dental caries
1. INTRODUCTION
Dental caries is an ecological disease in which the diet, the host and the microbial flora
interact over a period of time in such a way as to encourage demineralisation of the
tooth enamel with resultant caries formation. Dental caries is still one of the most
common diseases in the world today. Until recently almost everyone had experienced
tooth decay in their lifetime. However, today many people are caries free and there has
been a 40-60 % reduction in the incidence of tooth decay around the Western world.
Most developed countries and many non-industrialised countries are now well [NextPage]below the
World Health Organisation goal of less than 3 decayed, missing or filled teeth per 12
year old child.
2. THE HOST
Teeth are composed of a thin layer (1-2mm) of dental enamel which forms the hard
protective coating over the tooth. This consists mainly of calcium, phosphate and other
ions in a structure known as “hydroxyapatite”. Dental enamel is porous and is
susceptible to acid dissolution during the process of demineralisation. This
demineralisation process is offset by the repair process known as remineralisation.
Tooth susceptibility varies among individuals. The reasons are not fully know[NextPage]n, but
influences include:
* Shape, size and order of the teeth which affect the “washing” effects of saliva. This
is largely determined by hereditary factors.
* Salivary components which can be critical in controlling dental caries since they
affect bacteria, immune status, plaque formation, and enamel structure and can
neutralise acids. Saliva has a vital role in the balance between demineralisation and
remineralisation. These salivary factors will be outlined in greater detail below.
* Enamel structure can be altered by a selection of mineral ions and fluoride, as well
as by acid. The balance betwee[NextPage]n demineralisation and remineralisation of the
enamel determines whether caries occurs. Availability of fluoride favours
remineralisation.
3. SALIVA
Saliva is the body’s natural protective mechanism against decay. It contains salivary
proteins which adsorb strongly onto the teeth, protecting enamel against acid
dissolution. This adsorbed protective layer is referred to as the pellicle. Salivary proteins
also act as antibacterial agents.
Saliva is the primary resource of calcium, phosphate and fluoride, the materials used to
remineralise the enamel.
Saliva also acts quickly to clear away food debris fr[NextPage]om the mouth and to buffer the
organic acids that are produced by the bacteria.
Saliva is therefore a very vital and complex material in the prevention of dental caries.
Thus, salivary dysfunction can lead to rapid deterioration of dental enamel. Salivary
dysfunction can occur whenever certain medications are taken or medical treatments
such as radiotherapy are undergone.
4. THE BACTERIA
Dental caries will not occur if the oral cavity is free of bacteria. These bacteria are
organised into a material known as dental plaque which is yellowish coloured film on the
surface of the teeth. Of the many types o[NextPage]f bacteria in the mouth, the most caries active
appear to be Streptococcus mutans, Lactobacillus spp., Veillonella spp. and
Actinomyces spp. These bacteria can be transferred from mother to child and are
present at varying levels in all human mouths. A variety of carbohydrates provide
substrates for these organisms to grow on and the waste products of their metabolism –
acids – initiate the tooth decay process by dissolving tooth enamel.
Most research on the bacteriology of dental caries has focused on the ubiquitous
S. mutans and its ability to ferment sucrose. This organism preferentially ferments
s[NextPage]ucrose to produce significant amounts of acid and extracellular polysaccharide
(plaque). However, most researchers now agree that other organisms present in the
mouth are capable of plaque formation and acid production from a variety of
fermentable carbohydrate substrates besides sucrose which are present in the normal
mixed diet.
5. THE ROLE OF THE DIET
The dietary components that contribute most to the caries process are fermentable
carbohydrates. These need to be retained in the mouth long enough to be metabolised
by oral bacteria (principally Streptococcus mutans, but others can be involved) to
pro[NextPage]duce acid. The acid attacks the tooth enamel and gradually dissolves it
(demineralisation). This demineralisation process is offset by the repair process known
as remineralisation. The balance between remineralisation and demineralisation
determines whether caries occurs.Extensive data now exists to show that any foodstuff or drink containing fermentable
carbohydrate (sugars or cooked starches) has the potential to cause significant acid
production, followed by demineralisation of the enamel.
Biochemical Studies: Studies of plaque pH both in vivo and in vitro have shown that all
fermentable carbohy[NextPage]drates whether cooked starches, added or naturally occurring
sugars – have the potential to cause acid production in the mouth.
The amount of carbohydrate is not important.
Animal Tests: The cariogenic potential of foods has been assessed using laboratory
rats. Again, these tests demonstrate that all fermentable carbohydrate foods – whether
cooked starches or sugars – have the potential to cause decay. Again the amount of
carbohydrate is not important.
Food retention: The ability of a food to be retained in the mouth will alter its potential
cariogenicity. Tests to determine food retention indicate th[NextPage]at high sugar foods, often
perceived to be sticky, are not necessarily retained in the mouth for a longer time. In
practice starchy foods are retained longer in the oral cavity than some of the fast
clearance sugary foods.
6. FREQUENCY OF CARBOHYDRATE INTAKE
It is now widely recognised that it is not what one eats but how often carbohydrate is
ingested that is the most significant dietary factor in the aetiology of dental caries. In
subjects with normal salivary function an acid challenge occurs within 10 – 15 minutes
after ingesting fermentable carbohydrate foods or drinks, and it lasts for between 3[NextPage]0-60
minutes. Greater time between such acid attacks allows greater time for the repair
process – remineralisation – to occur.
Although there is now a consensus that frequent eating of carbohydrate foods and
drinks is the main dietary factor in the development of dental caries, no one has yet
determined precisely how many occasions per day are safe for all individuals. It is,
however, generally agreed that three meals plus three to four snacks per day is
acceptable. Research is needed to further establish the dynamic interactions between
frequency of eating/drinking and oral hygiene and the use of flu[NextPage]oride. There is however
an increasingly recognised view that, provided that oral hygiene is adequate and the use
of fluoride optimal, the frequency of eating diminishes in importance. This has been
demonstrated in human studies in New Zealand, UK, USA, Spain, Sweden, Norway and
Netherlands.
7. SENSIBLE SNACKING
It had been common practice among many in the dental profession to recommend that
‘three meals a day’ is safe for teeth, and ‘snacking’ is unacceptable. This advice is no
longer given as such. Some reasons why the dental profession has modified their
message are as follows:
1. It has been well [NextPage]documented that eating and drinking frequency has been increasing
in most industrialised countries over the last few years, and that the ‘three meals a
day’ pattern of eating has long been abandoned by most sectors of the population.
This change in frequency has occurred over a period when the incidence of dental
decay has declined. Sugar consumption has also remained static or increased.
This would suggest that another factor – which most believe to be fluoride (especially
in dentifrices) has counterbalanced and overridden the effect of increased frequency.
This is well documented in Sweden, Norwa[NextPage]y, UK and Switzerland.
2. An experimental caries model has been developed in the US and the Netherlands
which stimulates what happens in the human mouth, by alternating periods of
demineralisation and remineralisation. The model has been used to mimic human
eating experiences over a 24 hour period, and it demonstrated the power of fluoride
to ‘neutralise’ the effect of frequent snacking. Where fluoride was used twice daily,
there was less mineral loss following 10 challenges, than there was following 3 in the
absence of fluoride.
HOW IMPORTANT IS DIET ?
In most industrialised countries, the percentage [NextPage]of the population that is caries free has
been steadily increasing. It is generally accepted that the major factor has been the use
of fluoride in water, toothpastes, mouth rinses, and tablets. This decline in caries has
not been associated with any significant reduction in sugars ingestion or in snacking. In
fact as noted above, while frequency of eating has generally increased, sugars
consumption is either stable or increasing.
Additionally, recent epidemiological studies (UK, USA, Spain, New Zealand) have
shown that in both children and adults, the total of all dietary factors examined
(carbohydrat[NextPage]e amount, type and frequency) accounted for only a very small increase in
caries incidence. Dietary factors, although statistically significant were clinically
insignificant as they were overridden by the effects of fluoride and oral hygiene
programmes.
This contrasts markedly with the older studies of the pre-fluoride era where diet and
particularly sugars intake was directly related to caries experience in most countries and
in most population groups. Availability of fluoride, especially used topically in
toothpastes, has brought about a dramatic change in the aetiology of the disease.
9. CARING F[NextPage]OR TEETH
Dental caries is primarily a disease of children and teenagers. Its causes are complex,
but there are some quite simple methods for preventing it. This advice aslo applies to
the adults who are increasingly suffering from decay because of the greater number of
natural teeth that they maintain into adult and older life.
1. Sensible eating:
Eat a well balanced diet which includes a variety of foods. ‘Nibbling’ or drinking
constantly throughout the day should be avoided because it provides more
opportunities for demineralisation and less time for remineralisation.
Sensible snacking, that is six t[NextPage]o seven eating occasions a day, is acceptable, but
‘grazing’ is not.
2. Cleaning teeth:
Teeth should be cleaned thoroughly at least twice a day using a fluoride
toothpaste. Brushing helps to remove the plaque and food particles from the tooth
surface and flossing helps to remove the plaque and food particles from the areas
between the teeth. Regular brushing, also keeps gums healthy. Fluoride in the
toothpaste retards demineralisation and favours the remineralisation process and
thus prevents caries.
3. Visiting the dentist:
Visit the dentist for regular checkups and professional plaque removal.
10. IOCC[NextPage]C POSITION
The IOCCC welcomes the decline in dental caries around the world. The IOCCC
supports all reasonable and scientifically valid efforts to reduce tooth decay. The optimal
use of fluoride in toothpaste and mouthrinses is the most effective way of eliminating the
disease, as has been noted in many epidemiological studies. The very substantial
decline in caries incidence and prevalence in many parts of the world has generally
been attributed to the use of fluoride toothpaste.
Dietary measures can play a part, but will depend on the reduction in frequency of
intake of all fermentable carbohydrate [NextPage]foods and drinks whether cooked starches or
sugars. There is no scientific evidence for asserting that confectionery is the main cause
of tooth decay.
IBLIOGRAPHY
1. D. BIRKHED, B. SUNDIN, and S.I. WESTIN, 1989. Per capita consumption of sugar
containing products and dental caries in Sweden from 1960 to 1985. Comm. Dent. Oral
Epid. 17: pp 41-43.
2 . B.A. BURT, S.A. EKLUND, K.J. MORGAN, F.E. LARKIN, K.E. GUIRE L.A. OLIVE, and
J.A. WEINTRAUB, 1987. The effect of diet on the development of dental caries.
University of Michigan, School of Public Health. NTIS, Final report for Contract DE-
22438, National [NextPage]Institute of Dental Research.
3. W.M. EDGAR, 1981. Plaque pH assessments related to food cariogenicity in: Foods,
Nutrition and Dental Health, ed. , J.J. Hefferen and H.M. Koehler, 137-150.
Park Forest South Illinois: Pathotox.
4 . W.M. EDGAR, 1993. Extrinsic and intrinsic sugars: a review of recent UK
recommendations on diet and caries. In Efficacity of Caries preventive strategies. Caries
Res 27 (Suppl 1) pp 64-67.
5. J.D.B. FEATHERSTONE, M.M. O’REILLY ET AL, 1986. Enhancement of
remineralisation in vitro and in vivo. In Factors relating to demineralisation and
remineralisation of the teeth. IRL Pres[NextPage]s. Oxford and Washington.
6. J.D.B. FEATHERSTONE, 1987. The Mechanism of Dental Decay. Nutrition Today.
May/June, pp 10-16.
7. FORSYTH CONFERENCE, 1982. The first international conference on the declining
incidence of dental caries, ed, R.L. Glass, J. Dent Res. 61, Special issue, pp 1301-
1383.
8. S.R. GROBLER and J.B. BLIGNAUT 1989. The effect of high consumption of apples
and grapes on dental caries and periodontal disease in humans. Clin. Prev. Dent. 11: pp
8-12.
9. J.J. HEFFERENN. (ed). 1986. Proceedings: scientific consensus conference on
methods for assessment of the cariogenic potential of foods,[NextPage] San Antonio, 1985. J.
Dent. Re. 65 (Special Issue).
10. M.E. JENSEN AND C.F. SCHACHTELE, 1983. The acidogenic potential of reference
foods and snacks at interproximal sites in the human dentition. J. Dent. Res. 62, (8), pp
889-892
11. S. KASHKET, J. VAN HOUTE, L.R. LOPEZ and S. STOCKS, 1991. Lack of correlation
between food retention on the human dentition and consumer perception of food
stickiness. J. Dent. Res. 70: pp 1314-1319.
2. L.M. KEREBEL, M.T. LE CABALLEC ET AL, 1985. Report on caries reduction in French
schoolchildren 3 years after the introduction of a preventive programme. Comm. Dent.
Ora[NextPage]l Epidem., 13, pp 201-204.
13. J. KLIMEK, H. PRONZ ET AL, 1985. Effect of a preventive program based on
professional tooth cleaning and fluoride application on caries and -gingivitis. Comm.
Dent. Oral Epid. 13, pp 295-298.
14. K.G. KONIG 1990. Changes in the prevalence of dental caries: how much can be
attributed to changes in diet ? In Diet, Nutrition and Dental Caries, Caries Res 24
(Supplement 1): pp 16-18
15. K.G. KONIG 1993. Role of fluoride toothpastes in caries preventive strategy. In efficacy
of caries preventive strategies. Caries Res, 27 (Supplement 1): pp 23-28
16. H.A.B. LINKE, L. ARAV, P.M[NextPage]. CHIU and S.J. MOSS. 1989. Oral clearance and acid
production of foods containing either cooked starch or carbohydrate sweeteners.
(Abstract). Caries Res 23: pp 430.
17. L.S. MAJEM, R.G. CLOSAS, J.M. RAMON, C. MANUA, E. CUENCA and B. KRASS,
1993. Dietary habits and dental caries in a population of Spanish schoolchildren with
low levels of caries experience. Caries Res. 27, 488-494.
18. T.M. MARTHALER, 1990. Changes in the prevalence of dental caries: how much can
be attributed to changes in diet ? In Diet, Nutrition and Dental Caries. Caries Res 24
(Supplement 1): pp 3-15.
19. J. McMAHON, W.R. PARNELL[NextPage] and G.F.S. SPEARS, 1993. Diet and dental caries in
preschool children. Euro. J. Clin. Nutn. 47, 794-802
20. J.E. MORMANN AND H.R. MUHLEMANN, 1981. Oral starch degradation and its
influence on acid production in human dental plaque. Caries Res, 15, pp 166-175.
21. S.A. MUNDORFF, J.D.B. FEATHERSTONE ET AL, B.B. BIBBY, M.E.J. CURZON, A.D.
EISENBERG and M.A. ESPELAND. 1990. Cariogenic potential of foods. 1. Caries in
the rat model. Caries Re. 24: pp 344-355.
22. J.M. NAVIA, AND H. LOPEZ, 1983. Rat caries assay of reference foods and sugar
containing snacks. J. Dent. Res., 62, (8), pp 893-898
23. ROBERT WO[NextPage]OD JOHNSTON FOUNDATION, 1983. Preventing tooth decay: Results of
a four year national study/Special report, (2).
24. G. ROLLA and B. OGAARED. 1987. Reduction in caries incidence in Norway from 1970
to 1984 and some considerations concerning the reasons for this phenomenon. In
Strategy for dental caries prevention in European countries according to their laws and
regulations. Ed. by R. M. FRANK and S.O’HICKEY. pp 223-229. Oxford: IRL Press Ltd.25. A.J. RUGG GUNN et al, 1984. Relationship between dietary habits and caries increment
assessed over two years in 405 English adolescent schoolchildren, Arch[NextPage]. Oral Biol.29,
(12), pp 983-992
26. J.M. TEN CATE and Y.M. SIMMONS, 1989. pH cycling: a useful technique now being
automated. (Abstract). Car. Res. 23: pp 114-115.
27. WHO 1992. Dental caries levels at 12 years. World Health Organization.
28. WHO, 1988. An elemental success story. World Health Organization.