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Dietary Effects on Dental Diseases

Public Health Nutrition 4(2B), 569-591 2001.
Dietary Effects on Dental Diseases
Aubrey Sheiham *
Department of Epidemiolgy and Public Health, University College London,
1-19 Torrington Place, London WC1E 6BT, UK
Accepted: 1 August 2000


Dental caries is a highly prevalent chronic disease and its consequences cause a lot of pain
and suffering. Sugars, particularly sucrose, are the most important dietary aetiological cause
of caries. Both the frequency of consumption and total amount of sugars is important in the
aetiology of caries. "The evidence establishing sugars as an aetiological factor in dental
caries is overwhelming. The foundation of this lies in the multiplicity of studies rather than
the power of any one."1. That statement by the British Nutrition Foundation's Task Force on
Oral Health, Diet and Other Factors, sums up the relationship between sugars and caries in
Europe. There is no evidence that sugars naturally incorporated in the cellular structure of
foods (intrinsic sugars) or lactose in milk or milk products (milk sugars) have adverse
effects on health. Foods rich in starch, without the addition of sugars, play a small role in
coronal dental caries.

The intake of extrinsic sugars beyond four times a day leads to an increase risk of dental
caries. The current dose-response relationship between caries and extrinsic sugars suggests
that the sugars levels above 60g/person/day for teenagers and adults increases the rate of
caries. For pre-school and young children the intakes should be proportional to those for
teenagers; about 30g/person/day for pre-school children.

Fluoride, particularly in toothpastes, is a very important preventive agent against dental
caries. Toothbrushing without fluorides has little effect on caries. As additional fluoride to
that currently available in toothpaste does not appear to be benefiting the teeth of the
majority of people, the main strategy to further reduce the levels of caries, is reducing the
frequency of sugars intakes in the diet.

Dental erosion rates are considered to be increasing. The aetiology is acids in foods and
drinks and to a much lesser extent from regurgitation.

                Dental caries, sugars,erosion,  recommendations


There are two major dental conditions, dental caries and periodontal disease. As diet has not
been implicated in periodontal disease, this report relates to diet and caries. Factors
following eruption of the teeth are much more important than pre-eruptive nutrition in the
aetiology of caries2. Therefore this review is restricted to the effects of post-eruptive diet
on caries. Dental erosion is increasing, so the report will also review the relationship
between diet and dental erosion. Throughout the report, sugar refers to sucrose and sugars to
total sugars. Most of the reports referred to relate to extrinsic sugars as defined by COMA3
as  "Sugars not located within the cellular structure of food". Non milk extrinsic sugars
(NMES) are "Sugars found in confectionery, soft drinks, table sugar. Biscuits, cake, fruit
juices, honey and sugars added to recipes." 3.

1. The Burden of Disease
   Epidemiological analysis within EU
   Extent of problem
   Cost of treating dental caries

Dental diseases, particularly dental caries, are the most expensive part of the body to treat.
Caries is indeed the most expensive human disease in terms of direct costs. For example, the
direct costs of caries treatment in Germany was 20.2 billion, CVD 15.4 billion DM, diabetes
2.3 billion DM.4. In West Germany, the cost of dental care was 10.3% of the health budget in
19945. The high cost of treatment is directly related to the progressive nature of dental
caries. As a higher proportion of older people are retaining there teeth, and they are more
susceptible to caries than younger cohorts6, and they require more extensive treatment and
retreatment of their fillings, the cost of treatment of caries is likely to increase.

Dental Pain

Dental pain is mainly due to dental caries. Among a national sample of UK children aged 14-15,
49 per cent had experienced toothache7 and 40 percent of UK adults had dental pain (in the
past year8. In England, 47 per cent of 8-year olds in North London had experienced toothache9.
Dental pain caused crying in 17 per cent of children. 7.6 per cent of children had pain in the
previous 4 weeks. Among these 45 children, this recent pain resulted in stopping playing in 26
per cent, eating in 73 per cent, sleeping in 31 per cent and in going to school in 11 per

Dental caries in children

Despite the marked declines in caries in the past 30 years, dental caries in pre-school
children remains a major dental public health problem in most EU countries. The caries
condition of children of immigrants and refugees is particularly poor. Early childhood caries
(ECC) affects one in ten of all 3-4 year olds in the UK. A higher likelihood of caries
occurred in children given a sweetened comforter.  These findings highlight that ECC "... is a
serious public health problem in disadvantaged communities in both developing and
industrialized countries ..... " 10. A national survey in Britain indicated that 50% of
children in Scotland aged 3 1/2  to 4 1/2   had experienced caries and of children with active
decay, 30% had decay which extended into the dental pulp11.

Marthaler et al12 in an extensive review reported on the prevalence and severity of dental
caries in Europe between 1990 and 1995. The data reported here are mainly from their review.
Dental caries in the primary teeth of school aged children aged 5-7 year ranged from 0.9 to
8.5 dmft. National averages below 2.0 occurred in Denmark, Finland, Italy, the Netherlands,
Norway and England. Higher levels of decay were reported in Portugal (4.4), Lithuania (4.4),
Hungary (3.7) and Scotland (3.0). In some countries the percentage of the caries which was
untreated was between 71% (UK)13-15.

Dental caries is common in 12 year olds. In countries with relatively low DMFT scores, 65% of
children had experienced dental caries in their permanent teeth. The Scandinavian countries,
England and the Netherlands were the only countries were approximately half the 12 year-olds
had no decay experience. The majority of EU countries had DMFT averages below 3.0 at 12 years
of age.  Nine had DMFT scores above 3.0, the WHO goal for the year 2000. They include Austria,
Iceland, Germany, Greece, Israel, Spain, Yugoslavia, Hungary (4.3) and Poland (5.1). The
Baltic countries like Latvia (7.7) have high DMF levels. An indicator of the inability of
current dental services to cope with the dental caries problem is the relatively high
percentages of untreated dental caries lesions. The percentage of caries lesions untreated in
12 year olds was 29% in France, 45% in the UK, 46% in Hungary and 53% in Poland13-16.

Dental caries adults

Caries increases after the age of 20 years indicating that it affects children and adults17.
Adults have caries incidence rates similar to those of children. Increases in caries with
increasing age were reported in cohorts of Norwegians. The numbers of decayed and filled teeth
increased from 3 at 13 years to 8 at 23 years and to 15 at 33-34 years6. Caries has declined
and is occurring at later ages. The prevalence of DMFT was high in most young adults in
Europe; more than 90% were affected. Caries severity increased with age. In Ireland and in the
Netherlands the mean DMFT for 20-24 year olds was 9.5 and 11.3 respectively in 1985-1991. The
DMFT in 16-24 year old United Kingdom adults was 10.8, and increased to 16.0 at 25-34 and to
19.0 at 35-44 years. The mean DMFT in EU countries after 1988 varied between 13.4 and 20.8 at
35-44 years. In France the DMFT was 14.6 in Germany 16.3 and in the United Kingdom, 18.9. In
fluoridated areas of Ireland the DMFT was 18.9. The WHO classifies DMF levels at 35-44 years
as high when the DMF is above 14.0 and very high, at 18.0 or more18. Most EU countries fall
into these two categories.

Among older people with natural teeth free-living British people aged 65 years and older, the
average numbers of teeth with caries experience was 15.5. In Ireland, the DMFT in older people
was 26.5 in fluoridated areas19.

Dental caries in immigrants and refugees

Dental caries levels among most of the young in immigrant groups in Europe are higher than the
resident groups. Whereas disease levels are decreasing in the latter, it is increasing,
particularly among pre-school children, in the immigrants20. There are more than 20 million
immigrants and refugees in Europe. They carry a serious dental disease burden in addition to
their other problems. The higher caries levels of Asians and other immigrant groups has been
attributed to a higher intake of sugar containing drinks, including milk and a higher
frequency of sugary products21.

Root Caries

The prevalence of root caries ranged from 7-11% among Finnish adults aged 30-39 years to 27
-33% in the oldest group but the mean number of teeth affected was low, 0.32.  Higher rates
(15-80%) were reported in Sweden with 65-year-old men having an average of 0.9 teeth affected
by root caries17.

Tooth Erosion

Dental erosion has been defined as an progressive irreversible loss of dental hard tissue by a
chemical process, usually by acids other than those produced by plaque bacteria2,22. Erosion
can lead to reduction in size of teeth and depending upon the severity and length of exposure,
may lead to the total destruction of the dentition22. That requires extensive expensive
restorative treatment. Rates of dental erosion appear to be increasing. The prevalence of
erosion affecting dentine or pulp (severe erosion) increased from 3% in children in Great
Britain aged 1 1/2 to 2 1/2 years olds to 13% in 3 1/2 to 4 1/2  years olds11. Among 5-6 year
olds the prevalence of erosion was 52% in the primary incisors: 25% had erosion involving
dentine or pulp and among 11-14 year olds the prevalence in permanent teeth was 28%; in 2% the
erosion affected the dentine23. Based upon a review of population-based surveys ten Cate and
Imfeld24 reported that from 8 to 13% of adults had at least one facial surface erosion lesion
involving dentine. A further 30 to 43% had between 3.1 and 3.9 teeth affected by occlusal
lesions extending into the dentine. The main causes are intrinsic or extrinsic acids. The
intrinsic acids are from vomiting related to anorexia, bulimia, and cytostatic drug treatment.
The extrinsic causes are dietary acids such as fruit acids, ascorbic and phosphoric acid in
frequently consumed acidic fruit juices, squashes, sports drinks and carbonated beverages22
-25. Many drinks have pH values below 422. Smith and Shaw26 have drawn attention to the
erosive effects of baby fruit juices. Ten Cate and Imfeld24, in summarising a workshop
organized by ILSI stated that "the potential risk factors for dental erosion are changed
lifestyles and eating patterns, with increased consumption of acidic foods and beverages."

The current situation relating to dental erosion was outlined in the National Clinical
Guidelines and Policy Documents 1999 for Paediatric Dentistry of the Dental Practice Board for
England and Wales27. The report emphasised that erosion was a oral health problem. The causes
were  "All acids, whether from within the body or from external sources, are capable of
demineralising tooth tissue, and therefore of causing erosion." "The intrinsic causes include
intrinsic acids from gastric reflux and vomiting. Extrinsic causes are soft drinks, and some
dry wines and alcopops." Although there is increasing evidence of the role of soft drinks in
the development of erosion, it is not just drinks that contain acid. There are also other
potential dietary sources such as fresh fruit, pickles, and sauces, lactovegetarian foods and
yogurt  "Frequency of, rather than total intake may be critical in the erosive process. It is
the titratable acidity of the drinks that is more important in causing erosion than just the
actual pH." "Another important consideration is that dental erosion is frequently associated
with individuals with high standards of oral hygiene Š" 28.

2. Pathogenic mechanisms with observed relationship across Europe

To answer the question, why do we get caries, the patho-physiology of caries needs to be

Dental caries is a process of enamel and dentine demineralization caused by various acids
formed from bacteria in dental plaque. Caries "Š involves dissolution of the minerals of the
tooth surface by organic acids formed from the bacterial fermentation of sugars derived from
the diet."1. Saliva is capable of depositing mineral in porous enamel areas demineralized by
the acids (remineralization). The deposit of impure hydroxyapaptite crystallites is an
important protective property of human saliva. Saliva is always supersaturated with calcium as
well as phosphate at pH 7. If a porous lesion is formed in enamel, repair by remineralization
always takes place. However, remineralization is a slow process and has to compete with
factors causing demineralization. If the remineralization process can effectively compete,
repair of the enamel takes place. On the other hand, if the challenge is too great, it is
below the critical pH, and demineralization dominates, porosity of enamel increases with
lesion progression until finally a carious cavity forms29. The rate of demineralization is
affected by the concentration of hydrogen ions (pH) at the tooth surface and the length of
time, which is related to frequency that the pH of the plaque is reduced below the critical
pH. In other words, caries occurs when the balance of dissolution and repair is tipped towards
excess dissolution, when demineralization exceeds remineralization1. Fluoride enhances

Bioactive food components and caries

Caries is caused by acids produced mainly from the interaction of specific bacteria with
sugars. So although the bacteria produce the acids and are considered a 'cause' of caries, the
bacteria do not produce sufficient acids to demineralize enamel without sugars or sugars in
combination with finely ground and heat-treated starch or with cooked starchy foods. As the
pathogenic mechanisms of caries involves five main factors, tooth susceptibility, saliva,
bacteria, dietary sugars and the time the sugars are in contact with the bacteria, this
section of the report will outline the interactions and assess the role of nutrients .

The mouth is unique in the human body in having non-shedding surfaces (teeth) for microbial
colonisation. That results in the accumulation of bacterial biofilms especially at stagnant
sites around the dentition. Plaque-mediated diseases such as caries occur at sites with a pre
-existing normal resident flora30. Caries results from imbalances in the resident microflora
resulting from an increase of pathogens due to strong selective pressures from a major
disturbance to the local habitat. A common feature of disruptive factors is a change in the
nutrient status of the site. Changes to the local environment can disturb the microbial
balance found in health and select for organisms associated with caries30.

Brathall31 stated that "Bacterial plaque is the only, immediate, direct factor causing caries.
The level of bacterial activity in the plaque is determined by diet (sugars). In addition, the
outcome of the bacterial activity in terms of causing damage to the teeth is controlled by
several other factors such as fluorides, saliva secretion, buffer capacity, salivary
antibodies which collectively are said to represent the resistance to caries development, ie
the susceptibility of the host." The microbiology of caries revolves around important roles of
mutans streptococci and S. sobrinus in the bacterial community. The growth of some species of
bacteria are controlled by environment, including pH and nutrition. Mutans streptococci will
establish on the teeth in the absence of sucrose. probably because of their affinity to adhere
to the teeth and fermentation of lactose. The acids produced by mutans streptococci are mainly
influenced by the diet (sucrose), the cariogenicity in rats was related to the amount of
sucrose in the diet.

Sucrose can enhance production of insoluble plaque matrix polymers by specific bacteria,
including mutans streptococci and S. sobrinus. And the growth of those organisms is highly
dependent on the presence of fermentable monosaccharides, provided directly by sucrose and
glucose and indirectly through the degradation of complex carbohydrates, mediated by host
enzymes (amylase) or the combined activities of other oral bacteria degrading plaque matrix or
salivary mucins. Excessive exposure to monosaccharides provides a selective pressure via pH
for rapid growth and retention (matrix), which favours mutans streptococci and S. sobrinus
relative to the other acid-producing bacteria. Indirect provision of these monosaccharides
while generating acid may not have such an immediate impact, although the slower liberation of
monosaccharides may increase the time for acid production. However, excessive use of sucrose
would probably give an equivalent period of low pH.

In summary, given sucrose, mutans streptococci and S. sobrinus can begin the caries process
quickly, without intermediaries. Nevertheless there is a debate whether there is a specific
sucrose-mediated glucan effect on mutans streptococci32. The presence of sucrose-specific
glucosyltransferases (GTFs) in mutans streptococci led to a presumption of a unique
relationship between these bacteria and sucrose. The establishment of mutans streptococci on
the tooth surface results in a concentrated accumulation of acids in situ during bacterial
growth and fermentation of dietary sugars. Sucrose is split into glucose and fructose by
mutans streptococci invertase, fructosyltransferase or GTFs. These monosaccharides are easily
fermented by most plaque bacteria via the glycolytic sequence to produce primarily lactic, but
also to alcohol, acetic, and formic acids.

Thus it is clear that bacteria such as mutans streptococci interact with sugars.  Regular
periods of low pH in plaque select for bacteria like lactobacilli and mutans streptococci
because they are more competitive at low pH compared with those organisms associated more with
enamel health. Thus it is the low pH from sugars rather than the sugar itself that disrupts
the plaque ecology30. There is an increase in the levels of mutans streptococci in volunteers
who rinsed with low pH buffers30. The oral flora would be influenced by the diet, namely, it
is a dynamic relationship, and some species would increase and others decrease. Mainly, it is
the low pH generated from the diet rather than how much sugar per se, although the two are
strongly correlated.

Mutans streptococci ranks highest among the potentially cariogenic bacteria, playing an
important role in the initiation and progression of enamel caries33. Mutans streptococci have
three unique caries-inducing properties; their ability to adhere firmly to tooth surfaces in
the presence of sucrose by forming water-insoluble glucan (IG), and, second, to form acids by
fermenting various dietary sugars32; a key discriminatory property of bacteria such as mutans
streptococci and lactobacilli is their ability to grow and metabolise at the low pH values,
they generate30. The rate at which the bacterial plaque produce acids depends upon the type
and numbers of bacteria, and whether the bacteria have been 'primed' by frequent exposure to
sugars. The rate at which pH returns to the resting level depends on the amount and duration
of sugar exposure, the rate of salivary flow, and the buffering capacity of the saliva34. The
formation of acids from sucrose by glycolytic activity of a group of streptococci and
lactobacilli which are especially cariogenic, leading to a fall in pH at the tooth surface is
very well established35. The acid response of the plaque to sugary food is altered if it is
taken in combination with non-acidogenic foods.

The interaction of sugars and bacteria

Caries is associated with increases in the proportions of acidogenic and acid tolerant
bacteria, especially mutans streptococci. These bacteria are able to rapidly metabolise
dietary sugars to acid, creating locally a low pH. They grow and metabolise optimally at low
pH and under such conditions become more competitive, whereas most bacterial species
associated with enamel health are sensitive to acidic conditions30. It is indisputable that
mutans streptococci's role in caries development is conditional upon a frequent intake of
fermentable sugars33. They are strongly dependent on dietary carbohydrates32. Mutans
streptococci are able to rapidly metabolize dietary sugars to acid, creating locally a low
pH30. High frequency of fermentable carbohydrate intake with regular pH drops favour the
proliferation of mutans streptococci and there is a direct effect of sucrose on the numbers of
these micro-organisms in the mouth33. Reports on the relation between self-reported sugar
consumption and oral loads of mutans streptococci are equivocal. Some studies show only small
changes in mutans streptococci counts with decreased sugar intakes whilst others report two-
to five-fold reductions after 8 weeks32,33. They conclude that "Individuals with a high risk
of caries incidence are, almost by definition, exposed to a cariogenic diet." As most oral
streptococci, including mutans streptococci, produce little acid from starch33, the main
dietary cause of caries is sugars. Acid production is very rapid with a minimum pH occurring 5
-10 minutes following exposure to sugars. The demineralisation of enamel and later dentine is
affected by the concentration of hydrogen ions (pH) at the tooth surface. The characteristic
form of the pH response in plaque to sugars, plotted against time, is called the Stephan
curve. The episodic nature of the Stephan curve indicates that frequency and duration of
ingestion of dietary sugars are important aspects of caries1. As the pH falls calcium and
phosphate ions are lost from the enamel. The drop in pH below 5.4, the critical pH, is
sufficient to decalcify enamel and dentine. Glucose and fructose are fermented at a similar
rate to sucrose. Most oral streptococci, including mutans streptococci, cannot produce acid
from starch33. Starch can give rise to falls in pH only if hydrolysed by host amylase and
microbial glucosidases.

In summary, sugars particularly sucrose, are the most cariogenic of carbohydrates in animal
studies. The high affinity of mutans streptococci for sucrose coupled with the unique uptake
of the disaccharide molecule of sucrose and mutans streptococci interaction with dietary
carbohydrates particularly sucrose, to form acids. Complex carbohydrates such as starch
interacts to a lesser extent with oral bacteria including mutans streptococci and produce less
acids than sugars, suggesting that they are not as acidogenic as sucrose.

The influence of fluoride on the sugar/caries relationship

The biochemical mechanisms causing the dissolution of human enamel and dentine indicate that
dietary substrates are necessary for caries to occur. Fluoride is the main factor altering the
resistance of teeth to acid attack and interacting with sugars in plaque. Fluoride affects
tooth structure during tooth development and post-eruptively and reduces caries in three ways:
1. Reducing and inhibition of dissolution of enamel. Fluoride has a strong affinity for
apatite. Because of its small ionic size and its strong electronegativity, fluoride is
incorporated into the enamel lattice and/or binds to crystal surfaces. By converting the
apatite into fluorapatite, which is more stable than hydoxyapatite, fluoride reduces the
dissolution rate of enamel by replacing hydroxyl groups in hydroxyapaptite to form

2. Remineralisation is the process by which partly dissolved crystals are induced to grow by
precipitation  of mineral ions from solution, sothat the process  of mineral loss is reversed
to some extent. Both saliva and plaque fluid are supersaturated at near- neutral pH with
respect to hydroyapatite  and can thus support remineralisation. At the pH and supersaturation
levels found in resting plaque fluid, apatite crystal growth proceeds by formation  of
intermediate solids, especially octacalcium phosphate (OCP), which then hydrolyses to
hydroxyapatite. The hydrolysis of OCP is accelerated and the product of crystal growth is
fluorapaptite or fluoro hydroxyapatites (FHA) rather than hydroxyapatite. Thus
remineralisation in the presence of fluoride will not only replace lost mineral but will also
increase resistance to acids and to later demineralisation.

3. Effect of fluoride on bacteria. Fluoride affects plaque by altering the ecology of the
dental plaque and reducing acid production. The pH fall is reduced in the presence of

The main protective action of fluoride is topical, after the teeth have erupted. The inverse
relation between fluoride concentration in drinking water and caries is well established.
Topical fluoride, either in the form of toothpastes, rinses or varnishes, reduce caries in
children by between 20-40%. These findings from over 800 controlled trials shows that
fluoride, either in water or in toothpaste, is the most important prophylactic agent against
caries36. Does fluoride affect the sugar/caries relationship?

Recent studies on diet and caries have been confounded by the widespread use of fluoride
toothpastes. Nevertheless Hinds and Gregory11in England and Steckson-Blicks and Holm37 in
Sweden showed that the association between snacking and caries experience was only partially
negated by the frequent use of fluoride toothpaste. Caries progressed through enamel and
dentine in teenagers in a preventive programme which included a range of fluoride regimens38.
In the two major studies of diet and caries, the use of fluoride toothpaste did not affect the
relationship between sugar and caries39,40. In a cross-sectional study, Beighton et al41on 12
year olds who were using fluoride toothpaste and with a low mean DMFS of 3.05 +/- 3.85 and
5.72 +/- 5.00, the DMFS scores were significantly related to the number of eating events at
which sugar-containing foods or confectionery were consumed. In a study where the use of
fluoride toothpaste was controlled, the strong positive relationship between frequency of
sugary snacks and caries persisted42. The most objective view on the current sugar/caries
relationship is Marthaler's43. He concluded, after reviewing the literature on declines in
caries and associated factors, that "... within modern societies which are aware and make use
of prevention, the relation between sugar consumption and caries activity still exists". The
main conclusion by Marthaler43 is "Recent studies have demonstrated that sugar - sucrose as
well as other hexoses - continues to be the main threat for the dental health (1) of the whole
populations, some developed and many developing, and (2) for the individual in both developed
and developing countries, (3) in spite of the progress made in using fluorides and improved
oral hygiene". Marthaler43 concluded that in Spain, Portugal, Greece, Hungary, Iceland,
Poland, Yugoslavia, Albania and Italy the "Š high sugar consumption is still the most
important determinant of caries prevalence." Although dental caries levels have declined in
many European countries, a significant relationship between sugars and caries persists despite
the regular widescale use of fluoride toothpaste.

A combination of fluoride and lowered sugar has a synergistic effect on caries reduction.
Weaver44 showed that the caries in 12 year-olds declined by 50% in both South (fluoride) and
North Shields (no-fluoride) during wartime because of sugars rationing.  In 1943 the DMF in 12
-year-olds in North Shields was 4.3 and in 1949 it was 2.4. In South Shields the DMF was 2.4
in 1943 and 1.3 in 1949.

Side-Effects of Fluoride

There has been growing concern about the increasing problem of dental fluorosis. With the
widespread use of fluoridated toothpastes, and accidental ingestion by very young children, in
industrialised countries in the past 30 years there are more reports of unacceptable fluorosis
of the front teeth45,46. Recent studies have reported fluorosis prevalence ranging from 3% to
42% in communities with negligibly fluoridated water and between 45% and 81% in areas with
optimal fluoridation46-52. The association between fluoride in toothpaste and fluorosis has
been demonstrated in children in low water fluoride communities53,54. The difference in
prevalence of fluorosis in optimally and in negligibly fluoridated communities has narrowed

3. Some Epidemiological characteristics about caries; the nature of caries and its
distribution in populations

The progressive nature of caries

As with other chronic diseases, prevention ideally should stop or delay progression of caries
for long enough for the severe manifestations of the condition not to manifest. In this
section, two aspects of progression of caries are analysed; progression in patho-physiological
terms in teeth and in epidemiological terms

Analysing the rates of progression of a disease provides evidence of the extent of the
aetiological challenges and the resistance to them. If the challenge is sufficient to cause
progression that would suggest that the resistance is not able to overcome the challenge. On
an observational and policy level, it is clear that the rates of progression of dental caries
have not been sufficiently slowed to allow dental policy makers worldwide to change the health
education messages to the public to attend for a regular annual recall visits to diagnose and
treat dental caries. In all European countries recall intervals remain annual.

Caries occurs on the occlusal  (biting) and the approximal (fronts and backs of teeth). The
majority of approximal caries lesions in permanent teeth progress slowly, with an average
lesion taking at least 3 years to progress through enamel to dentine. At levels of caries
common in EU countries, the rates of progression of caries in people from 11 to 22 years is as
follows: the median number of new approximal lesions per 100 tooth surface-years (there are
156 tooth surfaces per person) were 3.9 from no caries to caries halfway through enamel, 5.4,
from halfway through enamel to spread into the outer half of dentine, and from broken enamel
dentine border to obvious spread in outer half of dentine, 20.338.    The DMFT increased from
3.2 at 12 years to 7.0 at 22 years. The cohort was exposed to  comprehensive topical flourides
including rinses, fluoride lozenges and varnishes over many years. The authors conclude that
"The slow but continuous progression of approximal caries and the relatively high prevalence
of enamel caries at 21 suggest that for the approximal surfaces in a long-term perspective,
the fluoride supplements simply retard the progression of caries" 38.

A further indication of the progressive nature of caries is the differing types of surfaces of
the teeth affected as the severity of caries increases. At low levels of caries (DMF-S below

10) the main parts of the teeth attacked are the pits and fissures. As the caries attack
increases, the disease extends to involve the approximal and smooth surface. The DMF increases
with increasing age and so does the extension of the disease to more surfaces. In
epidemiological terms, caries progresses with increasing age of groups of people. In all
humans studied, the DMFT for children of 6 years is lower than those of 12 years and 18 years.
The rates of progression of the disease varies according to the level of disease at the
younger age.

Distribution of dental caries in populations

Some claim that at current levels of caries most of the dental caries load in EU countries
occurs in a small proportion of the population55. Indeed the low prevalence of caries is
considered to be a justification for using a high risk strategy limited to the small
percentage who have the majority of caries. For example Pollard et al56  stated that  "This
decline (in dental caries) now means that over half the children in Britain never experience
dental caries and that 60-80% of the decay that does occur is found in 20% of the child
population." This is an inaccurate statement as the possession of a caries-free dentition
under the age of 10 is not a good predictor of zero caries incidence thereafter. Fejerskov and
Baelum55 warned against the term caries-free. That indicates "Š only that no cavities have
been found, not that the disease is not present".

Caries is considered to be "... a 'dichotomous disease' affecting mainly those in the lower
social classes and other disadvantaged groups." Pollard et al56 claim that there is no
persuasive argument to support reducing sugars intakes by the whole population. Such a policy
would only benefit the minority with a high caries prevalence56. Therefore it is worth
outlining the different policies or strategies to control dental caries.

Strategies to Control Dental Caries

Rose57 divides strategy approaches to control most chronic diseases into two distinct groups.
Those aimed at the population and those in which certain sections of the population are
identified, either as a group or as individuals, the risk approach. To decide whether to adopt
a population or the risk approaches, Rose57 poses the fundamental question, does a small
increase in risk in a large number of individuals generate more cases than a large increase in
risk in a few individuals?  The criticisms of the high-risk approach is that it is both
palliative and temporary. It neither addresses the underlying cause(s) of the problem nor
prevents new cases occurring. The pivotal factor that should be used to determine the choice
of preventive strategy is the distribution of disease within the population.

How do Rose's principles apply to preventing dental caries? Batchelor58 tested Rose's concepts
on caries distributions and concluded that at low levels of caries, the majority of lesions
occur in a minority of individuals. As DMF levels increase beyond DMFT of 1 for any age group,
the changes in caries levels are not confined to a group who some define as at 'high risk'.
The majority of new caries lesions occur in the group defined at 'low' risk. While those
individuals at an initial low DMF score had, on average, a lower annual caries increment than
those individuals with a high DMF score, both groups developed caries. Any changes in caries
levels are distributed throughout the population: a strategy limited to the 20% of individuals
'at risk' will fail to deal with the majority of the new caries. For example, per 100 7 year
-old children, 67 of children had a DMF score of 0 and developed 2.28 lesions over a 4 year.

Thus the number of new lesions was 152.7 (2.28 times 67). At the other extreme, although those
with an initial DMF score of 7 or greater had a 4-year increment of 4.27, only 2 children per
100 were at this disease level. The number of new lesions would be only 8.5. Those who would
be defined at low risk, with a DMF-S score of  0, accounted for 55% of the new lesions. Taking
a 'high-risk' approach even if 100% successful would deal with less than 10% of lesions58.
These studies show that contrary to some claims, caries does not only affect a minority of
Europeans. The percentages of children with caries is high. Whereas 40% are caries free at 14
years and caries free levels continues to decline in older groups, in Scotland 79% and in
Northern Ireland 85% of 15 year olds had experienced caries. The percentage of caries free
young adults is very low and on average 15 teeth are DMFT in dentate people18.

4. Major risk factors for dental caries

"The evidence establishing sugars as an aetiological factor in dental caries is overwhelming.
The foundation of this lies in the multiplicity of studies rather than the power of any
one."1. That statement by the British Nutrition Foundation's Task Force on Oral Health, Diet
and Other Factors, sums up the relationship between sugars and caries in Europe. Some claims
are made that the causes of caries are multifactorial. "Saying that dental caries is a
multifactorial disease merely reflects the fact that bacteria, as well as sugar and other
factors, are needed for the caries to develop. But refined sugars are a necessary factor for
the occurrence of the disease. The other factors such as the amount and type of sugar,
frequency of sugar intake, age of the dentition, and availability of fluorides are additional
to sugars, not alternatives to them" 59. When looking for causes of pathological states the
main emphasis should be in identifying those factors that determine whether or not the disease
develops60. To get caries you have to have certain types of bacteria present, and people have
to eat refined sugars frequently. The first condition is satisfied, as far as we know, in most
individuals. The second, however, varies and it is this variation that is responsible for a
high or low caries incidence.

There are extensive reviews of the same body of literature on diet and caries1,2. All conclude
that non-milk extrinsic sugars, particularly sucrose, are the main cause of caries.
Nevertheless,  some recent  reviews have argued that, because of the widespread use of
fluoridated toothpastes, the relationship between sugars and caries in children and young
adults has declined61, and they question whether sucrose reduction is important in food and
health policy in industrialised countries.  Burt and Ismail62 correctly pointed out that
"total consumption of all sugars does not correlate well with caries experience in populations
consuming high amounts of sugars, but it does so better where overall sugar consumption is
lower, such as developing countries today."

The Committee on Medical Aspects of Food Policy (COMA) on Dietary Sugars and Human Disease3
and Rugg-Gunn2 and other expert committees have reviewed the evidence on sugars and dental
caries. The positions of most expert committees which have reviewed the evidence on dietary
sugars and dental caries is encapsulated in the conclusions of the COMA report on Dietary
Reference Values for Food Energy and Nutrients for the United Kingdom63. They are; "There is
no evidence that sugars naturally incorporated in the cellular structure of foods (intrinsic
sugars) or lactose in milk or milk products (milk sugars) have adverse effects on health.
Apart from lactose in milk and milk products, extrinsic sugars in the UK, (principally
sucrose), contribute to the development of dental caries. ... There is evidence from
laboratory studies for the potential cariogenicity of fermentable carbohydrates other than
sugars, but the epidemiological evidence implicates non-milk extrinsic sugars as the major
dietary component contributing to dental caries. Factors other than dietary carbohydrate, in
particular fluoridation, are also important in determining the incidence of dental caries."

Laboratory and epidemiological studies support the relationship between diet and caries. Since
the identification by Stephan that the fall in the plaque pH below 5.5 following the ingestion
of sugary foods was a central mechanism to caries development, the results of many
investigations have confirmed the strong positive association between the frequency and/or
quantity of sugars intake and the occurrence of caries39,40,64,65. The sugars intakes of
children with high and low DMFT showed very large and systematic differences in sugar intake
according to the level of caries in a large survey in the USA in 1970. The data on 2514
adolescents shows  that there was twice as high intake of sugar-foods in adolescents with high
than those with low DMFT. Any increase in sugar-food consumption was associated with a
comparable increase in DMFT66. These results were not entirely reproduced in later
longitudinal studies. There were weaker associations between amount of sugars and caries in
the two well-controlled longitudinal studies of diet and caries. Both found only small
positive associations between sugar intake and caries39,40. In the UK study the correlation
between caries increment and weight of daily intake of sugars was +0.143. There were
considerable differences in caries increment between the highest and the lowest sugar
consumers. Children consuming the most sugar (>163g/day) developed 5.0 DMFS during the 2
years, 0.9 DMFS per year more than the children (3.2 DMFS over 2 years) who had the lowest
sugar intake (<78g/day)39. Both studies used total sugars intake, combining intrinsic and
extrinsic sugars. This may have concealed the more important influence of extrinsic sugars1.

Rose's57 observations on the difference between determinants of disease occurring in
individuals and determinants of populations' health can be applied to the epidemiology of
caries and sugars. For example, the correlation between individual cholesterol intake and
heart disease is weak whereas the populations' cholesterol levels are significantly associated
with  their levels of heart disease.  Turning to caries and sugar, there is a relatively low
correlation between an individual's sugars intake and caries increment39. But in comparisons
between high- and low-consumption populations, associations between sugar consumption and the
incidence of caries are high (r=+0.7 to 0.8)67,68. Thus, although dietary sugar is the main
determinant of a population's incidence of caries, measures of sugar intake in industrialised
countries generally fail to identify high risk individuals; the level of consumption is too
high, and moreover the variation in sugar consumption within populations is too low, to show
any measurable effect on caries incidence69,70. Burt et al40 pointed out that some of the
older studies have failed to demonstrate a correlation between amount or frequency of sugar
intake and dental caries activity. Marthaler43 explained the 'failures' by the fact that the
samples were too small. "Consequently, the power of the experiment was insufficient to level
out inter-individual variation." Indeed, Burt and Szpunar71 concede that in their study40 the
low relative risks of caries in higher sugar consumers was the small variances in the patterns
of both diet and caries and that a substantial increase in either the number of participants
or the length of the study would have been required to establish clearer relationships. In
addition some of the older studies had obvious methodological weaknesses. The fact that there
were relatively small variations between subjects' intakes of sugar in most of the
longitudinal studies71 must be considered when assessing those studies. They illustrate a
basic principle in epidemiology, namely that if all people are exposed to cigarette smoke then
the relation between smoking and cancer will not be apparent57.

Sucrose consumption was associated with the trends in the increase and decline of caries in
Japan and in Britain. Miyazaki and Morimoto72 (1996) reported a positive significant
relationship of 0.91 between the DMFT in 12-year-olds and per capita sugar consumption per
year in Japan between 1957 and 1987. The market share of fluoridated toothpastes was 10% until
1986 and has increased since then.  Downer68,73 used data from 13 extensive nationally based
point prevalence dental surveys of British 5 and 12 year olds. The sucrose data from both
sugar intake figures in the COMA8 report and from the Sugar Bureau. Neither included glucose,
honeys, and non-food use and wastage. The Spearman correlation between sucrose consumption and
mean dmft the populations of 5-year-old was 0.62 and for DMFT of 12 year olds, 0.84. The
relationship between sucrose availability and mean DMFT at 12 years was linear. These two,
detailed analysis based upon well-defined caries diagnosis and sugar available for
consumption, puts in perspective the relationship between national data on caries and sugars.

In an ecological study using data from 47 countries, Sreebny67 found a correlation
coefficients for sugar supplies and  dmft of  0.31  and 0.72 for DMFT. Marthaler43 calculated
from Sreebny's data that for each 25 g of sugar per day, one tooth per child would become DMF.
In the 47 countries studied there was a correlation of r=0.72  between sugar supply per capita
per day and caries at 12 years of age. In statistical terms a correlation of 0.72 means that
52% of the variation between the reported data on caries are explained by the variations of
the average sugar supply43.  On the other hand Woodward and Walker74 using DMFT data for 12
year-olds from 90 countries, 61 developing and 29 developed, found that the relationship
between sugar and DMFT was not significant. The shortcomings of their interpretations have
been highlighted by Nadanovsky75 who argued that the reason why the association between sugars
and caries was not high using ecological data, was that all the industrialised countries have
such high levels of sugars consumption that changing sugars intake by a few kilograms per year
does not affect the caries attack.  Nevertheless over 28% of the variation in DMFT was
explained by sugars in Woodward and Walker's study74. When problems of comparing DMFT derived
from different examiners are considered and the inaccuracy of sugar consumption data, and the
fact that children up to the age of 12 are only one fifth of the total population so the sugar
consumption is dominated by those over 12 years old and that the dental data were not from
representative samples, the important distorting effects of confounders such as availability
of fluoridated toothpaste and frequency of sugar intake, then a 28 coefficient of
determination is very impressive indeed. The data from Woodward and Walker highlights an
impressive ecological association between sugar and caries. Their data strongly reinforce the
view of a "safe" level of sugar. Almost all countries with sugar levels below 18.25
kilograms/head/year had DMFT below 3.0 at 12 years (23 out of 26 countries). Only half the
countries (36 out of 64) with sugar levels of 18.25 kg or more had DMFTs below 3.0. When the
10kg/person/year is used the difference is even more striking. Over 78% of countries with
sugar levels below 10 kg had a DMFT below 2.0.  On the other hand only 30% of the countries
with sugar consumption above 10 kg had a mean DMFT below 2.0 at 12 years.  Thus the caries in
populations is much lower when sugars consumption is below 18 kg/person/year.

Ruxton, Garceau and Cottrell76 from The Sugar Bureau used the data from Woodward and Walker74
and Sreebny's67 studies to assess whether there was a relationship between declines in caries
and declines in sugar supply in 67 countries between 1982 and 1994. They used a simple scatter
plot and no statistical analysis to control for confounding factors. Their plot showed that
whereas the DMFT  decreased  in 18 countries which had declines in sugar supply, in 25
countries dental caries declined despite increases in sugar supplies. In three countries
sugars declined and caries increased. However, in a further 18 countries caries levels
increased with increases in sugar supplies. So, overall the relationships between sugar supply
and increased caries was supported in 36 countries and not in 2876. Considering the
limitations of analytical methods used and the reliability of the data on caries and sugar
supply in this analysis, and the fact that for 17 countries the data points around the axis
were within 1 DMFT and 10 g/person/day, the conclusions are questionable that there are no
reliable information for setting population-based targets for sucrose or sugars in general.

Relationship between frequency and amount of sugar intake and caries

There is a debate about whether frequency or quantity of intake of sugars is more important in
causing caries. The discussion is complicated by the fact that the two are highly associated
in human diets2. Evidence from numerous studies suggests that caries rates in humans are
related to the amount of sugar consumed and the frequency of eating between-meal sugary
products. COMA63 stated: "In free-living people these three variables, mass, concentration and
frequency, are all closely and positively related to each other." A WHO expert committee  on
Diet, Nutrition & Prevention of Chronic Diseases77 concluded that "Numerous epidemiological
studies conducted at the population level suggest that there is a direct relationship between
the quantity and frequency of sucrose consumption and the development of caries." 77. Despite
those conclusions most of the emphasis on the sugar/caries relationship has been on the
frequency of sugar intake. There is conclusive evidence of a high correlation between the
frequency and the amount of sugar intake. Studies indicate that when more sugar is consumed,
the frequency increases. The correlation between frequency of sugary foods of intake per day
and weight consumed per day, by children aged 12 to 14 years was +0.772,39.  All the
correlations for a number of food groups were above +0.75, showing that as the amount of
sugary foods consumed per day increased, the frequency of intake also increased (Table 1)2,39.
The correlations were higher for the amount and frequency of all sugared drinks (0.86).
Similar high correlations  for amount and frequency of drinks between meals (+0.97) was
reported by Ismail et al78 for American children and for frequency and total sucrose intake
for South African Black people, Indians and Whites79. The correlations were between +0.78 and
0.84.  Similar correlations between frequency of sugars was reported by Rodrigues65. There was
a highly significant relationship between daily frequency of sugar intake and the daily weight
of intake at nursery and caries increment, after adjusting for all the other variables. In
addition, children with a frequency of sugar consumption of 4-5 times per day at nursery were
6 times more likely to develop  high levels of caries  over one year, compared to those having
the lowest frequency80,81.  Daily frequency of sugar intake at nursery showed a dose-response
trend with the risk of having high caries increment.

(Table 1  here)

Ismail et al78 reported a significantly higher risk of caries in persons aged 9 to 29 years
for both the amount and frequency of soft drinks consumed between meals. Those consuming 450
grams/day of soft drinks between meals were 1.86 more times likely to have a high DMFT. The
odds ratios increased from 1.28 for those drinking soft drinks once a day between meals, to
1.87 for twice and 2.79 three or more times a day. Ismail et al78 caution against considering
sugary drinks less damaging to teeth than sticky sugary foods.

At frequencies of intake of sweets and between meal sugars which are common in Europe at
present there are statistically significant relations between frequency of sugars intake and
caries. Rugg-Gunn et al39 found higher correlations between caries increments and total sugar
intake than between frequency of sugar intake. Szpunar et al82 confirmed the association
between amount but not with frequency. They found that children whose energy intake from
sugars was one standard deviation above the mean had twice the risk of developing approximal
caries relative to those with one standard deviation below the mean.

The two large longitudinal studies on caries and sugars39,40 were conducted on children with
relatively high average intake of sugars of about 100g/per/day (i.e. 36.5 kg/year).  As the
study by Burt et al40 is often mentioned, a more detailed analysis of their study is reported
here.  In the USA, Burt et al40 showed that sugar intake, especially sugary snacks were
positively correlated with caries. The initial and final DMFS differed between the children
grouped by sugar intake. Children with the lowest sugar intake of sugar from all sources (109
g), had a final DMFS of 5.86, whereas those with the highest sugar intake had a DMFS of 8.39.
The small difference in age at baseline cannot explain the difference of 2.51 DMFS as the
average increment of new caries per year was equal or less than 0.23 DMFS. Marthaler43 has
pointed out that there were not many children in the study with low sugars intake and there
was only limited variability in natural and added sugar of the food consumed by the children.
That would give a low correlation. In addition, the ratio, 175/109g is 1.6 and the
corresponding DMFS ratio 8.16/5.86 is 1.4. This agrees fairly well with regression line in
Sreebny's67 study in which passes through the origin. Sreebny67 had shown a strong positive
correlation of r=0.72 between sugar supplies and dental caries.

Most recent studies have found larger associations between frequency than amount of sugars
ingested and caries. The dmft in young children who were fed four sweetened snacks and drinks
a day was 1.67 compared to 1.25 in those fed them once a day42. The British National Diet and
Nutrition Survey assessed the relation between diet and dental caries in 1500 preschool
children11; 22% of children with low intakes of confectionery had caries and 40% of children
with a high intake. Grindefjord et al83,84 reported a significant relation between caries and
intake of sweets and with consumption of sugar-containing beverages in a longitudinal study of
3 year olds. Holbrook et al85 reported a mean dmfs of 10.7 in the 56% of children who consumed
sugars 4 or more times a day compared to dmfs 2.6 in those consuming sugars less frequently.
They found a threshold effect. Above the threshold of „4 sugar intakes per day or „3 between
meal snacks, the levels of caries rose markedly. In an earlier cross-sectional study on 4 year
-old urban children Holbrook et al86  reported a doubling of the dmft in children with intakes
of sugar of more than 30 times a week, which is comparable to „4 sugar intakes per day.
Frequency of sugars intake was also important in teenagers70. Between meal sugar consumption
and frequency of candy consumption were significantly related to approximal caries. The r2
ranged from 0.17 to 0.32 for the significant relationships. Bjarnason et al87 in a detailed

dietary study of 12-13year-olds in Iceland showed that there was a higher incidence of caries
surfaces with frequent intake of buns and cakes with meals and confectionery. These findings
were confirmed in a 3 year longitudinal study of Swedish 15-18 year olds88. The correlation
between sweet consumption and the incidence of posterior approximal caries was 0.25. The r
value increased to 0.70 in children with poor cleanliness and considerable dental plaque and
low salivary flow. They stated that the "... explanatory value of about 49%, ... is remarkable
and seems to be the highest value reported for any caries-etiologic factor in observational
studies"89. The authors concluded that "... consumption of sweets should still be considered
an important caries-related factor ... "89. Recent investigations in the Netherlands show a
strong relation between the consumption of sweets and caries experience in school children90.
Jamel et al91 reported a strong positive relationship between numbers of cups of sweet tea
consumed per day and caries (+0.43 for urban group). The correlation between weight of sugar
in tea and DMF was +0.71 for rural groups. Caries levels were related to preference for
sweetness (r=+0.58). A study on 6014, 14-year-olds in 20 districts in England reported a
highly significant relationship between consumption of sugared drinks and carbonated drinks
and caries (Jones et al 1999). Children adding two or more teaspoons of sugar to hot drinks
were 1. 87 times more likely to have caries than those who added less than two teaspoons92.
Kleemola-Kujala and Rasanen93 reported that with increasing total sugar consumption the risk
of caries increased significantly only when children did not clean their teeth properly.

Some studies did not find a relationship between frequency of sugary intakes and caries94.
Bergendal and Hamp95 did not find a relationship between diet and caries in 95 teenagers but
the numbers of subjects in subgroups was too small for rigorous analysis.

The findings from the studies reviewed here suggest that both the frequency of consumption and
total amount of sugars are important in the aetiology of caries because frequency of intake
and amount of sugars ingested are closely related. An increase in frequency of sugary intakes
of more than 4 per day increased the risk of caries.

The influence on caries of different carbohydrates

Oral bacteria utilize sucrose, glucose, fructose and other simple sugars to produce organic
acids in sufficient concentrations to lower the pH of plaque to levels that may result is
demineralization of enamel. It is only from sucrose that most bacteria are able to synthesize
both soluble and insoluble extracellular polymers which facilitate attachment of bacteria,
especially mutans streptococcus, to it. Unlike other disaccharides, sucrose can serve directly
as a gycosyl donor in the synthesis of extracellular polymers. Sucrose has been shown to be
more cariogenic than monosaccharides and other disaccharides in animal experiments in rats
infected with mutans streptoccoci.

Three trials on human caries have compared sucrose with other sugars. In the Turku experiment
in which xylitol, sucrose and fructose were compared, apart from the lower effects of xylitol,
the findings were indecisive; the cariogenicity of sucrose and fructose were similar96. Whilst
some aspects of the Turku studies  have been criticized97, the differences in caries between
the xylitol  and sucrose and fructose are considerable. Xylitol was the only sugar that the
xylitol group used. Their consumption of starch was not controlled.

A study compared a normal sucrose diet with one where invert sugar completely replaced
sucrose98. Children eating invert sugar had a lower level of caries. Studies on sorbitol99 and
hydrogenated glucose syrup (Lycasin) suggest that they are non-cariogenic100.

The role of dietary starch

After an extensive review on the relationship between starchy foods caries Rugg-Gunn2,101 and
Rugg-Gunn and Nunn102 concluded that:

… Cooked staple starchy foods such as rice, potatoes, and bread are of low cariogenicity in
… The cariogenicity of uncooked starch is very low but, since this is seldom eaten by humans,
 this finding is of little relevance.
… Finely ground and heat-treated starch can cause dental caries, but the amount  of caries is
 less than caused by sugars.
… The addition of sugar increases the cariogenicity of cooked starchy foods.  Foods containing
cooked starch plus substantial amounts of sucrose, appear to be as cariogenic as a similar
quantity of sucrose.

Similarly the COMA panel on Dietary Sugars and Human Disease3 concluded that "Simple starchy
foods, intrinsic sugars in whole fruit and milk sugars are negligible causes of dental caries.
Non sugar bulk and intense sweetners are non cariogenic or virtually so."3.  Therefore the
panel recommended that: "In order to reduce the risk of dental caries, the Panel recommends
that consumption of NMES by the population should be decreased. These sugars should be
replaced by fresh fruit, vegetables and starchy foods. ."3. And a later COMA on Dietary
Reference Values62 concluded that "There is no evidence that intrinsic sugars or milk sugars
have adverse effects on health."62. Furthermore a WHO expert committee on Diet, Nutrition and
Prevention of Chronic Diseases concluded that " ... an extensive review of evidence showed
that cooked staple starch foods such as rice, potatoes and bread appear to be of low

Less refined starchy foods may have properties which help to protect teeth from dental caries.
These properties, include: (a) a fibre content so that the food has to be chewed vigorously
which aids removal of the food from the mouth and increases salivary flow thus raising plaque
pH, and (b) possible protective factors - mainly organic phosphates (almost exclusively
phytate) - which may protect the teeth from dissolution.

Information on the potential cariogenicity of a carbohydrate can be obtained from a range of
experiments including: incubation studies, plaque pH studies, enamel slab studies, animal
experiments, human epidemiological studies and clinical trials.  The cariogenic potential of a
carbohydrate can be judged using information from these experiments.

First, plaque pH experiments. It is important to realise that these investigate acidogenicity
not cariogenicity. Certain 'protective factors' in starchy foods would not affect
acidogenicity, but would decrease cariogenicity since they affect solubility not acid
production. Almost all of the plaque pH experiments investigating starch either use the
sampling method or the indwelling glass electrode method of measuring plaque pH.  The sampling
method has tended to indicate that cooked starch, or starchy foods, are less acidogenic than
sugar or high sugar foods and that uncooked starches are virtually non-acidogenic. On the
other hand, indwelling glass electrode experiments show that starch depresses plaque pH below
the critical pH 5.5. Whether this accurately reflects what occurs naturally in humans is open
to question. Indwelling glass electrodes "tend to give an all-or-nothing response to foods -
any carbohydrate-containing food leading to a maximum drop in pH"103. Indeed, Edgar103
considers that "the pH response seen with glass electrodes might be hyper-responsive." "This
feature makes the application of the method to evaluating relative cariogenicity of snack
foods difficult, as bread, judged to be low relative cariogenicity by other methods, appear
highly cariogenic, and the technique is mainly used to verify the low cariogenicity of some
sugar substitutes" 103. These facts should be taken into consideration when assessing the
claim made by Edgar104 that after reviewing the same data "Š it would appear that while fresh
fruits (as consumed in a normal diet) do not contribute detectably to caries, they exhibit
properties which do not exonerate them in terms of cariogenic potential were they to be
consumed at a frequency similar to other foods which contribute to the cariogenic load".
Edgar's consideration that the cariogenic potential  of fresh fruits, if eaten as often as
sugars would be similar to other foods, is conjecture and not based upon evidence.

Enamel slab experiments are a little closer to the human situation since demineralization and
remineralization usually occur in vivo. Experiments which have investigated the cariogenicity
of starch have indicated that cooked starch is about one quarter to a half as cariogenic as
sucrose105106 but mixtures of cooked starch and sucrose are more cariogenic than sucrose
alone107. Many animal experiments have been undertaken with rather variable results. Raw
starches appear to have very low cariogenicity while cooked starches cause some dental caries;
less than that caused by sucrose. Mixtures of starch and sucrose cause more dental caries than
starch alone and the amount of dental caries was positively related to the amount of sugar in
the mixture. The degree of processing of starch in manufactured foods influences the
development of dental caries in rats, due to the partial hydrolysis of starch (for example in
fried potato chips and extruded starchy snack foods)102. Cooked starch causes about half the
caries caused by sucrose in rats106 but mixtures of cooked starch and sucrose are more
cariogenic than sucrose alone107. Starch (-0.06) and lactose (0.01) were not correlated to
caries in rats whereas glucose (0.43), reducing sugars (0.30) and sucrose (0.18) were highly
significantly related108. In an extensive series of studies on monkeys in captivity were fed a
range of diets Cohen 109,110 found that "Š in all the experiments I have carried out I have
never found it possible to induce caries in monkeys without the addition of sucrose to the
diet.". Lehner, Challacombe and Caldwell111 induced caries in the Rhesus monkey. Carious
cavities started developing in deciduous teeth within 4-8 weeks on a diet with sugars and
increased to a maximum at week 72.

Animal experiments are useful in giving some indication of the cariogenicity of foods in
humans, but caution in their interpretation is necessary. Although laboratory studies show
that starchy foods can reduce pH of plaque112, epidemiological studies suggest that starches
are of low cariogenicity in humans.

Human observational and intervention studies provide the most valid evidence of cariogenicity.
On a world-wide scale, whereas there is a strong positive correlation between availability of
sugar and dental caries, no such relation is seen for starch availability and caries. People
eating low sugar, high starch diets tend to have very low levels of caries. They are the only
types of study which actually record the development of caries in people and as such should
provide the most valid estimate of cariogenicity.  For millenia starchy foods were the staple
diet of humans with there was very little caries.  "Even now, in countries consuming high
starch, low sugar diets, caries remains low. It appears that only when sugar consumption
increases does caries increase. Starchy foods have become more processed - flour is heat
treated and finely ground, which breaks down the starch granules and some of the long-chain
starch molecules- which may make them more cariogenic. Frequency of eating may have increased
also (although there is no evidence for this), but it is unlikely that these aspects explain
the great rise in caries which has occurred in developed countries - the rise in consumption
of sugars remains by far the most reasonable explanation."102. In the Hopewood House study,
where children were fed a lactovegetarian diet with a little molasses and honey but high
levels of starch, children had one tenth the caries compared to non-institutional populations.
The children's oral hygiene was poor and they had no fluoride113. In the Turku study96, the
participants continued to eat starch, yet the xylitol group developed very little caries.
These studies corroborate the findings from studies of people with hereditary fructose
intolerance (HFI). Indeed these studies provide evidence of a direct link between sugar
sucrose ingestion and dental caries and the relatively low cariogenicity of starch. Persons
with HFI, who could not tolerate sucrose or fructose, had strikingly reduced dental caries
experience114.  In a longitudinal study of caries and diet in adolescents, Rugg-Gunn et al115
found no correlation between starch consumption and caries when controlling for sugar.
Children with high starch/low sugars intake had lower caries increments than children with low
starch/high sugars intake. Further evidence on the low cariogenicity of starch comes from
wartime dietary restriction. Dietary restriction in Norway and Japan resulted in an increased
consumption of starch, unrefined flour and a decreased consumption of fat, meat, sugar and
flour of low extraction. The caries rates decreased during wartime and increased sharply after
the rise of sugar in the post-war diets116,117.

Further evidence of the relative importance of sugars in caries compared to starches come from
studies on the effects of rationing during wartime. Weaver44 reported a halving of the caries
levels between 1943 and 1949 in 12 year olds living in North and South Shields. The main
decrease during that period was in sugar consumption and not starch. The Weaver study
highlights an important finding. Namely, that there is a synergistic effect of combining
decreasing sugar and optimum fluoride. In the low fluoride North Shields, caries declined from
4.3 to 2.4 whereas in fluoride rich South Shields the caries level in 1943 (2.4) was half that
in North Shields because of fluoride. Nevertheless, there was a further decline to 1.3 after
sugar rationing Weaver44. Similar results were reported by Künzel and Fischer118. They showed
that the beneficial effects of water fluoridation varied by levels of sugars consumption.
These studies demonstrate that dental caries can be reduced to low levels by the combined
effects of fluoride and low sugars.

Zeisenitz and Edmondson119 claim, without presenting any evidence, that caries rates increased
in developing countries such as Nigeria and China because the frequency of fermentable
arbohydrates, starches and sugars, have increased. Chinese and Vietnamese have eaten cooked
starch for many years, yet their caries rates were low120,121 and Ethiopians and South
American Indians who eat cooked starches such as wheat, rice, maize and quinoa have low caries
rates121. There are some well controlled studies showing that there is a low caries level
despite frequent consumption of cooked starches with low sugars intakes. One of the best
studies of increases in dental caries with change of diet is the Tristan da Cunhans122. Prior
to 1940 the diet was low in sugar but they did eat cakes, bread and biscuits. Yet the caries
rates in children and adults was very low. That shows that in modern groups eating cooked
starch relatively frequently, the caries levels were low. Similarly, as stated earlier,
Hopewood House children consumed high levels of cooked starches frequently and yet they had
low caries rates113. The Turku study showed very clearly that low increments of caries occur
when sugars were replaced with Xylitol. No changes in consumption of cooked starch was
introduced. All the foods consumed by the participants were supplied by the study team96 yet
the xylitol group developed very little caries.

Workers in the confectionery industry have higher caries rates than other workers. The DMFT of
confectionery workers was 15.6 compared to 9.1 in comparable textile workers123. The caries
rates in the confectionery workers increased more, the longer they worked in the industry.
Similar results have been reported in Japan124 and Denmark125.

The most convincing evidence on the low cariogenicity of cooked starches in  contemporary
humans are the data from 47 countries assessing the correlations between dental caries
experience, sugar consumption, and starch consumption. The correlations between caries and
cereal were reduced to near zero when sugar was controlled for, indicating that cereal
availability did not affect caries experience. The statistically insignificant partial
correlations, after controlling for sugars consumption in 47 countries were -0.03 and -0.13,
between total cereals, measured as calories per day or percentage of total calories; 0.05 and
0.03 for wheat and -0.24 and -0.26 for maize2. The strong positive relation between caries
experience and sugar availability was unaffected by standardizing the data on cereal
availability, thus indicating that sugar availability had a real effect on caries
experience2,67,126.  Similarly, in a longitudinal study of caries and diet in British
adolescents, Rugg-Gunn et al115 found no correlation between starch consumption and caries
when controlling for sugar. Children with high starch/low sugars intake had lower caries
increments than children with low starch/high sugars intake.

Evidence shows that milk sugars exhibit low cariogenicity and do not pose a threat to dental
health, therefore the extensive evidence that suggests that dental caries is positively
related to the amount of sugars in the diet and the frequency of their consumption largely
applies to non-milk extrinsic sugars.

Maltodextrins and glucose syrups

Research indicates that maltodextrins and glucose syrups are cariogenic, however, initial
studies on some synthetic oligosaccharides have suggested reduced cariogenicity compared to

Refined cereals

Because sugars and refined cereals are usually associated in diets it is difficult to
separate the effects of the two. Sreebny126 found a positive correlation of 0.45 between
availability of wheat and the prevalence of caries in 47 countries. When Rugg-Gunn2 reanalysed
the same data using partial correlation analysis, on the removal of sugar the correlation
disappeared. However, when the influence of wheat was removed, the correlation between sugar
consumption and caries levels only reduced from 0.70 to 0.60, indicating that sugar plays a
much greater role in the aetiology of caries than the availability of wheat1.


Fruit is sometimes implicated as a cause of caries. "... in experimental conditions, with the
fruit being a major dietary constituent, fruits may cause caries, however, as consumed as part
of the mixed human diet there is no evidence to support its cariogenicity."127. Observations
from human studies show a negative relationship between fruit consumption and the incidence of
dental caries, which supports the view that intrinsic sugars are of low cariogenicity. Clancy
et al128 found a negative correlation between DMFT and frequency of intake of apples, fruit
juice and sugarless gum. And Rugg-Gunn et al39 found no correlation between intake of apples
or other fruit and dental caries increment. Grobler and Blignaut129 found that a high intake
of apples or grapes was related to higher caries in adult farm workers. However, most of what
they claimed was caries should be queried as 20 of the 24 DMFT teeth were missing. The cause
of the loss of such a high number of teeth was not ascertained.

In summary the conclusions by Rugg-Gunn2,101 mentioned above are valid. Starches and fruit
have no or very low cariogenicity.

Fluoride and Dental Caries

The use of fluoride is the most effective tested method of controlling dental caries. Fluoride
can be ingested from water, tea, and a range of foods2. A common non-dietary source of
fluoride in industrialised countries is toothpaste. Fluoride in toothpaste is considered to be
the most important reason for the decline in caries in Europe130. Despite the reductions in
caries and the widescale availability of fluoride in toothpaste and other vehicles, caries
persists and progresses. The benefits of fluoride must be weighed against the disbenefits. In
many industrialised countries socially unacceptable levels of enamel fluorosis with
discolouration of the front teeth is increasing even in communities with no artificial water
fluoridation. The main source of the fluoride is from ingested fluoridated toothpaste. No
costings are available on the treatment of the discolouration. As additional fluoride to that
currently available in toothpaste does not appear to be benefiting the teeth of the majority
of children, the main strategy to further reduce the levels of caries, is reducing the sugars levels in the diet.

Oral cleanliness and dental caries

There is a widely repeated premise that dental caries occurs only after plaque has accumulated
on susceptible tooth surfaces in individuals who eat sugar frequently131. But the relationship
between toothbrushing and oral cleanliness on the one hand and dental caries on the other is
equivocal132. Bellini, Arneberg and von der Fehr132 concluded that toothbrushing habits had a
questionable effect on caries.

The position regarding toothbrushing and caries is summed up by the expert group advising the
Health Education Authority in England. Here is what they recommend: "Although caries cannot
develop without the presence of plaque, plaque removal by toothbrushing cannot in itself be
advocated for caries prevention.  Normal brushing inevitably leaves some plaque in fissures
and other stagnation sites where caries occurs, and plaque rapidly begins to reform on cleaned
tooth surfaces.  While toothbrushing is important for maintaining gingival health, numerous
studies have failed to establish a clear association between toothbrushing and caries
incidence. However, brushing with a fluoride toothpaste is the most important method of
delivering fluoride to the tooth surface. Other suggested methods for plaque removal such as
eating fibrous foods including apples and carrots are ineffective.  Plaque can be suppressed
using an antiseptic, but its acceptability for public use and its effectiveness for caries
control have not been established."133.

The relative ineffectiveness of toothbrushing in preventing caries is very clear. In practical
terms, it is physically impossible for the toothbrush bristles to remove bacterial plaque from
the depths of fissures and pits and from below the contact points between the teeth. On the
other hand there are many population studies where populations with poor oral cleanliness and
abundant dental plaque have low levels of caries. For example, in the Hopewood House study,
the children had abundant plaque and very low levels of caries as long as only small amounts
of sugars were eaten134. The relationship between oral cleanliness and caries is summarised by
Sutcliffe131. After an extensive review he concluded that:

… "Although tooth cleaning with unmedicated agents may be expected to reduce caries
experience, the lack of consistent epidemiological corroboration of the relationship has led
to questioning  of the value of oral hygiene practices against caries.

… Relatively few controlled prospective studies have been undertaken and the results point
towards a weak positive association between plaque and caries.

… Tooth-brushing with fluoridated dentifrices has been shown to be an effective caries
preventive measure. The effectiveness of fluoride toothpastes has been shown to improve with
increased brushing frequency and if the minimum amount of water is used to rinse after

5. Secular trends in EU dental caries patterns and projections of future caries

Dental caries has decreased in children and young adults in industrialized countries. For
example, in England and Wales in 1973, 65% of 8 year olds had experienced caries; by 1993 the
figure had dropped to 17%. In 12 year olds the mean number of DMF teeth decreased from 2.9 in
1983 to 1.2 in 199373. Similar changes have occurred in most industrialized countries. As
stated earlier, the different parts of teeth, pits and fissures mainly on biting surfaces and
fronts and backs (approximal) of teeth differ in their susceptibility to caries. The greatest
change in prevalence of caries has occurred in approximal tooth surfaces resulting in many
children having caries confined to the pit and fissured surfaces of first molars. As caries
prevalence falls, caries on the least susceptible surfaces (approximal and smooth surfaces)
decreases by the greatest proportion, while the most susceptible surfaces (pits and fissures)
have the smallest reductions135.

The consensus of expert analyses of the decline, agreed by 55 experts130, is that the
widespread use of fluoride, especially fluoride in toothpastes, was the main factor.
Nadanovsky and Sheiham135,136 found that all the countries where substantial declines in 12
year-old DMF-T occurred also had improvements in several general health indicators.

Changes in sugars consumption are frequently dismissed as having contributed to the
declines61. That viewpoint, which was not based upon a scientific analysis of data, was
challenged by Downer73 who showed that the rise and fall in caries in children in England and
Wales "Š was the concurrent increase and reduction in the sugar challenge, mitigated after the
early 1970s by the preventive effect of fluoride toothpaste"68. Downer68,73 has presented
detailed evidence that there was a high correlation (r = +0.85) between sucrose consumption
and caries levels in 12-year-olds in the United Kingdom and that sucrose made an significant
contribution to the trends in caries over the past 50 years. There was a close correspondence
between sucrose availability and caries until around 1970. After 1970, caries levels fell
rapidly with the introduction of fluoride toothpaste73. König138 argues that as caries has
declined and sugar supplies have remained the same in the Netherlands, sugars are not a cause
of caries. That is equivalent to concluding that if lung cancer decreased and smoking did not,
then smoking is not a cause of cancer. His conclusion does not address the fact that dental
caries does not occur without sugars. Despite König's claim that sugar supplies have been the
same in the Netherlands, they have declined. They decreased from 42.5kg to 38.5kg between 1965
and 1985  and there was as correlation of r =+0.92 between sugar supplies and caries levels in
12 year olds in the Netherlands.

Marthaler43 after asking the question "Is the relation between dietary sugar and individual
caries activity vanishing in countries where fluorides are used extensively?" said that
whereas sugar has lost its dominant role as the primary determinant of average prevalence, Š
the studies demonstrate that within modern societies which are aware and make use of
prevention, the relation between sugar consumption and caries still exists." One of the
reasons why the importance of sucrose is decreasing is that it is increasingly substituted  by
fructose, glucose and dextrose. In the USA sucrose constituted half of all sugars consumed in
1984 and in Ireland the average glucose consumption had risen to 23g per capita per day43.

The decline in dental caries appears to have stopped in most EU countries. Fejerskov and
Baelum55 came to the conclusion that "A gradual decline in caries incidence has occurred over
40 years and has stabilized at a "national" plateau". Poulsen139 concluded that in Denmark
"the constant decrease in dental caries in Danish children and adolescents observed during the
1970s and early 1980s has now come to a halt". His analysis shows that the caries increment
during preschool ages remained the same from cohort to cohort. Among 12-year-olds a plateau
was reached around 1991 with about 45% being caries free and with a mean DMFS of 1.8-1.9. The
DMFS in 15-year-olds has hardly changed since 1993 when the DMFS was 4.00 and 60% of children
were caries free53,139. In the Netherlands the caries rates in 6 year olds had  stopped
declining140. Pitts et al16 came to similar conclusions about trends in the UK. They found an
apparent slow down in improvements in caries and static levels of DMF.

Probable projections of future prevalence of caries

As indicated above, caries is a progressive disease and that although the prevalence and
severity is moderate in the very young, the severity increases with age. There are trend lines
for each level of caries.  Groups with the particular level of caries at 6 years of age follow
a rising trend line with a predictable dental caries increment. The slopes of the trend lines
change as the caries levels decrease135. What is the significance of the trend lines? Some
trend data are from countries such a Denmark, where there are annual national reports of
caries. It is unlikely that the levels of fluoride available can account for the year-by-year
decreases and the constancy of the trends. Two explanations for these trends are that:

1. There may be a change in the oral ecosystem, such as changes in numbers and virulence of
the cariogenic organisms, at the tooth surface and the mouth.

2. The reasons for the changes may be environmental. Arguably the dominant changes in the
environment which affects caries is fluoride, or changes in diet or social factors such as
changes in breast feeding patterns and sugars consumption137.  For a given cariogenic
challenge there is a specific intra-oral pattern of caries. The pattern is changed by either
altering the pathogenic challenge or increasing the resistance of tooth surfaces. The strength
of the dental caries challenge affects the site specific caries pattern within the mouth.

The trend lines also indicate that as people age, they get more caries. The epidemiological
trends of caries suggests that each new age cohort will have lower levels of caries and that
caries will occur at later ages than at present until they reach a plateau for caries in
children. The increase in severity in older people is related to the fact that with increasing
age, the root surfaces of the teeth become exposed and they are susceptible to caries. In
addition, there are a fair proportion of older people who have a reduced salivary flow, dry
mouth. That is a risk factor for caries, as the beneficial buffering effect of saliva against
acids is decreased. Therefore the pool of caries in older people will increase.

Unless broader measures are introduced to reduce the cariogenic challenge, new caries
increments will continue with increasing age, but at a lower rate than when caries levels were
high. Caries will affect mainly pits and fissures on molars. The rate of progression of
demineralization of enamel and dentine will decrease. That will allow longer intervals between
screening and dental check-ups. More people will retain more teeth and therefore more root
surfaces will be at risk of root caries.

Dental caries will continue to be a major public health problem in Europe. In the short term
future dental caries will continue to be a disease of children and young adults. In the longer
term future, within 20 years, instead of being a disease mainly of children it will be a
disease of adults. Later still, as the cohorts of middle aged adults become older people and
there will be higher proportions of older people in the next decades, severe caries will  seen
mainly in the old.

Life cycle features 

Infants and pre-school children

As reported earlier, early childhood caries (ECC) is related to the use of a sugar. Caries in
early childhood has been considered a 'dieto-bacterial disease'141. Bowen141 maintains that
"diet influences Š the virulence of cariogenic microorganisms". Persson et al142 linked diet
at age 12 months with caries at 3 years. In an extensive review of 40 cross-sectional
observational studies Rugg-Gunn and Edgar143 found that in most studies there were significant
correlations between caries experience and sugar consumption for children under five years
old. Among children 3_ to 4_ years olds in Great Britain, 30% had decay experience and among
those with active caries, 30% had some decay which extended into the pulp11. These patterns
are widespread in Europe indicating that dental caries in pre-school children is still a major
problem. In addition to dental caries, 50 % of the incisors of the 5-6 year olds are eroded by
acids from drinks11.

Older people

Three factors increase the susceptibility of older people to dental caries.

1. Older people have a higher taste threshold for sweet144.
2. Levels of xerostomia (dry mouth) increase with increasing age. In particular, dry mouth is
   associated with many drugs used by older people.
3. There is a high prevalence of exposed roots of teeth. Exposure increases vulnerability to
   caries. The pH required to demineralize exposed dentine is higher (pH 5.8) than for enamel
   (pH 5.5). Therefore, roots of teeth are more susceptible than enamel to acids from sugars
   and starches.

The following factors contribute to the increasing rates of dental caries in older people:
… The progressive nature of dental caries - even with slow rates of progression,
… demineralization undermines the enamel and creates cavities in later life on
… the coronal parts of the tooth.
… More teeth are present than in previous decades so more teeth at risk.
… Recession of the gums, getting long in the tooth, exposes more tooth, and particularly the
  roots of teeth. The cementum covering the roots is more susceptible to caries and
  demineralizes at lower pH than enamel.
… Poorer saliva flow - the buffering capacity of saliva against acids decreases.
… Increased numbers of older people taking medicines that leads to dry mouth.
… Increased intake of sugars, sometimes to stimulate saliva

As more older people are retaining more teeth into later life, the numbers of teeth at risk of
caries will increase6. The risk is increased because older people with dry mouth use strong
gustatory stimuli such as sugars to increase salivary flow. Sugars used frequently in older
people with reduced salivary flow and buffering capacity will result in caries on the
vulnerable exposed tooth roots145. In an extensive national study of a randomly selected
sample of 437 free living older people aged 65 years and older and with natural teeth in Great
Britain, Steele et al145 reported that those with a high frequency of intake of sugar-rich
foods were significantly  more likely to have new root caries than those with low intakes.
Frequent intake foods rich in sugars more than doubled the chance of having caries on roots
(OR=2.4). They concluded "frequent sugars intake is an important contributor to the
development of root surface decay, even when all other major contributory variables are taken
into account"145.

6. Dose response relationships between caries and sugars

This question is central to the argument about the level of extrinsic sugars that are
compatible with low levels of dental caries. Newbrun146 suggested that the relationship
between caries and sugars was a S-shaped curve, rising steeply when the sucrose-containing
food is eaten frequently by children when newly erupted teeth are more susceptible. When
sugars are eaten less frequently or if the teeth have been longer in the mouth, or if most of
the susceptible tooth surfaces are already decayed or filled as in adults, then it may take a
higher level of sucrose to cause caries and the resulting caries will be less extensive - the
curve will shift to the right. The rate of increase also depends on the availability of
fluoride.  Sheiham147 suggested that where fluoride is present in drinking water at 0.7-1.0
ppm, or over 90 percent of the toothpastes available are fluoridated, the dose-effect curve
shifts to the right and the 'safe' level of sugars increases. Following the rise in caries,
the curve flattens out, so that increasing the sucrose content of the diet beyond a certain
level does not increase caries to an appreciable extent. This explains the findings in some
human studies of a weak relationship between total sugar consumption and caries: the sugar
intakes of all the individuals in the population are so high that they lie on the upper flat
part of the S-shaped curve147,148 .  Significant lowering in caries rates occur only when
sugars levels are on the slope and not on the flat of the curve. The benefits of prevention
are larger at high levels of sugars below the 'saturation level'. Newbrun's proposal of an S
-shaped curve was based upon  animal  and human studies and is probably correct. Evidence
suggests that in populations without fluoride, below a consumption rate of 10 kg   sugars per
person per year (27.4 grams per day), the caries rate is very low; increasing levels of sugars
are followed by increasing levels of caries; at 15 kg per person per year the intensity of the
caries attack increases.  Above 35 kg a year  the curve eventually flattens out, and further
increases in sugars do not lead to appreciable increases in caries.

The main studies on the dose-response relationship are those carried out by Takeuchi117 in
Japan and by Sreebny149. Wilska150 was the first to show a relationship between caries and
amount of sugar consumed. In countries where the annual per person sugar consumption was below
20 kg, high proportions of adults were caries-free. Above 20 kg the percentage with caries was
over 98%. The most comprehensive evidence of the dose-response relationship between sugar and
caries comes from studies of the changing levels of caries when sugar consumption decreased
and then increased, as occurred during and after the 1939-45 war. Toverud116 and
Takeuchi117,151,152 and his co-workers have carefully documented the effects on caries of a
wartime decrease in sucrose. Takeuchi found that the S-shaped dose-response reached a plateau
at 35 kg per person per year. Takeuchi showed that the annual caries incidence rate was
positively correlated with the annual sugar consumption in Japan (r=+0.8) with increases in
sugar consumption from 0.2 kg to 15 kg per person per year. Takahashi153, using data from
Japan collected between 1941 and 1958, showed that at 13.2 kg of sugar per person per year the
annual caries incidence in first molars was 17%, at 8 kg the incidence was 10% and at 5 kg,
6%. When sugar consumption decreased to 2 kg the incidence was 2% and when no sugar was
available the incidence was zero.  When cavities did occur at low sugar levels, they were
small and progressed very slowly. What is most significant is that Takeuchi found that, when
the sugar consumption rate went beyond 15 kg per person per year, the caries occurred in the
first posteruptive year and the attack rate increased154. These studies show that when the
annual sugar consumption increased above 15 kg, caries intensified. The incidence rate of
caries increased more rapidly when annual sugar levels rose  - the incline of the dose
-response curve became steeper - suggesting a more intensive dietary challenge. Wartime data
from Norway and Britain support the Japanese findings. Schulerud155 concluded that when
Norwegian children aged 6-12 years consumed about 28.5 g of sugar a day (10.4 kg per person
per year), a good state of dental health was achieved in comparison to pre-war levels. In
Britain, evidence that annual levels of sugar consumption below 10 kg per person are
compatible with good dental health is provided by a comparison between children evacuated from
Jersey during the war and those remaining. Children on the island of Jersey had about 8.3 kg
of sugar per person per year until 1944. They had markedly healthier teeth than children
evacuated from the island to England. The average number of carious teeth was 1.8 among Jersey
children and 5.1 among evacuees aged 5 to 7156.

Buttner157, using data from 18 countries in 1959 on the relationship of sucrose consumption
and the average number of decayed, missing, and filled (DMF) teeth of children of 10-12 years
old, revealed a high positive correlation (r=0.95). Countries with sugar consumption levels
below 20 kg per year had very low DMF scores. Sreebny149 also found a strong positive
correlation between per person sugar supplies and dental caries for 12-year old children in 47
populations (r=0.72). The data clearly suggest that low caries rates are associated with a low
availability of sugar, and higher rates with larger sugar supplies. For the 21 (mainly
underdeveloped) countries with a daily sugar supply per person of less than 50 g, the caries
level was less than 3 DMF. For seven countries at the other extreme - a daily supply of 120 g
(43.8 kg per person per year) - the DMF was greater than 5. Sreebny considered that 50 g of
sugar per day (18.25 kg per person per year) may represent an upper limit of 'safe', or at
least 'acceptable' sugar consumption. Künzel158 in studies on 200,000 Germans found an
increase in caries in fluoride-free Plauen when the sugar consumption increased from 19 kg in
1950, to 27 kg in 1955 and 39 kg in 1979.  The DMF increased from 4.2 at 11-15 years to 5.5
and then declined with partial water fluoridation to 3.4 in 1979.  In fluoridated Karl-Marx
Stadt the lowest DMFT at 11-15 years and at 39 kg sugars was 3.4158.

The dose-response relationship is supported by a recent analysis of caries trends and sugar
consumption in Japan by Miyazaki and Morimoto72.  The caries rate in 12 year-olds increased as
per capita sugar consumption increased up to a peak at 29 kg/year in 1973. Thereafter, sugar
consumption decreased and so did caries levels, the correlation was 0.91. And the recent study
by Downer68 which reported a linear relationship significant between caries in children and
sucrose availability supports a dose-response relationship.

Rodrigues65 reported that after adjusting for confounding, children having more than 32.6
grams of extrinsic sugar daily (12 kg per child per year) at nursery were 2.75 times more
likely to have high caries increment compared to those who consumed up to 32.6 g/child/day.
There was a 29% higher risk of high caries increment among children who consumed more than
32.6 g of sugar daily at nursery. Those children with the highest overall sugar intake were
6.2 times more likely to have a high caries increment.

In summary, the studies reviewed show that when annual sugar availability exceeds 15 -20 kg
per person per year dental caries increases with increasing levels of sugars intake.  When the
caries rates reported by Rugg-Gunn et al39 in their low-sugars group (<78g sugars/day) are
considered, they developed 1.5 new caries surfaces a year, then levels of sugars intake of
about 60g/day as recommended by COMA63  for teenagers and adults appears to be a reasonable

Recommended intakes of sugars

The following are recommended targets for non milk extrinsic sugars intakes:
… Citing its own 1986 report on sugars, the FDA accepted the fact that added sugars contribute
to tooth decay  in 1993. The Surgeon General's Report on Nutrition and Health stated:
"Frequent consumption of sugars, especially sucrose, promotes formation of dental plaque, the
key predisposing cause of both caries"  "Evidence exists that sugars as they are consumed in
the average American diet contribute to the development of dental caries, suggesting that the
general public should reduce its sugar consumption."159.

… Free Sugars - Lower Limit 0% of energy, Upper Limit 10% of energy77.

… " .... average intake of non milk extrinsic sugars should not exceed about 60 g/day or 10
 per cent of total dietary energy."63.

… "Quantified targets for extrinsic sugars consumption are set in a minority of cases (27
reports). However the commonest recommended level is 10% of total energy intake as a maximum
level." 160,161.

Most authoritative international consensus document(s) on the quantitative relationship
between the specified nutrient and the disease or risk profile for that disease. Twenty three
national reports set targets for added sugars, the average being 10 percent or less of
calories161. The following are a list of recent consensus reports which concluded that caries
levels will be low when dietary sugars  are below 10% of total calories:
1986 Netherlands, Ministry of Health 0‚10%

1987 Australia, Department of Health 12%

1987 Finland, Nutrition Board 10% or less

1989 Poland, National Institute, less than 10%

1990 WHO 1990 - Diet, Nutrition & Prevention of Chronic Diseases less than 10%

1991 United Kingdom, Department of Health, COMA 10%

1996 Nordic Nutrition Recommendations. The upper limit of 10% fabricated sugars  for children
and adults with a low energy intake.

1997 Swedish. Most 10% from purified sugars.

7. Preventability

Known intervention  and observation studies


The majority of trials to prevent caries have involved fluorides. The reductions in caries
with fluorides range from 10 to 40%. At lower levels of caries, the reductions are smaller in
terms of numbers of tooth surfaces prevented from caries. Many of the trials, which were
conducted in the 1970s and 80s, have limited application now that the most people are using
fluoride toothpaste and the levels and intra-oral patterns of caries are different. A large
meta-analysis, which is due to be published soon, indicates that combinations of fluoride
vehicles, at low levels of caries, are not very effective in further reducing caries levels in
children162. Furthermore, in countries such as Denmark, where a range of fluoride methods have
been used, the decline in caries has stopped139.


There is some intervention studies on reducing sugar consumption in the 1950s. As they were
not well controlled, they were not reviewed. There are three intervention studies of the
effect of changing the types of sugars on caries; the Turku studies and four quasi
experimental observational studies on children where sugar intakes were reduced; Hopewood-
House Study, the Malmo study, the Synanon Study and the Recife study.

The Turku studies investigated the effects of either almost totally replacing or partial
replacement of dietary sucrose with xylitol, a natural polyol sweetener. In addition to the
first Turku studies where sucrose was replaced by either fructose or xylitol, there are a
number of intervention studies using xylitol chewing gum. Later there were some WHO
commissioned demonstration trials in Hungary, Thailand and French Polynesia. Whilst there are
some shortcomings in the later studies, the total replacement study showed that xylitol was
non-cariogenic in adults96,163.

The Roslagen Study. The cariogenic effects of sweets made with sucrose were compared sweets
made with a hydrogenated potato starch containing a mixture of sorbitol, maltitol, maltotritol
and higher saccharide alcohols, Lycasin.  Compliance was inadequate and the dropout rate from
the study was too high (50%) to allow adequate evaluation100.

The Malmo Study. In a two-year trial, sucrose was compared with one where sucrose was
completely replaced by invert sugar. There was less caries in children eating invert sugar98.

Observation in non-experimental studies

Hopewood House Study.  Children aged 5 to 13 in this institution in Australia was followed up
for 15 years. Children were fed a lactovegetarian diet with a little molasses and honey.
Comparison was made with non-institutional Australian children and New Guinea villagers. The
13 year olds had a mean DMF of 1.6 compared to the general populations DMF of 10.7.  When the
children were relocated and changed to the Australian diet their caries levels increased
rapidly indicating that the preventive effect of a low sugar diet is not long-lasting113.

Synanon Study. In a study with no control group, 73 children aged 11-17 years were exposed to
a preventive programme, which included fluoride supplements since birth, daily brushing and
flossing and the elimination of sugar from the diet164. The mean DMFS was very low for the 5
-10 year olds (0.53).  It is not possible to ascribe the decrease to any single aspect of the

Recife Study. The objective of this study was to test the effect of adoption of dietary
guidelines on sugars by nurseries on levels of sugar consumption and on one year dental caries
increments in low-socio-economic 3-year-old children. There was a statistically significant
difference in frequency and weight of sugar intakes between children attending nurseries
adopting and not using guidelines  (p<0.001). Children at nurseries adopting guidelines
consumed less than half the amount of sugar a day than children at non-adopting nurseries;
22.9 vs 53.5 grams. Children attending nurseries not using guidelines on reduction of sugar
intake were 4.8 more times likely to develop caries in one year than those attending nurseries
with guidelines. Attending nurseries not using guidelines on reduction of sugar intake
increased by 3.6 times, the risk of developing a high caries increment. Children who had a
daily sugar intake of more than 32.6 grams had nearly 3 times the risk of developing a high
caries increment than those consuming less than 32.6 grams65.

The findings from these few studies suggests that reductions in sugars consumption at
nurseries would have a significant effect on dental caries in pre-school children.
Substitution of sucrose by other sweeteners in confectionery and drinks will reduce caries.

8. Conclusions

1. Sugars, particularly sucrose, are the most important dietary cause of caries in children
and adults. At current levels of sugars intake in Europe, there are statistically significant
relationships between the frequency and amounts of sugar intake and caries severity. The
quantity and frequency of extrinsic sugars intake are strongly related. Both the frequency of
consumption and total amount of sugars is important in the aetiology of caries. Health
education messages should emphasize that relationship and not concentrate mainly on snacks,
confectionery and drinks as the main causes of caries.

2. The intake of extrinsic sugars beyond four times a day leads to an increase risk of dental

3. There is no evidence that sugars naturally incorporated in the cellular structure of foods
 (intrinsic sugars) or lactose in milk or milk products (milk sugars) have adverse effects on
 health. Foods rich in starch, without the addition of sugars, play an insignificant role in
 coronal dental caries.

4. There should be an independent review, by statisticians, of the data from the controlled
trials on caries and sugars. A question that is not addressed by most authors who question
whether there is currently a significant relationship between sugars and caries is "If the
sugars levels are not significantly affecting caries at present, what is causing caries to
progress at rates sufficiently rapidly to control the increase in caries, with increasing age,
in all populations in Europe"?

5. The current dose-response relationship between caries and extrinsic sugars consumption and
data from the observational studies on teenagers suggests that the sugars levels should not
exceed 60g/person/day for teenagers and adults. For pre-school and young children the intakes
should be proportional to those for teenagers; about 30g/person/day for pre-school children.

6. Research should be carried out to analyse the claim that there is a sugars/fats seesaw.
Some argue that if sugars levels are decreased, there will be an increase in fats consumption
with a concomitant increase in CHD and obesity.

7. Fluoride, particularly in toothpastes, is a very important preventive agent against dental
caries. At low levels of caries in people using fluoride toothpaste, the preventiveness of
combinations of fluorides, is low. As additional fluoride to that currently available in
toothpaste does not appear to be benefiting the teeth of the majority of children, the main
strategy to further reduce the levels of caries, is reducing the sugars levels in the diet.

8. Dental caries and its consequences cause a lot of pain and suffering. The treatment is
expensive and palliative. The costs account for between 4 to 11% of the health budgets of
European countries. On a population basis, dental caries is the most expensive part of the
human body to treat.

9. Caries has declined in Europe and is occurring at later ages. Caries is far from being a
negligible health problem in a segment of the population.

10. The decline in dental caries has stopped in some EU countries where levels of DMF are 1 at
12 years of age.

11. Caries increases with increasing age. Dental caries will continue to be a major public
health problem in Europe in the medium-term future.

12. Although the distribution of caries is skewed to the left, most of the caries increases
occurs in the majority, who have low DMF, and not in a minority with high levels of caries.

13. Dietary aetiological factors are still causing dental caries in a significant proportion
of population.

14. Caries levels in young immigrants and refugees are increasing.

15. Dental erosion rates appear to be increasing.

Table 1. Correlations between frequency and weight of intake of dietary items which are high in sugars,
observed in 405 English children aged 11-14 years. All correlations are positive and significant

Sweets        		0.74
Confectionery   		0.77
Chocolate   		0.85
Biscuits and cake   		0.80
Biscuits, cake, puddings	0.71
Sweet puddings      		0.86
Sugared tea 		0.98
Other hot drinks    		0.93
Sugared drinks      		0.86
Sugared cordials     		0.79
All foods and drinks    	0.32
All foods with > 10% sugars 	0.59

Source: Rugg-Gunn et al39.


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