clarify
the terms they are using. An obvious
example is the very simple way in which
dental caries is defined. Mostly, the
word dental caries is used synonymous-
ly with a carious cavity.
Any single factor which has been
speculated to play a role in caries devel-
opment has been presented as a pos-
sible "cause" and as such dental re-
search is fraught with aneedotal sup- agnostic cut-off point chosen (5), Clear-
port for various theories and ly, the vast differences which are re-
hypotheses as to how dental caries oc- ported between and within populations
curs. Many of these factors have been depending on which diagnostic criteria
thought to be so important that in are used will have important conse-
attempts to model the disease in human quences on the type of conclusions we
populations by, for example, employing draw, especially if we are looking at the
complex multivariate models involving occurrence of caries as being the out-
as many as 20-40 of these variables (so- come of a given "treatment", etc.
called predictor variables), they are We have therefore reeommended that
brought together without due consider- the signs of the disease be recognized as
ation as to the biological rationale be- being a eontinuum of ehanges of inereas-
hind them. As such, it may not be sur- ing severity (and tooth destruction).
prising that the attempts in ereating They are not the disease itself. What we
such models have resulted in R^ values refer to as caries is not a singular event,
which typically are less than 0,30 and but rather the outeome of an accumula-
sensitivity and speciflcity values which tion of events, a process, spread over a
combined in most studies at best vary period of time. Thus, the carious process
between \AQ% and 160% (review (4)), is the dynamic de- and remineralizing
Therefore, it is important to clarify processes resulting from microbial me-
certain terms, and make an attempt to tabolism on the tooth surface which over
exemplify how a focus on single vari- time may result in a net loss of mineral,
ables, such as certain micro-organisms, and subsequently possibly, but not al-
diet or tooth susceptibility, may result ways, will lead to eavitation.
in eause and effect conceptual models It seems to me most appropiiatc to
which deeply influence the way in which use the term dental caries only to refer
preventive programmes are designed or to the reeorded mineral loss (and cavi-
maintained without adequate consider- ties) as it presents itself in the clinic. At
ation as to whether caries reduction can which stage of progression we should
be better obtained through different record the symptoms, and the sensitivi-
and more cost-effective approaches that ty and specificity of the different diag-
have a scientific rationale. nostic methods, are matters dealt with
elsewhere in this issue. From a public
health point of view - and in daily clin-
ical practice - it is therefore important
Dental caries - recording disease to appreciate that what is referred to
and/or symptoms imprecisely as dental caries covers a va-
Beeause we use the term dental earies riety of hard tissue dissolution and
often rather imprecisely, it is important breakdown stages each of which may
to remember that in most clinical/epide- respond somewhat differently to the
miological studies, this term reflects re- various non-operative treatment meth-
cording of symptoms or signs of ongo- ods (often referred to as "preventive
ing and past disease. Often signs are re- methods"). Thus, the therapeutic win-
corded only at the level of frank dow for fluoride may be very different
eavitation, and interpretation of data when dealing predominantly with non-
ignores that such a sign represents an cavitated stages of lesions from that
advanced stage of tissue destruetion. which should be considered in cases of
This too often leads to statements frank cavitated lesions.
about prevalence and severity of the With the above considerations in
disease in different populations which mind, certain statements are important
eause substantial confusion. An exam- for further discussion:
ple is the claim that "caries-free" gen- - dental caries measured as signs and
erations occur when all this means is symptoms is cumulative in nature
that in contemporary populations of and may progress with time if not in-
children at any given age, no sites yet terfered with (6, 7).
exhibit lesions which have progressed to - caries incidenec rates vary highly
the stage of eavitation. We have pre- within and between populations, and
viously emphasized how much our con- are as high in adults as in comparable
cept about presence/absence of disease child populations (8, 9).
in a population is dependent on the di- - in the last two decades the caries pro-
 Concepts oj dental caries

gression rate has slowed down in chil-

dren whereby an increasing propor- TIME
tion of children at any given age pres-
ent with signs, symptoms at the non-
cavitated stage, only (10), ABSORPTIVE BARRIER
- the disease is ubiquitous in all popu-
lations around the world and the
prevalence of signs/symptoms of on- LOSS
going or past carious activity reaches
100% by adulthood (5),
TIME
- the severity of carious manifestations
has been dramatically redueed in GAIN
most industrial populations during
recent years (1, 11, 12), ABSORPTIVE BARRIER
- dental caries is up to old age the pre-
dominant cause of tooth loss in all
populations worldwide (6, 13-18).
The consequences of these statements
for health care planning and delivery
are obvious.
TIME
Having defined dental earies as a
symptom the most important issue in ca-
riology is to understand what causes the
symptoms. We have previously suggest-
ed that the disease should be defined as
a dynamic process taking place within a
ABSORPTIVE
microbial deposit covering a tooth sur-
BARRIER
face at any given site in such a way that
over time the outcome of the process re-
sults in a disturbance ofthe equilibrium
belween the mineral and the surround- TIME
ings. However, the metabolie processes
in the biofilm on teeth is certainly a phys-
iologieal phenomenon and, as such, it GAIN
should be questioned whether dental Fig. I. a) A simulation of random fluctuations of plaque pH over time at the plaque-enamel
earies (the symptoms) are a result of a interface, b), c), d) Three examples from a potentially inlinitc scries showing erratie loss and
disease as such. Rather, available evi- gain of minerals from dental hard tissues caused tw accumulating (integrating) the effects of
small random pH Hucluations (noise) such as (hose illustrated in Fig, la. The solid horizontal
denee suggests that mineral loss and pos- line in each case represents the "origin", while the dashed horizontal line represents the posi-
sible subsequent cavity formation in tions of an arbitrary absorptive barrier. Note how loss and gain occur erratically in each ease,
teeth is a result of imbalance in the dy- the absorptive barrier being reached at different times (and in Fig, Ib. not at all). The path
natnic equilibrium between tooth miner- of the process, had it been allowed to continue without an absorptive barrier, is shown as a
al and surrounding plaque fluid. As bio- dotted line (19),
films on teeth are physiological phenom-
ena in an oral environment, we can
conclude that dental caries is a simple re- ization, should be considered a random the stage of frank eavitation can be pre-
flection of disturbances in a normal process as well. Therefore, we suggested
vented" (20).
physiological balance brought about by that the caries lesion, observed clinical-
The ease is argued in the following
a multitude of factors which in concert ly, is the accumulation of numerous epi-
with brief comtncnt on some implica-
determine the actual composition ofthe sodes of de- and remincralization. It is
tions of the above considerations for
plaque fluid at the tooth surface. itnportant to acknowledge that these our understanding of caries as a multi-
To better understand this eoneept we processes are not linear, and at any faetorial disease.
may use a model previously suggested stage of lesion development the physio-
(19), In Fig, I the relationship between logic balance between de- and reminer-
the metabolic events in plaque (shown alization may be restored and hence the Multifactorial disease - but dental
as random pH fluctuations) and pos- outcome clinically will be an arrested piaque is the oniy cause
sible consequences for loss and gain of lesion. The relative importance of oral hygiene
minerals from dental hard tissues is With this in mind, 1 therefore postu- (plaque removal) in caries control is
shown. The hypothesis and assumption late that: "Dental caries cannot be pre- often debated (21), but no one wotild
is that the effect on enamel of random vented - but the disease can be con- question the old concept that "a clean
pH fluctuations, i.e, de- and remineral- trolled, so that lesion progression into tooth does never decay". That microbi-
 FEJERSKOV

al deposits on the tooth surfaee cause also Hausen later in these proceedings). have to use proxy variables (eg, measur-
caries - and at a rapid speed when When drawing inferences about associ- ing numbers of CFU of mutans strepto-
sucrose is metabolized to avoid bacteri- ations, we must return to the problem eoeei from saliva as a reflection of actual
al sugar-kill (22) - has been shown ex- of defining the outcome or response concentration at the tooth surface).
perimentally in man (23), Moreover, variable, e.g. the caries lesion. As If we cannot measure the risk factors
tneticulous plaque control can on a stressed, dental caries is a process oc- direetly or accurately, then the measure-
population basis prevent lesion forma- curring at a subclinical level. The clos- ment error involved will be unavoidably
tion (24, 25), est we can come to measuring the pro- large. Even if the eausative relationship
It is therefore obvious that lesions de- cess itself is to look for evidence of between the risk factor and caries were
velop where microbial deposits are al- where it has been. There is, as will be very strong, we could not expeet statisti-
lowed to remain for prolonged periods discussed later, no gold standard con- cal analyses to show more than mostly a
of time, e,g. the occlusal surfaces during cerning diagnosis of caries, so there is weak association when there is large
eruption into functional occlusion, in some degree of imprecision about meas- measurement error in one variable. Link
interproximal areas below contact uring the response variable itself. As this to the problems of rneasuring pre-
points/facets, and along the marginal such, we are not measuring the disease cisely the continuum of changes that
gingiva. In the latter case, therefore, itself, but in reality a proxy variable. characterize carious lesions and we are
active root surface caries lesions are Precisely because of this, there rnay be left with a rather unsatisfactory situa-
predominantly confined to the retention problems in determining the strength of tion when trying to measure appropriate
sites at the enamel-cementum junction association between various (risk) fac- associations.
approximally and corresponding to the tors and dental caries. When we then
position of the retracted gingiva. In consider the fact that almost all the risk
other words, these areas do not repre- factors thought so far to be of interest Why predominantiy focus on a few
sent particular susceptible sites because are themselves very diffieult to measure determinants?
of "deficient composition of the precisely, we must appreciate that the is- It is a common postulate that the neces-
tissues", but merely reflect local envi- sue is very complex. In faet, several fac- sary causes of earies are: susceptible
ronmental conditions. Once a frank tors we cannot even measure directly, but teeth, presence of sufficient atnounts of
cavity is formed, this site represents an
ecological niche and unless such lesions
arc subject to plaque control and/or
have access to free salivary flow, the
lesions will progress, as the plaque me-
tabolism results in much more extensive
and prolonged pH drops in such cavi-
ties than in plaque covering sound or
inactive caries surfaces (26),
Once this is appreciated, the multi-
factorial concept is relevant as the nu-
merous biological factors which may
influence the outcome (i.e, net loss of
mineral ultimately resulting in cavity
fortnation) should be considered as de-
terminants (see Fig, 2).
The complex interplay between sali-
vary secretion and composition com-
bined with the way in which diet, the
local immune response in the oral cavi-
ty, pH fluctuations at various sites etc,
influence the plaque composition and
metabolism will then, in concert with
innumerable other factors such as fluo-
ride ion concentrations in the oral
fluids, determine the likelihoocl for a net
loss of mineral and the rate at which
this occurs at any plaque covered site.
If this concept about the disease and
its manifestations is accepted, it could
be understood why it is so difficult to
interpret data about associations con-
cerning dental caries; and why no good Fig. 2. A schematic illustration of the relationship between llic etiological factor - denta
predictor models are available (4) (see plaque - and determinants and conlounders in dental caries (84),

cariogenic microflora and easily fer-
mentable carbohydrates (Kcyes' host-
agent-environtnent model). Each of
these factors has therefore been dealt
with over the years in numerous reviews
(27). However, from a public health
point of view, it often results in a situa-
tion where it may be difficult "to see the
wood for trees". As the dental profes-
sion has invested extensive resourees in
trying to increase tooth resistance, cotn-
bat the use of sugars and change diet-
ary habits, and identify and eliminate
specific micro-organisms, it is impor-
tant from a cost-effectiveness point of
view to address the question as to
whether these resources could be better
spent elsewhere in health protnotion.
It is, of course, not possible in a few
sentences to pay tribute to the vast
numbers of studies in these different
disciplines. The problem is, however,
that very often major eonclusions are
derived out of /;; vitro or animal studies
whereas well-conducted human studies
from recent years are much more scarce.
The main question to address within
the aim and scope of this workshop is
whether we are able to achieve better
caries control in our populations by ap-
plying present knowledge on causality
more appropriately?
Tooth susceptibility ("The Host") -
For long it was thought that earies-re-
sistant teeth existed and numerous
attempts were tnade to identify struc-
tural and chemical factors of import-
ance (28-30), Such a thing as relative
resistance of enamel to caries attack
does not exist as concluded by WEATH-
ERELL, ROBINSON & HALLSWORTH in a
review in 1983 (31), Nevertheless, the
major concept prevailing in the past
was that fluoride incorporated into the
apatites of the enamel surfaee would
increase the resistance towards caries.
This led to the extensive systemic use
of fluorides in caries prevention. At a
certain stage, it even resulted in such
terms as "fluoride-deficient teeth".
However, it is now realized that fluoride
exerts its predominant cariostatic effect
by interfering with the carious process
(the dynamic equilibrium at the inter-
face between mineral surface and oral
fluid) - for reviews see (32-36). From a
publie health point of view, it is there-
fore extremely important to appreeiate
the fact that fluoride most likely acts as
a therapeutic agent on active ongoing
disease processes through its presence in
elevated concentrations in the oral
environment (32, 37),
This does not mean that exposure of
the tooth surface to the oral environ-
ment may not modify the structural and
chemical properties of the tissues so as
to make them less susceptible, /// situ
caries tnodel experiments have indi-
cated that arrested smooth surface
enamel caries lesions (despite subsur-
face loss of mineral) are less susceptible
to a renewed acid attack (38, 39).
The concept that pits and fissures in
and of themselves are particularly sus-
ceptible to caries should be reappraised
as data indicate that these sites do not
easily develop lesions if good overall
oral hygiene is prevailing (40, 41),
Finally, exposed root surfaces consti-
tute areas which require more extensive
studies before conclusions concerning
relative susceptibility can be drawn. The
root surface undergoes substantial
chemical changes when gradually ex-
posed to the oral environment as a re-
sult of periodontal reeession (42). This
is most likely a result of caries processes
which do not result in lesions of clinical
significance. As such, there is a substan-
tial increase in crystal size in exposed,
but clinically sound outer cementum,
and even more in (he surface cementum
covering subsurface small lesions (42).
Root cementum suddenly exposed to
the oral environment (as a result of, for
example, periodontal surgery) is highly
susceptible to mineral loss resulting
from plaque metabolism (43), This
might explain why it is very difficult to
prevent new root caries lesions from de-
veloping in periodontally treated pa-
tients eveti when extensive fluoride
treatment is provided (44, 45), In this
context, it is of interest that root earies
prevalence in adult and elderly Chinese
is low despite no oral hygiene and ex-
tensive gingival recession (6). The
plaque covering these root surfaces ex-
hibits a profound and long-lasting pH
drop following suctose exposure (46).
However, in these populations the bad
oral hygiene results in severe gingivitis
with extensive exudation of erevicular
fluid with a high pH. This would facili-
tate a conditioti where the plaque fluid
would be supersaturated with respect to
calcium and phosphates and certainly
extensive amounts of subgingival calcu-
lus are present in these populations
Concepts of detital earies
(47), It is tempting to combine this in-
formation and postulate that the envir-
onment resulting frotn gingival in-
flammation over time might result in
substantial chemical modification ofthe
root surface and hence make it less sus-
ceptible to the caries challenge. Pure
speculation, but maybe also a hypo-
thesis which requires research. As we at
present apparently can do very little if
anything in the clinic to improve tooth
resistance, let us turn to the causative
role of specific micro-organisms in den-
tal caries.
The cariogenic niicro-organisnts
( "The Agent") - As all types of micro-
organisms in the oral cavity are not
equally able to ferment carbohydrates,
it has been logical to look for major
caries pathogens. While research in the
first half of the century focused on the
role of lactobacillus and used salivary
counts as a caries susceptibility measure
(48), the latter half has predotiiinantly
dealt with the role of mutans strepto-
cocci (for reviews see 49-53), The ap-
preciation of earies as an infectious and
transmittable disease derives from the
studies by FITZGERALD & KEYES (54)
and KHYtiS (55) who studied certain
streptococci in hamsters fed a sugar-
rich diet. However, while the oral flora
of rodents is relatively simple, humans
harbour a very complex flora (53, 56).
Nevertheless, most studies in man have
dealt mainly with mutans streptococci
and that their relative contribution even
in plaque from active carious lesions
may vary from not detectable to a max-
imum mean percent of 30"/) of the total
viable counts is often ignored (57),
Moreover, it is important to note that
mutans streptococci are not primary
colonisers of tooth surfaces (58),
In protected sites, plaque develop-
ment may result in a climax community
within 2 weeks comprising a complex
flora whereas constant disruption of
microbial cotnmunities (from tooth-
brushing) results in constant secondary
succession and a more simple plaque
composition (56). The following obser-
vations are important.
- 5, nnitans is often found at higher
concentrations in plaque covering
early enamel caries lesions (59) and
baeterial succession with increases in
5, mutans (and lactobacilli) is ob-
served in many sites developing white
spot lesions (57).
10 FEJERSKOV
- there is no assoeiation between ap-
proximal caries lesions, presence/ab-
sence of S. mutans or the plaque
mutans counts, and plaque pH re-
sponse in children (EMILSSON,
ScHEiE & FEJERSKOV, unpublished),
- children with increased numbers of
carious cavities have higher salivary
mutans eounts, but subgrouping of
children based on different levels of
salivary mutans counts does not al-
low a distinction between caries
active and inactive children (60, 61),
- the explanatory power of mutans
streptococci and lactobacilli for den-
tal caries is low and diminishes
further when controlling for con-
founders such as variation in oral hy-
giene (62, 63).
- the number of mutans streptococci or
lactobacilli in plaque does not ex-
plain the variation in caries experi-
ence (64),
- a dramatic decline in caries has been
documented over a few years without
apparent ehanges in salivary tnutans
levels in the population (65),
- a review of the literature concludes
that no single type of micro-organism
can be claimed to be the pritnary
cause of either root or enamel caries
(52).
- the overall low predietive power of
mutans group streptococci in ran-
domly selected groups, aecentuated
in subjects with caries, speaks for the
need for some kind of re-evaluation
of this risk factor (66),
The problem at present is highly im-
portant for any public health approach.
If mutans streptococci are of key im-
portance for carious lesion develop-
ment (if it is a necessary cause), it is re-
levant to consider antimicrobial treat-
rnents and maybe even vaccines.
However, if we instead favour the con-
cept that mutans streptococci are "indi-
eator miero-organisms" which increase
in number when the pH of the environ-
ment is low (because they are aciduric),
the clinical consequences are very dif-
ferent and vaccination irrelevant. Eco-
logical theory suggests that the local en-
vironment of a habitat has a major im-
pact on its associated microflora (67),
Therefore, in areas where lesions devel-
op - and cavities occur - growth in
numbers of aciduric micro-organisms
(lactobacilli and mutans streptococci) is
to be expected. If lesions are arrested
due to plaque removal, and control
and/or access of stimulated saliva to the
cavity is favoured, succession of other
bacteria will result in a reduced propor-
tion of S, mutans and Lactobacillus. In
other words: they are not causative fac-
tors as such, but indicator micro-organ-
isms reflecting the environmental condi-
tions.
Diet ( "The Environment") - The role
of sugar as a determinant which en-
hances acid production in dental plaque
and hetice carious dissolution is indis-
putable. However, the associations ob-
tained from the gross comparison of
DMFT data and per capita sugar con-
sumption in different populations are of
limited value because of great varia-
tions in the way in which data are ob-
tained, SREEBNY (68) found a positive
association between g-sugar/person/day
and caries experience of 12-year-olds
from 47 countries (a country average of
DMFT!?), On the other hand, a cotn-
parison of annual per capita sugar con-
sumption in all European countries
shows absolutely no association with
the caries experience of children in
these countries by the mid-1980s (69).
It eould be argued that European
countries are not that different, and
that a variation in per capita sugar con-
sumption in kg/year ranging from 27,4
kg to 52.2 kg will not be reflected be-
cause everyone in the populations is ex-
posed. The cause is universally present
(70). The really important issue is the
relationship between diet and dental
earies, which has often been reviewed
(68, 71-73). It is apparent that diet is
extremely difficult to "measure" with
any degree of accuracy. We have pre-
viously pointed out that it is unclear
whether in fact increasing the aeeuracy
of measurement of the food items con-
sumed is likely to help, sinee the nutri-
ent content and amounts consumed
nevertheless remain a proxy for what
actually occurs at the tooth surface
(74). Dental epidemiologists have, in
the words of BLOCK (75) sometimes
"been captured by the nutritionists'
dream of developing a method which
will yield precise and aeeurate quantita-
tive amounts of nutrients. This may be
an appropriate goal for nutritionists
who would like to be able to set quanti-
tative standards for nutrient intake ...
but at the present level of knowledge
about the relationships between nutri-
tion and disease, such precision may be
unnecessary".
Very few up-to-date studies on the as-
sociation between diet and caries are
available in contemporary populations
with low caries experience and the re-
sults from two well-designed longitudi-
nal studies (76, 77) showed a poor corre-
lation, if any, with frequency of sugar
consumption and caries, and the caries
increment was only weakly correlated
with total intake of sugars. However, it
should be kept in mind that these studies
are conducted in populations where the
total sugar consumption overall is very
high. As stressed by ROSE (70), it may be
an unsuccessful approach to do such
studies within a population if there are
not sufficient differences in exposure at
the time of the study. Even in countries
throughout Africa where the overall car-
ies experience amongst children is rather
low (78), there are very few good studies
on the relationship between diet, sugar
and dental caries (for review (73)), In
East African populations the diet is pre-
dominantly starch. Even meticulous
analyses of dietary habits and food com-
position have not been able to explain
within-population variation in caries ex-
perience within African children. How-
ever, gross differences in dietary tradi-
tion and snack frequency between Afri-
can and Asian children in Kenya
certainly show that Asian children have
a much higher caries experience.
With the appreciation of the fact that
the majority of the world's populations
experience a low caries progression rate,
and that subfraetions account for the
majority of earies experience, it is tints
highly recommended that much better
and more relevant data on the relation-
ship between dietary habits and earies
are provided.
Conclusion
It will be apparent that much of the em-
phasis on improving tooth resistance
and reducing or eliminating specific
bacteria and changing dietary habits
may have had little impact - and yet we
are able to control dental caries through
a combination of appropriate oral hy-
giene and use of fluorides. In some
populations fissure sealants are also re-
commended. We should, however, real-
ize that the caries decline cannot be ex-
plained from these factors alone. A

ehange in diagnostic criteria and treat-
tnent decisions has occurred (79, 80). In
parts of the world, where fluorides are
not cotiimonly used, a substantial re-
duction in caries experience has been
reported (81, 82), In water-fluoridated
communities a comparable reduction
has occurred without apparent changes
in oral prevention strategies (12, 83),
Fluoride beyond doubt is a eornerstone
in controlling dental caries, but we do
not yet have appropriate data on the
intraoral therapeutic window of this
drug.
It has become clear during the recent
decades that several paradigms about
the nature of dental caries have to be
reconsidered in order to provide the
tnost cost-effective dental services in
different parts of the world. Therefore
alone, there is a strong need for more
appropriate research in cariology in
man ranging frotn basic sciences to
public health applications.
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