DIET AND DENTAL CARIES

presented by

OONYU THOMAS BDS-III 21/U/18563

 OUTLINE
• The role of diet in dental caries.
• Cariogenicity of different sugars
• Influence of different sugar intake patterns; amount, form and
frequency in dental caries.
• Studies showing the relationship of diet to dental carries.
• The influence of fluoride on sugar-caries relationship.
THE ROLE OF DIET IN DENTAL CARIES:

• Dental caries occurs due to demineralization of enamel and dentine

(the hard tissues of the teeth) by organic acids formed by bacteria in
dental plaque through the anaerobic metabolism of sugars derived
from the diet
• . When sugars or other fermentable carbohydrates are ingested, the
resulting fall in dental plaque pH caused by organic acids increases the
solubility of calcium hydroxyapatite in the dental hard tissues and
demineralization occurs as calcium is lost from the tooth surface. The
pH at which demineralization occurs is often referred to as the critical
pH and is approximately 5.5.
• Saliva is one of the mouth’s natural defenses against this process.
• Saliva promotes remineralization, i.e. it is capable of depositing mineral in porous
areas where demineralization of enamel or dentine has occurred. Saliva is super-
saturated with calcium and phosphate at pH 7; this favors the deposition of
calcium.
• If a demineralized lesion is formed it will be demineralized; although this is a
slow process that competes with factors that cause demineralization. If the pH in
the mouth remains high enough for sufficient time then complete
remineralization of enamel may occur. However, if the acid challenge is too great,
demineralization dominates and the enamel becomes more porous until finally a
carious lesion forms.
• The rate of demineralization is affected by the concentration of hydrogen and
fluoride ions (i.e. pH at the tooth surface). Fluoride inhibits the demineralization
process and the frequency with which the plaque pH falls below the critical pH
without subsequent remineralization. So overall, caries occurs when
demineralization exceeds remineralization.
. The development of caries requires sugars and bacteria to occur but is influenced
by the susceptibility of the tooth, the bacterial profile, quantity and quality of the
saliva, and the time for which fermentable dietary carbohydrates are available for
bacterial fermentation.
• Streptococcus mutans and Streptococcus sorbrinus are important bacteria in the
development of dental caries. Both these bacteria readily produce organic acids
from dietary sugars and like most aciduric bacteria can synthesize insoluble
plaque matrix polymers (extracellular dextran) from dietary sugars—a factor that
aids bacterial colonization of the tooth surface. Growth of these streptococci
requires the presence of fermentable monosaccharides. Mutans streptococcal
invertase splits sucrose into glucose and fructose, which can be metabolized to
produce mainly lactic acid but also other acids including acetic and formic acids.
The resulting low pH alters the plaque ecology.
• A low pH in plaque is ideal for aciduric bacteria such as streptococci, lactobacilli
and bifidobacteria as these are more competitive at low pH than bacteria not
associated with dental caries.
 CARIOGENICITY OF DIFFERENT SUGARS
• The cariogenecity of the different sugars was experimented in the Vipeholm study
which was carried out on close to 400 isolated sample of people fed on different
sugars including sucrose, sweetened bread, sweets(toffees, caramels or
chocolate) to study the cariogenicity of the different sugars.
•COMPOUND
INFLUENCE OF DIFFERENT SUGAR INTAKE PATTERNS; AMOUNT, FORM AND
FREQUENCY IN DENTAL CARIES:
• Sticky forms such as caramel which clings to teeth, solid carbohydrates, soft
retentive foods that are cleared slowly, monosaccharides and disaccharides are
more caries-producing as they continuously release substrates over a long time. A
given amount of sucrose is more cariogenic when fed to animals in small
increments at intervals than the same total at once.
• The cariogenicity of different sugars varies as shown by the Turku study found no
significant difference in caries development between those consuming sucrose
and those consuming fructose.
• Free sugars are the monosaccharides and disaccharides added to foods by the
manufacturer, cook or consumer plus those naturally present in honey, fruit juices
and syrups. This excludes the naturally occurring sugars in vegetables, whole
fruits and milk.
 STUDIES SHOWING RELATIONSHIP
OF DIET AND ENTAL CARIES.
1. Early studies and research by Willoughby D. Miller in his Acidogenic or Miller’s
chemico-parasitic theory of 1882 put forward that the dental caries are based on 2
processes that is; decalcification of enamel and dentin, and dissolution of softened
tissue brought about by the acids or low pH produced by the oral microorganisms.
• The acids(lactic acid) is produced from the fermentation/anaerobic respiration of
starch and sugars lodged in the retaining centers of teeth such as ridges by the
acidogenic oral microorganisms on either the plaques or circulating within the
saliva.
• The lactic acid shifts the pH in the mouth which reacts with enamel
hydroxyapatite and produces apatite lactate salt that significantly compromises the
strength and resistance of enamel.
2. VIPEHOLM DENTAL STUDY;(1945-1953)
• One of the first large scale study in the history of dentistry. It was carried out in
the 20th century at the vipeholme hospital in Sweden. The study positively
established that sticky sweets consumed between meals, rather than during
meals significantly increased the incidence rate of dental caries. It showed a
major involvement in the development of the carious tooth surface.
• Subjects who consumed 24 pieces toffee a day developed 4.02 new carious tooth
surfaces per person per year, relative to the control group which developed only
0.30 carious surfaces per person per year. By the end of the study, a total of 2125
new dental caries had been induced among the study population.
3. Robert Stephan study of 1943:
• He used a curve to explain that there is a fall in saliva or plaque PH
during consumption of fermentable carbohydrate, acidic liquids, or
sugar below the critical PH (5.5) in the presence of acidogenic bacteria.
After consumption there is an elimination of the acid and a return to
normal saliva or plaque PH, at which point repair of any destruction of
enamel structure takes place following the intake( remineralization).
Repeated intake of fermentable carbohydrates causes the low PH to be
maintained for longer periods, thereby not allowing remineralization to
take place.
Stephan’s curve of dental Caries.
THE INFLUENCE OF FLUORIDE ON THE SUGARS–CARIES RELATIONSHIP
• Fluoride alters the resistance of the teeth to demineralization as well as the
speed with which the enamel surface remineralizers following a plaque acid
challenge. Fluoride affects the tooth post-eruptively in three ways.
• First, it reduces and inhibits demineralization: Fluoride is incorporated into the
enamel lattice and/or binds to enamel crystal surfaces and replaces the hydroxyl
groups in hydroxyapatite. By converting hydroxyapatite into fluorapatite which is
more stable, fluoride reduces the susceptibility of the enamel to
demineralization.
• Second, remineralization of enamel in the presence of fluoride results in the
porous lesion being demineralized with fluorapatite rather than hydroxyl apatite
(the former being more stable and more resistant to further attack by acids).

• Lastly, fluoride also affects plaque by inhibiting bacterial metabolism of sugar

thus reducing acid production. The main action of fluoride is topical at the
enamel surface after eruption. The inverse relationship between fluoride in
 THAKYOU

REFERENCES
• 1. Cawson’s Essentials of oral pathology and oral medicine 9th edition.
• 2. Public Health Nutrition: 7(1A), 201–226
• 3 Online www.wjahr.com