PREVENTION OF CARIES

INTRODUCTION

LEVELS OF CARIES PREVENTION

CHEMICAL MEASURES OF CARIES PREVENTION

NUTRITIONAL MEASURES OF CARIES PREVENTION

MECHANICAL MEASURES OF CARIES PREVENTION

CONCLUSION

REFERENCES

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PREVENTION OF CARIES

INTRODUCTION:

Dental caries and periodontal disease are probably the most common

chronic disease in the world. Although caries has affected human since prehistoric

times, the prevalence of this disease has greatly increased in modern times on the

world wide basis and increase strongly associated with the dietary changes.

However evidence now indicates that this trend peak and began to decline

in many countries in the late 1970s and early 1980s and the decline was most

noticeable in certain segments of population in developed countries. A similar

polarization is occurring on the world wide basis where the prevalence of caries is

declining in developed countries, is increasing in less developed countries and is

epidemic in countries with emerging economies. Thus caries being localized in the

segment of populations that can least afford the necessary dental treatment.

A caries prevention program is complex process involving multiple

interrelated factors. The primary goal of caries prevention program should reduce

the number of cariogenic bacteria. Prevention should start with a consideration of

the overall resistance of patients to infection by the cariogenic bacteria. Although

general health of the patient, fluoride exposure history and function of immune

system and salivary glands have a significant impact on the patient’s caries risk.

Caries control methods are the operative procedures used both to stop the

advance of the individual lesions and to prevent the spread of pathogenic bacteria

to other tooth surfaces and in this sense, they are preventive procedures.

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Management of dental caries and its consequences remain the dominant

activity of dentists. However preventive and diagnostic service, percentages of

practice activities are increasing. Although these activities relate to variety of

dental problems, diagnosis and prevention of caries are major part of these

increases.

No longer is the restoration of carious lesion considered to be cure. Rather

the practitioner must identify those patients who have active carious lesions and

those at high risk of caries and institute appropriate preventive and treatment

procedures.

METHODS OF CARIES PREVENTION:

The control of dental caries presents one of the greatest challenges that

must be met today by the dental profession. It has been a general failing of healing

profession that the treatment of disease has been overemphasized and prevention

is minimized.

Kauffman has stated that “The supreme ideal of dental profession should be

to eliminate the necessity for its own existence”.

This suggestion emphasizes the necessity for more forceful approach to the

problem of preventing dental caries, although the ideal has not been reached, there

have been definite accomplishments in the field of caries control.

The levels of prevention of dental caries:-

Primary prevention

Secondary prevention

Tertiary prevention

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The methods to control dental caries can be classified into 3 general groups

(types):

Chemical measures

Nutritional measures

Mechanical measures

CHEMICAL MEASURES:

1) Substances which alter the surface of tooth structure

a. Fluoride

b. Iodides

c. Bis-biguanides

d. Silver nitrate

e. Zinc chloride and potassium ferrocyanide

2) Substances which interfere with carbohydrate degradation through

enzymatic reaction/ alterations

a. Vitamin K

b. Vitamin D

3) Substance which interfere with bacterial growth and metabolism

a. Urea and ammonium compounds

b. Chlorophyll

c. Nitro furans

d. Caries vaccine

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FLUORIDES:

History:

1874: The first reference to prophylactic role of fluoride by Erhadt. In

contribution to ‘Memorabilia’ – A monthly publication he reported. As for a

long time, iron was given for blood, calcium, and phosphorus for the bones, so

it has been successfully to add fluoride to tooth enamel in soluble and

absorbable form. It is fluoride that gives hardness and durability to the tooth

enamel and protects against the caries.

1965 – Pindborg & 1982 – Hunsfordbraten both refer to pamphlet published,

entitled “Flourides” How to remedy the decay of the tooth? The text of the

brochure stated that various substances were essential for health of the teeth,

above all fluorine.

1986 – Dr. A Dennigar gave a lecture entitled ‘fluorides’ an agent to combat

dental diseases. Fluorine is an element which is close to chlorine, bromine and

iodine and most frequently bound to Ca, occurs as CaF2 in minerals. The lack

of fluorine in food stuffs still seems to be a very important factor in the cause

of dental diseases.

ANTICARRIES MECHANISM OF FLUORIDE:

The mechanism by which fluoride increases caries resistance may arise

from both systemic and topical applications of fluoride and can be broadly

grouped into –

1) Increased enamel resistance

2) Increased rate of maturation

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3) Remineralization of incipient lesion

4) Interference with microorganism

5) Improved tooth morphology

1) Increased enamel resistance:-

When enamel is exposed to a pH of about 5.5 or lower, it will dissolve

according to the following equation.

Ca10 (PO4)6 (OH)2 + 8H+ 10Ca2+ + 6HPO4 + 2H2O

Hydroxyapatite

The presence of fluoride in the dissolution medium effectively reduces the

solubility of enamel by promoting the formation of fluoroapatite and preventing

the formation of more soluble calcium and phosphate minerals.

Ca10(PO4)6 (OH)2 + 2F Ca10 (PO4)6 F2 +2OH

Fluorapatite

2) Increased rate of maturation:-

The resistance of teeth to caries appears to increase posteruptively with age

and greater benefits are obtained by topical fluoride application shortly after

eruption of the teeth. The newly erupted teeth has areas where minimal deposition

is not complete. These hypomineralized areas may become fully mineralized

within few months after eruption. The presence of even small amounts of fluoride

in a mineralizing solution enhances the precipitation of the mineral

hypomineralized areas that mature in the presence of fluoride contain more

fluoride than enamel that was fully mineralized upon eruption. These areas will

therefore be made more resistant to acid. The presence of fluoride in mineralizing

solution also increases the rate of maturation.

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3) Remineralization of incipient lesions:-

Incipient lesions are opaque, white areas on the enamel having relatively

sound surface but with substantial mineral loss 30 to 60 m below the surface

layer. When the environment is cariogenic, demineralization continues until the

cavity is formed. However, if the environment is changed to allow free access to

saliva, the lesion becomes arrested or actually disappears because of redeposition

of mineral within the lesion.

Although saliva is the natural remineralizing solution, there is evidence that

fluoride is more effective. Brown color of an arrested lesion in presence of

fluoride is due to the precipitated proteins and minerals.

4) Interference with microorganisms:-

Interference with the metabolism of microorganisms involved in caries

formation has been proposed as the possible mechanism for anti-cariogenic

property of fluoride.

Fluorides can affect microorganisms in several ways. At low fluoride

concentrations it inhibits acid formation, at higher concentrations it can affect

growth and metabolism and at very high concentrations it is lethal.

Inhibition of bacterial growth and metabolism is related to effect of

fluorides on enzymes. The enzymes most sensitive to fluoride during the

formation of acid is enolase and in the formation of polysaccharides it is

phosphoglucomutase. Also it inhibits the glucose transfer across the cell wall.

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5) Improved tooth morphology:-

The areas of teeth most susceptible to dental caries are the occlusal surfaces

and those with the deep fissures. The fluoride tend to make the teeth slightly

smaller and more important, shallower fissures.

Fluorides for Caries Prevention:

Systemic

Topical

Systemic fluorides Topical fluorides

Water fluoridation

Salt fluoridation

Milk fluoridation

Fluoride supplements

Sodium fluoride

Stannous fluoride

Acidulated phosphate fluoride

Fluoride varnish

Fluoride dentifrices

Fluoride mouth rinse

2) Salt fluoridation:

In Switzerland in the early 1950’s, initially the fluoride concentration used

was 90mgF/kg, later they increased the concentration to 250mgF/kg, because the

initial concentration used was too low for the most effective cariostasis.

3) Milk fluoridation:-

Milk fluoridation is the addition of a measured quality of fluoride to bottled

or packaged milk. Although, substantial reduction in caries is observed with milk

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fluoridation. Milk fluoridation started in Swiss city of Winterthen in 1955,

promoted by Zeigler.

4) Fluoride tablets:-

They are manufactured as,

a) tablets or drops, intended to be swallowed

b) tablets of chewing

c) lozenges

Supplements contain a measured amount of fluoride, typically 0.25 mg,

0.5mg or 1.0mg, usually as sodium fluoride but sometimes as acidulated

phosphate fluoride, potassium fluoride or calcium fluoride.

Daily dosage of fluoride, recommended by ADA:-

Age Fluoride concentration in drinking water

<0.3 0.3 – 0.7

0 – 2 years

2 -3 years

3 – 16 years

0.25 mg

0.5 mg

1.0 mg

0

0.25 mg

0.5 mg

Topical Fluorides:

Topical fluorides for the prevention of dental decay are the most widely

used dental products at home and in dental clinics. Generally, high fluoride

concentration agents are applied professionally and low-fluoride concentration

agents or products are applied by the individuals themselves.

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Professionally applied fluorides:

1) Sodium fluoride:- Introduced by Bibby and Knutson in 1940

The most accepted method of NaF application is Knutson’s technique,

where 2% NaF solution is used.

Mechanism of action:-

Ca10 (PO4)6 (OH)2 + OH 10CaF2 + 6PO4 + 2OH

High concentration of fluoride (9,000 ppm) in 2% NaF due to which

solubility product of CaF2 gets exceeded fast and this initial rapid reaction is

followed by drastic reduction in its rate, this phenomenon is called as choking off.

Further CaF2 reacts with hydroxyapatite to form fluoridated hydroxyapatite.

CaF2 + 2Ca5 (PO4)3OH 2Ca5(PO4)3 F + Ca(OH)2

2) Stannous fluoride:- Introduced by Dudding & Muhler in 1962

Muhler compared the effectiveness of NaF and SnF2 & found that SnF2 of

the same concentration as that of NaF is more effective in reducing the incidence

of caries.

Concentration available 8% to reduce the number of applications. SnF2 is

prepared freshly as it has no shelf life. it is prepared by dissolving 0.8 gms of

powder in 10 ml distilled water.

Topical applications:-

Mechanism of action:-

At low concentration

Ca5(PO4)3 OH + 2SnF2 2CaF2 + Sn2 (OH)PO4 + Ca3(PO4)2

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At high concentration (19500 ppm)

Ca5 (PO4)3 OH + 16SnF2 CaF2 + 2Sn3 F3PO4 + Sn(OH) PO4 + 4CaF2 (SnF3)2

Stannous trifluoro Calcium phosphate trifluoro

stannate

2 Ca5(PO4)3 OH + CaF2 2Ca5 (PO4)F + Ca(OH)2

3) Acidulated phosphate fluoride:-

Introduced by Brudevold and his coworkers who systematic investigation

to find out an optimal fluoride acid solution which would provide maximal

fluoride deposition while causing minimal demineralization and reported that

phosphate containing fluoride maximum beneficial effect.

APF solutions usually contains 1.23% fluoride in 0.1M phosphoric acid at

pH of 3.0.

Topical application:-

Mechanism of action:- When APF is applied to the teeth, it initially leads to the

dehydration and shrinkage in the volume of hydroxyapatite crystal which on

further hydrolysis forms an intermediate product called Dicalcium phosphate

dehydrate. This is highly reactive with fluoride and start forming immediately

when APF is applied and fluoride penetrate into the crystals more deeply and leads

to formation of fluoroapatite.

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Comparative clinical characteristics of topical fluoride solution:-

Characteristic NaF SnF2 APF

Percent 2% 8% 1.23%

Ppm fluoride 9000 19500 12,300

Frequency of application

4 times at weekly interval at age 3, 7, 10 & 13

Once/ year Twice/ year

Taste Bland Metallic Acidic

Stability Stable Unstable Stable in plastic container

Tooth pigmentation

No Yes No

Gingival irritation No Occasional No

Average effective 29% 32% 28%

Fluoride Varnish:

The cariostatic effect of topical fluoride agents has been related to their

ability to deposit fluoride in the enamel and their depth of penetration. The most

commonly used varnishes are:-

1) Duraphat (NaF varnish containing 2.26% fluoride in organic lacquer).

2) Fluorprotector (saline fluoride containing 0.7% fluoride in a polyurethane

based lacquer).

Duraphat hardens into a yellowish brown coating in the presence of saliva

(22600 ppm fluoride).

Fluorprotector leaves a clear, transparent film on the teeth (7000 ppm

fluoride)

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Method of Application:-

Mechanism of action:- When duraphat is applied to the surface, a reservoir of

fluoride ions gets built up around the enamel. From this, fluoride keeps on slowly

releasing and continuously reacting with the hydroxyapatite crystals of enamel

over a long period of time leading to deeper penetration of fluoride and formation

of fluorapatite.

10 Ca(PO4)3 OH + 10F 6Ca5 (PO4)3 F + 2CaF + 6Ca3

Fluoride Dentifrices:-

Tooth brushing with a fluoride dentifrice is by far the most common form

of caries control in use today and can be used effectively in individuals of all ages.

Dentifrices contain different types of fluoride compound such as NaF, SnF2,

sodium monofluorophosphate or amine fluoride.

Commonly used abrasives with sodium fluoride are calcium

pyrophosphate, hydrated silica, sodium bicarbonate, insoluble sodium

metaphosphate, acrylic polymer.

Recommendations for fluoride dentifrice in children:-

Below 4 yrs Fluoride tooth paste is not recommended.

4 – 6 yrs Brushing once daily with fluoride tooth paste and other two times

without fluoride tooth paste.

6 – 10 yrs Brushing twice daily with fluoride tooth paste and once without

fluoride tooth paste.

Above 10 yrs Brushing thrice daily with fluoride tooth paste.

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Fluoride Mouthrinse:-

The benefits from fluoride mouthrinsing range from 20% - 50% less decay.

Mouthrinses can be used daily or weekly based on the concentration of the

compound used.

Composition and usage of fluoride mouthrinses:

Source of fluoride Fluoride % Content ppm Recommended usage

NaF

NaF

NaF

APF

SnF2

0.2%

0.02%

0.05%

0.025

0.10%

900

90

225

200

243

Weekly

Twice daily

Daily

Daily

Daily

IODINE:

Miller (1980) reported the intraoral use of iodine solution as an

antibacterial mouthrinse. The bactericidal effectiveness is not time dependent i.e.

it kills microorganisms immediately once contact with the organisms is

established.

Disadvantage:-

- Metallic taste

- Tendency to stain silicate or composite restoration

Bis-Biguanides:

The two most common commercially available bis-biguanides are –

a) Chlorhexidine b) Alexidine

They are effective anti-plaque agents and thus potential anticaries agents.

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Topical antiseptics characterized by molecular structure having both

hydrophobic and hydrophilic constituents and possess a net positive charge at

physiologic pH.

Mode of action:

a) Ionic adsorption of negatively charged bacterial surface

b) Interaction with and damage to permeability barrier of cytoplasmic

membrane

c) Penetration into cells and subsequent penetration of cytoplasmic

constituents and culmination in membrane leakage and cell death.

SILVER NITRATE:

Silver nitrate impregnation of teeth was used clinically for many years to

prevent or arrest dental caries. The earlier worker believed that silver ‘plugged’

the enamel, either the organic invasion pathways such as the enamel lamellae or

the organic pathways, combining with the soluble inorganic portion of enamel to

form less soluble combination.

Zinc Chloride and Potassium Ferro cyanide:

Gottleib proposed that importance of protein matrix of the enamel in dental

caries process. The use of zinc chloride and potassium Ferro cyanide would

effectively impregnate the enamel and seal off caries invasion pathways.

Substances which interfere with the degradation through enzymatic alterations:-

a) Vitamin K

b) Sarcoside

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Substances which interfere with bacterial growth and metabolism:-

a) Urea & ammonium compounds

b) Chlorophyll

c) Nitrofurins

CARIES VACCINE:

The belief that bacteria are involved in the pathogenesis of dental caries

was clearly expressed in a paper by Underwood and Miller published in 1881.

Since the dental caries fulfills the criteria of the infectious disease, the

possibilities of the vaccination have been considered. ‘Vaccine’ is an immuno-

biological substance designed to produce specific protection against the given

disease. It stimulates the production of protective antibody and other immune

mechanism.

Over the past many years, there has been a study accumulated of evidence

the S.mutans is the bacterium most intimately associated with the initiation and

development of carious lesion.

Mechanism of action of a vaccine:

Since immune response cannot be mounted via enamel, the only way in

which immune element can reach the organism responsible for dental caries is for

them to liberate into saliva or in the cases of cell to migrate over the tooth surface.

Protection against dental caries by immunization would be achieved by immune

components from serum, by IgA antibodies in salivary secretions.

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The major immunoglobulin in saliva is secretory IgA and 80% of IgG is

present in 80% of the total immunoglobulin in serum. The molecular configuration

renders the secretary IgA antibody exceptionally resistant to digestion by

proteolytic enzymes consequently, it can function highly effectively in oral

environment which contain microbial proteases.

Even if an anticaries vaccine were developed, the concern remain that may

affects its widespread use.

First:-the potential side effect of caries vaccine should be identified. Safety of such

vaccines has not been demonstrated in fact there is concern of a possible cross

reaction with human heart tissue.

Second:- Its cost must be compared with public water fluoridation which is

inexpensive and already very effective in the fluoride therapy.

Third:- Limitation imposed by governmental regulatory agencies may affect the

widespread use of anticaries vaccine.

NUTRITIONAL MEASURES:

Diet:- The role of diet and nutritional factors deserve special consideration

because of the often observed differences in caries incidence of various population

who subsist on dissimilar diets.

Objectives of Dietary Analysis:

1) To provide an opportunity for patient to study, objectively personal dietary

habits.

2) To obtain an overall picture of the type of food in the patient diet, food

preference and quality of food eaten.

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3) To study the food habits with particular reference to frequency and regularity

of eating and the order in food is taken.

4) To record for study and future comparison of the types and frequency of use of

potential cariogenic food.

5) To determine the overall frequency of cariogenic exposure with clinical and

radiologic findings resulting in caries activity test.

6) To provide a basis for making individual recommendation for changes in diet,

important to the health of the oral mucosa and the prevention of dental caries.

Role of Carbohydrates in caries development:

Dental caries is the common plaque dependent bacterial infection that is

strongly affected by diet. Development of clinical caries is contingent upon the

interaction of the three local factors in the mouth.

a) Susceptible tooth

b) Cariogenic bacteria

c) Fermentable carbohydrates

Absence of any one of the factors dramatically reduces the caries risk.

Mutans streptococci are the predominant oral bacteria that initiate the caries

process. When the starches and sugars are fermented by cariogenic bacteria,

organic acids are produced which demineralizes the dental enamel. Thus for the

patient with high risk of caries, the dietary counseling about the damaging effect

of fermentable carbohydrates on the teeth are essential.

Decay promoting eatables are sugar (sucrose), corn sweeteners (45%

glucose + 55% fructose), milk (lactose), honey (45% fructose + 35% glucose + 5%

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sucrose) and highly refined cooked starch sugar combination such as Doughnuts,

cookies, potato chips and ready to eat breakfast cereals which produce a prolonged

acidogenic response when retained in the interproximal spaces. When the starches

are cooked they are partially degraded. This allow -amylase to convert starch

particles retained on the tongue, oral mucosa and teeth to maltose. Making maltose

available to plaque, pH will remain low and permit more demineralization to

occur.

Other factors affecting dental decay:

Frequency of eating:- The positive relationship between the frequency of sugar

intake in humans and dental caries was first demonstrated in Vipeholm study.

Subjects who consumed candies in between the meals developed more caries

than those who were fed equal amount of sugars with meals.

One snack between the meals is not harmful because there is a time for

remineralization of carious lesions. However snacking many times throughout

the day keeps the plaque pH low and extends the time for enamel

demineralization.

Physical form of carbohydrates:- Bacterial fermentation can continue as long

as carbohydrate adheres to the dental enamel surface. Solid foods that are

retained on the tooth surfaces for prolonged periods of time and can extend the

acid production beyond 60 minutes. Thus retentive foods are more likely to

produce more tooth decay than sucrose sweetened solutions like juices and

punches which are cleared from the mouth easily.

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Sequence of food:- Coffee with sugar consumed at the end of a meal causes the

plaque pH to remain low for longer time than when unsweetened food is eaten

following intake of coffee with sugar. When cheese is eaten following the

sucrose rinse, the pH remains higher than those when no cheese follows a

sucrose rinse.

Review articles on the relationship between sugar (diet) and dental caries:

Author(s) Main conclusions

Marthaler (1967) Food stuffs containing simple sugars are far more cariogenic than common starchy foods.

Newbrun (1969) Called for the specific elimination of sucrose or sucrose-containing foods rather than restricting total carbohydrate consumption.

Bibby (1975) Snack foods share importance with sucrose in caries causation.

Sreebny (1982a) Total consumption and frequency of intake contribute to dental caries; lacking evidence about the precise definition of the relationship.

Newbrun (1982b) Compelling evidence that the proportion of sucrose in a food is one important determinant of its cariogenicity.

Sheiham (1983) Sugar is the principal cause of caries in industrialized countries; recommended that sugar consumption be reduced to 15 kg/person/year or below.

Shaw (1983) Studies in animals consistent with the clinical evidence on the relationship between sugar and caries.

Rugg-Gunn (1986) Cariogenicity of staple starchy foods is low; the addition of sucrose to cooked starch is comparable to similar quantities of sucrose; fresh fruits appear to have low cariogenicity.

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Bowen and Birkhed (1986)

Frequency of eating sugars is of greater importance than total sugar consumption.

Walker & Cleaton-Jones (1989)

Degree of incrimination of sugar as a cause of caries is grossly exaggerated; questioned predictions of reductions in caries from decreases in sugar and snack intakes.

Marthaler (1990) In spite of dramatic reductions in caries due primarily to widespread use of fluoride, sugars continue to be the main threat to dental health.

Rug-Gunn (1990) Dietary modification involving restriction on the frequency and amount of extrinsic sugars can be more effective than other control measures.

Konig and Navia (1995)

Acknowledged the relationship between frequency and sugar intake and caries: recommended removing the focus away from elimination of sugar and towards improved oral hygiene and use of fluoride toothpaste.

Ruxton et al. (1999) Evidence strongly supports formulation of advice on frequency of consumption, not amount.

Konig (2000) Dental health problems do not require any dietary recommendations other than those required for maintenance of general health.

Van Loveren (2000) If good oral hygiene is maintained and fluoride is supplied frequently, teeth will remain intact even if carbohydrate-containing food is frequently eaten.

Sheiham (2001) Sugars, particularly sucrose, are the most important dietary cause of caries; the intake of extrinsic sugars greater than 4 times a day increases caries risk; sugar consumption should not exceed 60 g/day for teenagers and adults and proportionally less for younger children.

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Classic evidence from humans supporting the role of sugar in dental caries:

Study Reference(s) Main conclusions

Vipeholm study Gustafsson et al. (1954)

The more frequently sugar is consumed the greater the risk; sugar consumed between meals has much greater caries potential than when consumed during a meal.

Turku Sugar Study

Scheinin et al. (1976)

When sugars are almost completely replaced by non-fermentable sugar substitutes (xylitol), caries increment is dramatically reduced; fructose is less cariogenic than sucrose.

World War II Toverud (1957a,b) Tekeuchi (1961)

Caries decreased and increased with sugar consumption during and after the war, respectively.

Hopewood House

Harris (1963) Modern diet ore cariogenic than vegetarian low sugar diet.

Tristan da Cunha

Holloway et al. (1963), Fisher (1968)

Introduction of a modern diet including sugar and refined carbohydrates to this remote island greatly increased caries prevalence.

Hereditary Fructose Intolerance

Marthaler (1967), Newbrun et al. (1980)

Less caries in individuals that must avoid sucrose and fructose, but not other sugars and complex carbohydrate.

Experimental Caries in Man

Von der Fehr et al. (1970), Geddes et al. (1978)

Incipient caries can be rapidly induced by frequent rinsing with high-concentration sucrose solutions in the absence of oral hygiene.

Stephan Plaque pH Response

Stephan (1940, 1944)

Demonstrated the relationship between sugar exposure resulting in the acidification of dental plaque and caries experience

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Data from national Surveys:

Reference Parameters Main findings/ conclusions

Sreebny (1982b) dmft in 6-years olds

from 23 nations and

DMFT in 12-year-olds

from 47 nations; sugar

supply (g/person/day)

Significant positive correlation

(r=0.72; p<0.005) between caries

prevalence and national sugar

supplies for 12-year-olds only;

ingestion of 50 g of sugar/day may

be the upper limit of ‘safe’ or

‘acceptable’ sugar consumption.

Woodward and

Walker (1994)

DMFT in 12-year olds

from 90 nations; sugar

supply (kg/person/year)

Linear relationship between

DMFT and sugar consumption

when all 90 nations were included;

no evidence of a relationship with

a separate analysis of 29

industralized nations.

Miyazaki and

Morimoto (1996)

DMFT in 12-year olds

(kg sugar/years); 1957-

1987; low fluoride

exposure

Excellent correlation (r=0.91;

p<0.01) between DMFT and per

capita sugar consumption in Japan.

van Palenstein

Helderman et al.

(1996)

Caries experience in

Africa, Europe and

North America; salivary

mutans Streptococci

Caries experience on three

continents is attributable to dietary

differences and not prevailing

mutans streptococci species.

Dawner (1999) dmft in 5-year olds and

DMFT in 12-year olds;

available sugar

(kg/person/ year)

Strong positive correlation over

time (50 years) between caries

experience and national sucrose

availability in the UK.

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Form Frequency Points

Liquid: soft drinks, fruit drinks, sugar and honey in

beverages, ice cream, gelatin dessert, flavored yoghurt

___ x 5 =

Solid & sticky: Cake, cupcakes, donuts, sweet rolls,

pastry, canned fruit in syrup, bananas, cookies, chocolate

candy, jelly beams, chewing gums, jams.

___ x 10 =

Slowly dissolving: hard candies, breath mints, antacid

tablets, cough drops.

__ x 15=

Total score =

Evaluation of sweet scores:

Short:- To assess the cariogenic potential of the diet the client records a 24 hr diet

that represents the clients typical eating patterns. Type and amount of each food

eaten, food preparation and time of day the food was not eaten are reported.

The 24 hr diet recall is then used to calculate the cariogenic potential of the

diet. The sugar ingested reported on the 24 hr diet form is categorized according to

liquid sugars, solid and sticky sugars and slowly dissolving sugars. The frequency

with which each sugar is ingested and multiplied by 5, 10 or 15 depending on the

sugar source.

A sweet score of 15 or more indicates that the individual is needed of the

nutritional counseling to reduce the cariogenic potential of his or her diet.

Weak long:- The same procedure is done for a week long to evaluate the caries

potential of the different eatables.

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Dietary recommendations for the reduction of dental caries:

Limit the use of fermentable carbohydrates to mealtime. Foods other than

carbohydrates serve as buffer to help neutralize the plaque acids.

Omit sweet foods even with meals if the client is susceptible to caries.

Between meal snacks should consist of protective non-cariogenic food such as

raw vegetables. Raw, unrefined foods in the vegetable and fruit group require

chewing. The chewing action increases the salivary flow, thus aiding the

removal and dilution of sugars and their harmful byproducts.

Use a few concentrated sweets in the preparation of foods as possible.

Do not eat sweets before bedtime unless the teeth are brushed. Salivary flow

decreases at night and foods are not readily cleared from the mouth as they are

during waking hours. Acid left undisturbed remain in the mouth for 1 ½ to 2

hrs.

Avoid natural sugars as they are detrimental to the tooth surface as refined

sugars.

Avoid sticky foods because they are retained in the mouth longer than non-

sticky food.

Use of sugar alcohols, the most widely sued sugar alcohols are: xyliol, sorbitol,

mannitol, maltitol, lactitol and the products lycasin and palatinit. Xylitol in

chewing gum may reduce the dental plaque. Chewing sugar free gums 3 or

more times daily for prolonged periods of time may reduce caries incidence

irrespective of the type of sugar alcohol used.

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Using current diet patterns as the basis for discussion patient should be taught

the role of diet in caries, differences between cariogenic and non-cariogenic

eating patterns and how to adapt current diet to lower the cariogenic risk.

The methods of control of caries can be classified into 3 general types:-

a) Chemical

b) Nutritional measures

c) Mechanical measures

A) Chemical:

A last number of chemical substances have been proposed for the purpose

of controlling dental caries.

Bisbiguanides:- Chlorhexidine – anticarious effectiveness of chlorhexidine is more

pronounced for smooth surface caries than for pit and fissure caries.

Side effects:-

a) Transient diminution of the taste sensation

b) Parotitis

c) Mucosal irritation and desquamation

d) Allergic reaction

1) Silver nitrate:- Some studies show that silver nitrate is ineffective in caries

prevention.

It interferes with carbohydrate degradation through enzymatic alteration.

There are many substances that have ability to interfere with the enzyme systems

responsible for carbohydrate degradation and subsequent formation of acid. If

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such an inhibitor is effective in clinical preparation of dental caries, it must reach

the susceptible areas of the mouth in sufficient concentrations.

Vitamin K:

Synthetic vitamin K (2 methyl-1,4-napthoquinone) in prevention of caries

in vitro studies. He found that vitamin K prevents the acid formation in incubated

mixtures of glucose and saliva.

In another studies have tested the clinical effectiveness of vitamin K. a

group of students received a chewing gum containing the synthetic vitamin K and

sodium bisulfite and were instructed to chew this germ for at least 10 min after

eating any food.

The control group received the same chewing gum without the vitamin K.

The occurrence of new cavities were determined at 12 and 18 months intervals, it

was found that the incidence of new carious lesions was decreased by 98% and

42% respectively for the two intervals in the experimental group.

Sarcoside:

Fosdick and his co-workers in 1958, tested several hundred compounds and

noted that sodium-N-lauroyl sarcosinate and sodium dehydroacetate were

promising enzyme inhibitors or ‘antienzyme’.

Brudevold and Little (1954) continued investigation of this sarcoide in

patients who brushed their teeth with solution of the material and then measured

the fall in pH of plaque material from proximal surfaces after a sugar rinse. The

test was negative and it was concluded that the sarcoside did not reduce acid

production in subsurface.

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Substances which interfere with bacterial growth and metabolism:

Degradation of carbohydrates to acid is prevented by bacterial growth and

metabolism.

1) Urea and ammonium compounds:-

Urea and ammonium compounds have been tested extensively for use in

the oral cavity as anticariogenic agents. Wach and his associates (1942) reported

that a quinine-urea solution prevented acid formation in tests in vitro on

carbohydrate saliva mixtures. They also noted that oral bacteria count was

decreased after the use of quinine urea mouthwash.

Stephan (1943) continued the study of urea applied to dental plaques for

several minutes prevented the typical pH fall, following a carbohydrate rinse for

periods up to 24 hrs.

Although some studies indicate that ammoniated dentifrices are capable of

producing some reduction in dental caries incidence, the magnitude of this

reaction is not so great as to justify recommending them for widespread use as an

anticariogenic agent.

2) Chlorophyll:-

Chlorophyll is the green pigment of plants, as has been proposed as an

anticariogenic agent. Shafer & Shafer (1950) reported that a water soluble form of

chlorophyll. Sodium copper chlorophyll was capable of preventing or reducing the

pH fall in carbohydrate – saliva mixtures in vitro.

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Griffitts & Rapp (1950) and Knutson & Bibby (1951) reported the

bacteriostatic with respect to many oral microorganism including lactobacilli,

streptococci and micrococci.

Nitrofurans:-

They are the derivatives of Furans. They have been found to exert a

bacteriostatic and bacteriocidal action on many gram positive and gram negative

microorganisms.

John and associates (1951) reported that even in low concentrations, acid

production in saliva from caries active person was prevented.

Antibiotics:

1) Penicillin:- Anticariogenic compared because of antibiotic property. Hill

studied the effect of dentrifices containing 1000 units of Penicillin per gram,

on the oral lactobacillus counts of a group of 10 students. A remarkable

reduction from an average of 72,000 colony count to an average of 300 was

found after use of the dentifrices for 5 weeks.

2) Erythromycin:- Ripa and associates found that a 35% decrease in plaque

formation after a seven day test period of rinsing, then swallowing the agent 4

times a day.

3) Kanamycin:- Loesche (1976) reported that Kanamycin has been shown to

reduce plaque weight and to improve oral health in human being retarded

subjects when used a topical paste. It reduced the S.mutans and S.sanguis

population in the plaque. Other antibiotics like Lipnamycin, Tetracycline,

Tyrothricin, Vancomycin have been shown to be anticariogenic.

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Caries Vaccine:

The belief that bacteria are involved in the pathogenesis of dental caries

was clearly expressed in a paper by Underwood and Milles published in 1881.

Since the dental caries fulfills the criteria of the infectious decrease, the

possibilities of the vaccination have been considered. ‘Vaccine’ is an immuno-

biological substance designed to produce specific protection against the given

disease. It stimulates the production of protective antibody and other immune

mechanisms.

Vaccine derived from Latin word – a suspension of attenuated or killed

microorganism (bacteria, viruses or ricketsiae) administered for prevention,

amelioration or treatment of infectious diseases.

Over the past many years, there has been a study conducted with S.mutans

is the bacterium most intimately associated with initiation and development of

carious lesion. Laboratory studies have further shown that streptococci is a

heterogenous collection of the organism which can be subdivided into at least 6

distinct species (Containing strains of serotypes C, E and F).

Cariogenicity of S.mutans has been related to:-

- Its unique combination of properties i.e. ability to colonizes on the teeth.

- To produce extra and intra cellular polysaccharides

- To produce large amount of acids even at low pH values.

- To utilize salivary glycoproteins.

Appropriate immunization agents:-

The subcellular component which are currently being seriously proposed as

vaccines are (a) Glucosylatransferases (GTF), (b) Wall associated proteins.

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a) Glucosyltransferase (GTF):- Group of the extracellular enzymes involved

in synthesis of polymer (glucans) from sucrose.

b) Wall associated proteins:- Two purified proteins from surface of S.mutan

serotype C are currently being suggested for the use of the dental caries

vaccine. This antigen B shows some basis of the human caries vaccine and

has the advantage of being found in all serotype of S.mutans and

S.sorbinks. It could therefore give a wide-ranging protection. The other

wall associated protein of interest is antigen A which is a small molecular

weight cell wall protein.

Mechanism of action of a vaccine:

Since local response cannot be mounted via enamel, the only way in which

immune elements can reach the organisms responsible for dental caries is for them

to liberated into the saliva or in the case of cells to migrate over the tooth surface.

Protection against dental caries by immunization would be achieved by

immune components from serum, by IgA antibodies in salivary secretions.

The various studies have done to find out the mechanism of action of vaccine:

Challacombe et al. (1978) stated that IgG antibodies from serum reach the

oral cavity through the gingival crevicular fluid.

Seward (1971) stated that when the teeth erupted the local inflammation is

common and during this time serum antibodies may stimulate opsonisation and

phagocytosis of bacterial cell.

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Williams and Gibbon (1972) showed that the secretory IgA antibodies in

human saliva have been found to inhibit the attachment of S.sanguis to epithelial

cells.

Diagrammatic illustration of the two main immunological mechanism

involved in protecting the host against dental caries by immunization.

The first mechanism involves the secretory IgA secreted in saliva.

The second mechanism involves the systemic immune system an

production of antibodies that travel through the gingival epithelium into the

crevicular fluid that bathes tooth and plaque.

The major immunoglobulin in saliva is secretory IgA and 80% of IgG is

present in 80% of the total immunoglobulin in serum. The molecular configuration

renders the secretory IgA antibody exceptionally resistant to digestion by

proteolytic enzymes consequently, “It can function highly effectively in oral

environment which contains microbial proteases”.

Even if an anticaries vaccine were developed, the concerns remain that may

affect its widespread use. First, the potential side effect of the caries vaccine

should be identified, safety of such vaccines has not been demonstrated in fact

there is concerns of a possible cross reaction with human heart tissue. Second, its

cost must be compared with the public water fluoridation which is inexpensive and

already very effective at the fluoride therapy.

Third, limitations imposed by governmental regulatory agencies may affect

the widespread use of anticaries vaccine.

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Nutritional Measures:

Diet: The role of diet and nutritional factors deserves special consideration

because of the often observed differences in caries incidence of various population

who subsist on disseminator diets.

Objectives of Dietary Analysis:

a) To provide an opportunity for patient to study, objectively personal dietary

habits.

b) To obtain an overall picture of the types of food in the patient diet, food

preference and quantity of food eaten.

c) To study the food habits with particular reference to frequency and regularity

of eating and the order in which the food is taken.

d) To record for study and future comparison of the types and frequency of use of

potential cariogenic food.

e) To determine the overall frequency of cariogenic exposure with clinical and

radiologic findings and resulting in caries activity test.

f) To provide a basis for making individual recommendation for changes in diet,

important to the health of the oral mucosa and the prevention of dental caries.

Dental caries: role of carbohydrates in caries development:

Dental caries is the common plaque dependent bacterial infection that is

strongly affected by diet. Development of clinical caries is contingent upon the

interaction of the three local factors in the mouth – (a) susceptible tooth, (b)

cariogenic bacteria, (c) fermentable carbohydrate.

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Absence of any one of these factors dramatically reduces the caries risk.

Mutans streptococci are the predominant oral bacteria that initiate the caries

process. When the starches and sugars are fermented by cariogenic bacteria,

organic acids are produced which demineralized dental enamel.

The presence of other mineral such as Ca, F, and P in plaque and saliva

promote remineralization of incipient lesion. Other host factors that in addition ar

the saliva containing the buffering agents, bicarbonates and phosphates that

neutralizes the organic acids.

Other host factors that influence the caries risk; immune status, genetic

predisposition, malnutrition during tooth formation, education level and income

status. Thus for the patient with the high risk of caries the dietary counseling about

the damaging effects of fermentable carbohydrates on teeth are essential.

Decay promoting dietary products:

1) Sucrose:- Predominant role in development of the caries on smooth surface.

One of the sucrose metabolic by product, an extracellular polysaccharide called

glucan enables the mutan streptococci to adhere to the smooth enamel surfaces.

2) Corn sweeteners:- High fructose com syrup is mixture of 45% glucose and

55% fructose.

3) Milk:- A source of lactose has low cariogenicity except when used in nursing

bottle at bed time.

4) Honey:- 45% fructose, 35% glucose and 5% sucrose.

Highly refined cooked starch sugar combinations such as doughnuts,

cookies, potato chips and ready to eat breakfast cereals produce a prolonged

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acidogenic response when retained in the interproximal spaces. When the starches

are cooked they are partially degraded. This allows the -amylase to convert

starch particles retained on the tongue, oral mucosa and teeth to maltose.

Making maltose available to plaque pH will remain low and permit more

enamel demineralization to occur. Thus retentive, high starch foods may be more

acidogenic than high sugar/ low starch foods that are rapidly eliminated from the

mouth.

Other factors affecting the dental caries:

1) Frequency of eating

2) Physical form of carbohydrate (liquid vs. solid)

3) Retentiveness of a food on the tooth surface

4) Sequence in which the foods are consumed (e.g. cheese eaten before a

sweet food limits the pH drop).

5) Presence of minerals in a food.

1) Frequency of eating:-

The positive relationship between the frequency of sugar intake in humans

and dental caries was first demonstrated in Vipeholm study. Subjects who

consumed candies in between the meals developed more caries than those who

were fed equal amounts of sugars with meals.

One exposure of sugar between the meal is not harmful because there is

time for remineralization of carious lesions, however snacking many times

throughout the day keeps the plaque pH low and extends the time for enamel

demineralization.

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2) Physical form of the carbohydrate:-

Bacterial fermentation can continue as long as carbohydrate adheres to the

dental enamel surface. Solid foods that are retained on the tooth surfaces for

prolonged periods of time and cane extend the acid production beyond 60 minutes.

Thus retentive foods are more likely to produce more tooth decay than sucrose

sweetened solutions like juice and punches which are cleared from the mouth

easily.

3) Sequence of food:-

Coffee with sugar consumed at the end of a meal causes the plaque pH to

remain low for longer time than when an unsweetened food is eaten following

intake of coffee with sugar.

When cheese is eaten following the sucrose rinse, the pH remains higher

than those when no cheese follows a sucrose rinse.

Evaluation of cariogenic potential of diet using a sweet score: (Food diary)

- Short (one day)

- Week long

Short:- To assess the cariogenic potential of the diet, the records of a 24 hour diet

that represent the clients typical eating patterns. Type and amount of each food

eaten, food preparation and time of day the food was not eaten are reported.

The 24 hour diet recall is then used to calculate the cariogenic potential of

the diet. The sugar ingested reported on the 24 hour diet form is categorized

according to liquid sugars, solid and sticky sugars and slowly dissolving sugars.

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The frequency with which each sugar is ingested is tallied and multiplied

by , 10 or 15 depending on the sugar source. A sweet score of 15 or more indicates

that the individual is needed of the nutritional counseling to reduce the cariogenic

potential of his or her diet.

Weak long:

The same procedure is done for a week long to evaluate the caries potential

of the different eatables.

Decay promoting potential

Mean cariogenic potential indices in ascending order for 22 foods using the

rat model.

Dietary recommendations for the reduction of dental caries:

Limit the use of fermentable carbohydrates to mealtime foods other than

carbohydrates serve as buffers to help neutralize plaque acid.

Omit sweet foods even with meals if the client is susceptible to caries.

Between meal snacks should consist of protective, non-cariogenic food

such as raw vegetables. Raw, unrefined foods in the vegetable and first

group require chewing. The chewing action increases the salivary flow,

thus aiding in the removal and dilution of sugars and their harmful

byproducts.

Use of concentrated sweets in the preparation of foods as possible.

Do not eat sweets before bedtime unless the teeth are brushed, salivary flow

decreases at night and foods are not as readily cleared from the mouth as

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they are during waking hours. Acid left undisturbed remains in the mouth

for 1 ½ to 2 hours.

Avoid natural sugars, they are detrimental to the tooth surface as refined

sugars.

Avoid sticky foods because they are retained in the mouth longer than non-

sticky foods.

Nutritional needs of clients with dental caries risk:

Nutritional counseling for dental caries prevention must emphasize

decreasing the frequency with which the sugar is consumed and replacing

cariogenic food with nutritionally sound foods.

Acid producing microorganism (Lactobacillus, Streptococcus mutans)

A fermentable carbohydrate

A susceptible tooth surface

Nutritional counseling for dental caries prevention targets the elimination

or reduction of fermentable carbohydrates from the diet. Acid production

demineralization formation of dental caries.

Counseling points for caries prevention:

Dietary education and guidance is important for prevention and control of

dental caries. Patient should be carefully assessed to determine the level of

prevention and nutrition guidance needed.

1) Primary prevention

2) Secondary prevention

3) Tertiary prevention

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Primary prevention:- The patient does not appear to be risk for developing caries

at present education should be provided on diet caries relationship to prevent

fracture problem.

Secondary prevention:- The patient is risk for developing caries based upon

factors such as cariogenic diet pattern, xerostomia, family history, oral

bacteriologic test results.

Using current diet patterns as the basis for discussion, patient should be

taught the role of diet in caries, difference between cariogenic and non-cariogenic

eating pattern and how to adapt current diet to lower cariogenic risk.

Tertiary Prevention:-

- Patient presents with active caries and need the immediate targeted

intervention.

- Reduced cariogenicity of current diet.

- Factors influencing the current habits and working with the patient to develop

strategies for improvement which are appropriate and acceptable.

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