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Diet and dental caries
Contents
• Introduction
• Definitions
• Classifications of food
• Studies on relation to diet and caries
• Pathogenesis of caries
• Conclusion
• References
• Every part of the body is derived from nutrients
contained in the diet. The nutrients form an essential
and continuing component in the complex process of
maintaining optimal health throughout life.
• Diet plays a major in development of dental caries.
• A dynamic relation exists between sugars and oral
health.
• Diet affects the integrity of the teeth; quantity, pH, and
composition of the saliva; and plaque pH.
• Sugars and other fermentable carbohydrates, after
being hydrolyzed by salivary amylase, provide
substrate for the actions of oral bacteria, which in turn
lower plaque and salivary pH.
• The resultant action is the beginning of tooth
demineralization
Food- Any substance which when
taken into the body or an organ may
be used either to supply energy or
build a tissue.
• Diet refers to the local action of the foods in oral
tissues and encompasses the composition of the food,
its consistency pattern and frequency of eating. It
encompasses the food that is eaten regardless of its fate
and exerts local/direct effect upon the dentition.
Nizel (1989): Diet is the total oral intake of
a substance that provides nourishment.
DIET- Diet is defined as the types
and amounts of food eaten daily
by an individual. (FDI, 1994)
NUTRITION-It is
defined as the sum of
the processes by which
an individual takes and
utilizes food
(FDI,1994)
NUTRITION-It is
defined as the sum of
the processes by which
an individual takes and
utilizes food
(FDI,1994)
W.H.O: Nutrition is the
science of food and its
relationship to health. It is
concerned primarily with
the part played by the
nutrient in body growth,
development &
maintenance
• Nutrition differs from diet. In that it deals with
those elements of food that are absorbed
through the intestinal tract and enter into
metabolic processes in the body in the
formation and replacement of the tissue. It
exerts systemic effects upon the dentition via
the pulpal blood supply and the saliva.
• BALANCED DIET:
Def: A balanced diet is one in which each nutrient from each
food group in recommended servings is present for the
optimal functioning of the human.
• It contains variety of foods in such quantities and
proportions that the need for energy, amino acids,
vitamins, minerals, fats, carbohydrates, and other
nutrients is adequately met for maintaining health, vitality
and general well-being and also makes a small provision
for extra nutrients to withstand short duration of leanness.
DENTAL CARIES
Def: Dental caries is an irreversible microbial
disease of the calcified tissues of the teeth,
characterized by demineralization of the inorganic
portion and destruction of the organic portion
substance of the tooth, which often leads to
cavitations. (Shafer’s)
CLASSIFICATION OF FOODS
By origin:
• Foods of animal origin
• Foods of vegetable origin
By chemical origin:
• Proteins, fats, carbohydrates, vitamins, minerals
By predominant function:
• Body building foods – milk, meat, poultry
• Energy-giving foods – cereals, sugars, roots
• Protective foods – vegetables, fruits, milk
By nutritive value:
Cereals and millets, pulses, vegetables, nuts
and oilseeds, fruits, animal foods, fats and
oils, sugars and jiggery.
FOOD GUIDE PYRAMID
• The food guide pyramid can help to choose a variety of foods to
help achieve a balanced diet. Selecting foods from each group will
provide the many nutrients needed by the body.
• The dietary goals (prudent diet) recommended by the expert
committees of WHO are:
• Dietary fat should be limited to 15-20% of total daily diet.
• Saturated fats – not more than 10% of total energy intake
• Excessive consumption of refined carbohydrate to be avoided
• Salt intake reduced to not more than 5gm/day
• Protein – 10-15% of daily intake
• Reduced consumption of colas, ketchups and other foods that
supply empty calories
Studies providing evidence for the relationship
between diet and dental caries
CONCEPT OF NOBLE SAVAGE:
• Developed during later part of the 18th century.
• An understandable development from this ideal was the
belief that the apparent freedom from caries enjoyed by so
called primitive races should be attributed to the natural
diet on which they existed.
• Eating hard, fibrous, unprocessed food to better
development of the jaws and teeth helped to clear the food
debris from the teeth.
• Humans started eating soft processed food, highly
fermentable carbohydrate which did not properly exercise
the masticatory apparatus and lead to dental decay.
• WALLACE-1902, was a firm proponent of cleansing
foods, stated that the accumulation of fermentable
carbohydrate were the cause of caries and that such
deposits could be removed by eating hard and fibrous
foods(cleansing/detersive foods)
• PICKERILL – 1923, stated that if a meal was finished
with a salivary stimulant like apple, the mouth would be
kept free of fermentation both by physical cleansing
effect of fibrous food and also because of induced
salivary flow.
OBSERVATIONAL STUDIES
1.) EPIDEMOLOGICAL OBSERVATION:
• Modern diet v/s primitive diet
• Caries prevalence of ancient Hawaiians was
extremely low in contrast to the present scenario
• Dental caries incidence in native population –
Australian Aborigines, Bantu tribes of South Africa,
the New Zealand Maoris, The Eskimos were low
before introduction of modern
2). WORLD WAR II STUDIES:
• Toverud 1957 Scandinavian countries:
• Decrease in dental caries among 7 and 8 years old
children about 1-3 years after reduction in sugar
intake.
• Caries rates increased 12 years after rise of
sucrose in postwar diets in children
HOPEWOOD HOUSE STUDY
SULLIVAN (1958)
• 80 children – entered soon after birth
• Duration – 12 years (1947-1962)
• Diet – lacto vegetarian
• Whole meat flour - brad, biscuits
• Strictly vegetarian, restriction of refined carbohydrate
• Vitamin supplements and fluoride concentration of water is very
less
• Oral hygiene was virtually absent
At the end of 12 years, 13 year children represented:
• Mean DMFT – 1.6, while of general population – 10.7
• 53% of hopewood house population is caries free while only 0.4%
of state school children were caries free
VIPEHOLM STUDY –
GUSTAFFSON (1954)
Vipeholm Hospital, Lund(Sweden) - an institution for
mentally defective individuals.
• Duration: 5 year study
• The 436 patients involved in this study were divided into 6
• control groups. They were as follows:
• Sucrose group (300gm)
• Bread group (345gm)
• Chocolate group (65gm)
• Caramel group (22 – 70gm)
• 8 toffee group (60gm)
• 24 toffee group (120gm)
CONCLUSION
Increase in carb – increase dc
RISK OF CARIES – GREATER – FOOD
RETAINED ON THE SURFACE
TURKU SUGAR STUDY –
SCHEININ, MAKINEN (1975)
• STUDY PERIOD = 2 years; n = 125
SUCROSE
N = 35
FRUCTOSE
N = 38
XYLITOL
N = 52
• Location – Turku, Finland
• Aim: to compare the cariogenicity of sucrose, fructose and
xylitol as xylitol is a sweet substance not metabolized by
plaque microorganisms.
• Mean age of subjects: 27.6 yrs
Findings:
• After one year: sucrose and fructose are equal cariogenic
whereas xylitol produced almost no caries
• After 2 years: caries had continued to increase in sucrose
group but remained unchanged in the fructose group
whereas xylitol produced almost no caries.
SEVENTH DAY ADVENTIST
CHILDREN STUDY
• Limitation of sugar sticky elements, highly refined
starches, between meal snacking.
Level of DC was much lower.
Plaque pH studies
• Measures acidogenic potential
• Four methods:
• Metal probes (which can be inserted in situ into plaque)
• Glass probes
• Miniature glass electrodes (built into partial dentures that
stays in the mouth for several days to enable plaque to
grow on surface)
• Harvesting method: most accepted (removing small
samples of plaque from selected tooth and measuring pH
outside the mouth)
• Stephen (1940, 1944) – demonstrated the relationship between
sugar exposure resulting in the acidification of dental plaque
and caries experience.
• These studies have been used to rank the acidogenecity of
snack foods
• Boiled sweets: lowest plaque pH
• Sweetened tea and coffee: low pH
• Foods sweetened with nonsugar sweeteners (e.g. sugar free
chewing gum {pH-6.8}, diabetic chocolate sweetened with
sorbitol) and salivary stimulants {peanuts}:high pH
Survey of dietary habits in children
AVAILABILITY OF SWEET AND CANDY:
• Fanning et al
• Examined 1226-found fewer DMFS where sweets are
not available
• Study on south Australian children
• Frequent users of canteen sweets had high caries
• Infrequent users had less
• Dentist children had better oral health than others
SPECIAL POPULATION GROUP:
• NURSING BOTTLE CARIES
• Jacobi found the relation between the practice of
feeding infants with sucrose containing beverages and
milk at bedtime
• Lactose is responsible
Added sugar or sugar dipped pacifier at bedtime –
• Breast feeding – primary dentition 8 in infants
• 7.2% lactose by wt in human milk: 4.5% in bovine
• CEREAL STUDIES
Sugar coated cereal – highly cariogenic
• Eating sucrose during mealtime as a part of diet does not
increase dental caries – swallowed before the sweetness
is extracted – increased salivation during meal time
removes dissolved sugar.
• Buffering capacity of milk proteins or high phosphate
content
• Shaw suggested that amount of presweetened cereal is
less than total amount ingested daily
• Still controversy exists regarding cariogenicity of cereal
HEREDITARY FRUCTOSE INTOLERANCE
• Caused by reduced level of fructose
• Person learns to avoid food containing fructose
or sucrose
• Dental caries in theses is extremely low
• Siblings of theses showed similar incidence of
caries
INDIVIDUAL RISK
• Persons in bakery and candy factories showed
higher incidence of caries than the workers in
textile industries.
• Employees in chocolate factory showed more
caries than person in shipyard.
• Sugarcane workers had more caries incidence
than workers in textile industry.
Major Factors in the Dental Caries
Process
• Dietary factors must be modified to reduce the risk of
caries. Dietary recommendations need to address the
following dietary factors:
– Frequency of eating meals and snacks
– Oral retentiveness of foods (sticky, chewy, starchy)
– Sequence of food consumption
– Amount of fermentable carbohydrate consumed
– Sugar or acid concentration of the food or drink item
– Physical form of the carbohydrate
– Proximity of eating to bedtime
Important factors in caries determination
Physical properties of food
– Liquids include fruit juice, soda, sports
drinks, energy drinks, liquid medications
• An acidic medium that further demineralizes
the tooth
• Diet soft drinks contain added citric and phosphoric
acids
– Retentive CHOs include bakery items, crackers, potato
chips, pretzels
– Slowly dissolving CHOs include antacids, cough
drops, breath mints
Physical form
– Linear relationship between caries rate and number of
meals and/or snacks consumed
• Each time a food containing carbohydrates is eaten,
the salivary pH drops below the critical level for
approximately 40 minutes
• Enamel demineralization occurs
• Acid exposure is additive throughout the day
• Eventually demineralization progresses to the point at
which decay may be detected clinically
• The calcium and phosphorus in saliva need time to
remineralize the tooth between meals/snacks
Frequency of intake
– Amount of acid is reduced if a fermentable carbohydrate
food is eaten before or between other non cariogenic
foods
• Dairy products, such as cheese, reduce
demineralization of the tooth and help buffer acids
produced by the bacteria
• Sialagogues, like sugar-free chewing gum, stimulate
the saliva and promote buffering of acids produced
by bacteria and aid in oral clearance of the food
• Coffee with sugar after a meal decreases pH which
increases cariogenicity
Timing and sequence in a meal
Food constituents

The four carbohydrates starch, sucrose, fructose and glucose
comprise the greatest proportion of food consumed by man.

Starch is not cariogenic in humans.

Glucose & fructose are minor constituents of human foods
as they are present only in dried fruits, honey and milk
Natural versus processed food

Saliva incubated with refined food cause a
greater dissolution of enamel than when
incubated with unrefined foods.

Mixtures that included bran, wheat germ and
unrefined treacle contained protective factors
Acidity of foods

Natural foods such as lemons, apples, fruit juices
and carbonated beverages are sufficiently acidic
when in prolong contact with tooth.

Habitual use of these foods and beverages may
cause etching of enamel with cavitation
Cariogenic vs. Cariostatic
• Cariogenic: containing fermentable
carbohydrates that can cause a decrease in
salivary pH to <5.5 and demineralization when
in contact with microorganisms in the mouth;
promoting caries development
• Cariostatic: not metabolized by
microorganisms in plaque to cause a drop in
salivary pH to <5.5
Cariogenic Foods
• Promote formation of caries
• Fermentable carbohydrates, those that can
be broken down by salivary amylase
• Result in lower mouth pH
• Include crackers, chips, pretzels, cereals,
breads, fruits, sugars, sweets, desserts
Cariostatic Foods
• Foods that do not contribute to decay
• Do not cause a drop in salivary pH
• Includes protein foods, eggs, fish, meat and
poultry; most vegetables, fats, sugarless gums
Anti cariogenic Foods
• Prevent plaque from recognizing an acidogenic food
when it is eaten first
• May increase salivation or have antimicrobial
activity
• Includes xylitol (sweetener in sugarless gum) and
cheeses
ETIOLOGY OF DENTAL CARIES
• Dental caries is a multifactorial disease.
According to the current concepts, mainly four
factors are responsible for the causation of the
dental caries. i.e.
Diet
Bacteria
Susceptible tooth surface
Time
EFFECTS OF NUTRTION ON DENTAL
CARIES
PRE-ERUPTIVE EFFECTS
• Mineral malnutrition may be due to inadequate
quantities of calcium, phosphorus and iron.
• In deciduous teeth the dental dysplasias caused are
Odontoclasia
Yellow teeth
Infantile melanodontia
Lesion cauque: it occurs due to deficiency of
vitamin A or neonatal infection
Pulpal stone formation: due to L- ascorbic acid
POST-ERUPTIVE EFFECT
Role of vitamin D in maintaining dental health
MULTI-FACTORIAL PROCESS
• Involves the interaction of host factors (tooth surface,
saliva, acquired pellicle), diet, and dental plaque
(biofilm).
• Caries does not occur in the absence of either plaque or
dietary fermentable carbohydrates.
• Therefore, caries must be considered a dietobacterial
disease.
• Dental caries can be conceptualized as an interaction
between genetic and environmental factors, in which the
biopsychosocial components are expressed in a highly
complex, interactive manner.
MULTI-FACTORIAL PROCESS
Diet and dental caries
1 2 3 4
Prediction
based on
socio-
economic
status,
oral hygiene
and dietary
factors
Prediction
based on
behavioral
factors
Prediction
based on
past caries
experience
Prediction
based on
salivary
factors and
microbial
colonization
Messer, 2000
Microbial
Colonization
Caries
Experience
Behavior
SES,
Oral Hygiene,
Diet
Saliva
• Low indices of socioeconomic status (SES) have been
associated with elevations in caries, although the extent
to which this indicator may simply reflect previous
correlates is unknown
• Low SES is also associated with reduced access to care,
reduced oral health aspirations, low self efficacy, and
health behaviors that may be enhance caries risk
NIH 2002
Multifactorial disease
External (environmental factors)
Internal (endogenous factors)
Four factors
HOST
MICROFLORA
SUBSTRATE OR DIET
TIME
Microorganisms
Substrate
Time
Host &
teeth
CURRENT CONCEPTS OF CARIES
ETIOLOGY
ENAMEL PELLICLE + BACTERIA
PLAQUE FORMATION
PLAQUE BACTERIA + FERMENTABLE CARBOHYDRATE
( FOOD)
ACID PRODUCTION
DEMINERALISATION AND DISSOLUTION OF INORGANIC
AND ORGANIC STRUCTURES OF TOOTH
DENTAL CARIES
PATHOGENESIS OF
CARIES
• Factors that proved in cross-sectional studies, to be significantly
associated with increased prevalence of specific disease – Risk
indicators (RIs)
• Factors that have proved, in well- controlled prospective studies, to
increase significantly the risk of onset or progression of a specific
disease- Risk factors (RFs) and Prognostic risk factors (PRFs)
Education
Social class
Incom
e
Knowledge
Attitude
Behaviour
Fluoride
Diet
composition
frequency
Microbial Species
Buffer
capacity
Sugar
Clearance
rate
Saliva
(flow rate)
Saliva
(composition)
Time
Tooth
Tooth
Among external modifying
RIs, RFs, and PRFs, for
dental caries are…
Fermentable
carbohydrates
Poor socioeconomic statue
Systemic disease
Medication that impairs
salivary function
Irregular dental care
habits
METHODS TO MEASURE THE CARIOGENIC POTENTIAL
– In vitro caries models
– In vivo/ In vitro caries models
– Adhesiveness of foods
– Plaque PH measurements
ASSESSMENT OF CARIOGENIC
POTENTIAL OF FOOD STUFFS
• Food consumption and dietary habits – favorable and unfavorable
• Influence the type and proportions of specific cariogenic
microorganisms found in the dental plaque
• Sequence of eating pattern
• Ideal test: should include host and micro flora as well as
substrate- combination of tests
Currently accepting methods: pH
measurements and animal
testing ( control –sucrose)
– No cariogenic potential: do not lower plaque pH
significantly
– Low cariogenic potential: causes less than 40% of the caries
– High cariogenic potential: similar to positive control group
Large group fall into an intermediate category between low
and high – becos of overlap of standard deviation
• Food is mixed with an inoculum of salivary flora- amount of
acid formed
• Adhesiveness of food
• Enamel demineralization
• Production of titratable acid an artificial mouth
Limitation –
– Remote from the real life.
– Salivary flow
– Salivary flora is not representative of the plaque microbes
• Two tests ICT and IPT
• Intraoral Caries Test – Enamel hardness.
• Iodine Permeability Test – Permeability.
• Bovine enamel block mounted on the prosthesis – worn
intraorally
• Limitation – Food only in solution and Patient compliance.
• Cohesion: tendency of food to stick itself
• Adhesion: pressure applied to food – inter proximal and occlusal
sites : masticatory stress
• Adhesiveness: firm attachment between the food and the tooth
surface
• Tackiness : ability of food to stick to the tooth when minimal force
is involved
• Adhesion test : tensile force required to break a bound between
mixtures of food and saliva and the enamel surface of the teeth
• High adhesiveness : corn flakes and milk, sugar coated flakes,
toffee, chocolate, plain cake, tomato, apple etc
Methods –
– Sampling
– Touch electrode
– Built-in electrodes
• Sampling : plaque is removed from the teeth at intervals
after ingestion of the test food
limitations: plaque is disturbed
pooling of different sites
measurements is intermittent
• Microelectrodes placed with in plaque on the tooth surface
at intervals after food ingestion
• Direct reading of pH
• Antimony and glass electrode-
Limitations:
– Disrupts the plaque structure
– Outer surface of plaque pH
• Miniature electrode built in to prosthesis
• pH
readings taken continuously by either wire or radio
telemetry
• Previously glass electrode- slow response(30 sec)
• Hydrogen ion sensitive field transistor
Extremely small : 1mm2
-si3N4
– Low electric resistance
– Rapid response time (10sec)
• Indwelling bimetallic ( palladium/ palladium oxide)- versatile
• Criticism:
– Pattern and sequence of food intake – influence
plaque pH
– used in small no. of persons
– Permutations of sequence and frequency intake
- impossible
Swiss Office of Health
– Plaque pH
below 5.7 during and up to 30 min
• “Safe for teeth” or Zahnschonend
• Labeling the product: non cariogenic (nicht
kariogen)
STEPHEN CURVESTEPHEN CURVE
• First described by Robert Stephen in 1943
• Stephen curve is a graph plotted on pH level
against time
• This graph will show the food intake will
reduce pH level in the mouth to a level bad
for teeth and then rises again with time
• Stephen curve shows how the pH level at
neutral in the mouth is 7 and every time it drops
below 5.5 and is seemed to be critical and acid
attack happens
• First described by Robert Stephen in 1943
• Stephen curve is a graph plotted on pH level
against time
• This graph will show the food intake will
reduce pH level in the mouth to a level bad
for teeth and then rises again with time
• Stephen curve shows how the pH level at
neutral in the mouth is 7 and every time it drops
below 5.5 and is seemed to be critical and acid
attack happens
PRINCIPLE OF STEPHEN
CURVE
PRINCIPLE OF STEPHEN
CURVE
• To assess the cariogenecity of different
foods
• Represents the change of plaque pH over a
period of time
SIGNIFICANCE OF RESEARCH:
• Frequency of food intake is important which
determines cariogenecity
• Total amount of food intake is not important
• To assess the cariogenecity of different
foods
• Represents the change of plaque pH over a
period of time
SIGNIFICANCE OF RESEARCH:
• Frequency of food intake is important which
determines cariogenecity
• Total amount of food intake is not important
PRINCIPLE OF STEPHEN CURVEPRINCIPLE OF STEPHEN CURVE
• Relationship of food intake with PH level with respect to time
GRAPH DESCRIPTIONGRAPH DESCRIPTION
• The graph shows a pH below the critical level of
5.5 at which demineralization of enamel occurs
following the intake of fermentable carbohydrates,
acids and liquids
• After consumption, there is an elimination of acid,
and return to normal saliva or plaque PH, at which
repair of any destruction of enamel structure takes
place (remineralization)
• The graph shows a pH below the critical level of
5.5 at which demineralization of enamel occurs
following the intake of fermentable carbohydrates,
acids and liquids
• After consumption, there is an elimination of acid,
and return to normal saliva or plaque PH, at which
repair of any destruction of enamel structure takes
place (remineralization)
CRITICAL pHCRITICAL pH
Critical pH:
• The critical pH is the pH below which enamel
will begin to dissolve
• For enamel, critical pH is between 4.5-5.5
moles/L
Critical pH:
• The critical pH is the pH below which enamel
will begin to dissolve
• For enamel, critical pH is between 4.5-5.5
moles/L
STEPHEN CURVESTEPHEN CURVE
•Gradually over the following 30 minutes, the PH of the mouth begins
to return neutrality and dissolving of enamel stops and products of
saliva can begin to remineralize any dissolved enamel
•Gradually over the following 30 minutes, the PH of the mouth begins
to return neutrality and dissolving of enamel stops and products of
saliva can begin to remineralize any dissolved enamel
Behavior
SES,
Oral Hygiene,
Diet Saliva
Microbial
Colonization
Caries
Experience
Mutan streptococci
Ecological Plaque
Lactobacilli
Association of
Lactobacilli and
dental caries.
Association of
Lactobacilli and
fermentable
carbohydrates.
Innoculation of
S.mutans shows
higher caries
activity.
High acid
production activity
of S.mutans
Other oral bacteria
are sufficiently
acidogenic.
Adherence of
plaque without
mutan
streptococci.
Xerostomia
subjective
report of oral
dryness related
to gender
Salivary Flow Rate
Hyposalivation
Objective salivary flow rate
that is under 0.1 or 0.16
ml/min (or 0.1 ml/min;
relate to medication and
systemic disease
Tanathipanont & Korwanich, 2008
Lenander-Lumikari & Loimaranta, 2000
Buffer Capacity
• Effects of Carbohydrates.
• Effects of Proteins.
• Effects of fats.
• Effects of Vitamins.
• Effects of Calcium and
Phosphorus.
• Effects of Trace elements
• Types of sugars and uses
• Classification of sugars
• Sucrose a unique substrate for cariogenic flora
• Factors affecting cariogenecity of Sucrose in
diet
• Starches and dental caries
Types of sugar
• Raw sugar , Turbinado sugar ,White granulated refined
sugar, Corn syrup , Honey
Sugar manufacture’s :
– Blended sugar.
– Pure invert sugar.
– Common invert sugar
Uses of sugars :
– Sweetening agent
– Flavor blender and modifier
– Texture and bodying agent
– Dispersing/ lubricating agent.
Total Sugars
Intrinsic Sugars Extrinsic Sugars
Milk Sugars Non Milk Extrinsic Sugars
( NMES)
Classifications of Sugars –
saliva Plaque micro organisms
starches
sucrose
sucrose
Energy +
Organic
acids
glycogen
Sucrose
phosphate
Glucose
fructose
Sucrose
phosphateSoluble
polysaccharides
Glucose/fructose
Insoluble
polysaccharides
extracellular intracellular
polysaccharides
Bacterial
capsuleMaltose
Glucose
Lactose
fructose
PTS
b) Newbrun 1982- S- shaped curve
c) Woodward and walker 1994-
linear
d) Zero 2004- individuals with
good oral hygiene and regular fl
exposure, higher level of sugar can
be tolerated
• Smooth surface caries- biochemical ground depends on
growth of dental plaque
St. Mutans - Synthesize dextrans /glucans and levans.
– Glucans: insoluble ,serve as structural Components of
the plaque matrix- gluing certain bacteria to the tooth
– Levans – soluble, serve as transient reserves of
fermentable carbohydrates- prolonging duration of
acid production
• Polysaccharide built: glucose units are transferred from
sucrose to the active sites of enzyme- to growing chain
• Enzymes : Sugar 1- phosphate, nucleosidediphosphate-
sugar: transfer glucose/ fructose units directly to growing
polymer.
• Enzymes conserves: high energy( dihemiacetals) btn two C1
of glucose and C2 of fructose ( 6600Cal/ Mol)
Streptococcus sanguis and S.mutans:
– Glucosyl 1- transferases- Plaque matrix material
– Fructosyl transferses- Organic acids.
Clinical relevance
– Highly specific for sucrose
– Broad pH
optimum 5.2 to 7 coinciding with pH
range of dental
plaque
– Sucrose is not required : formation of above enzymes
n C12H22O11 (C6H10O5)n + n C6H12O6
sucrose
glucan fructose
polysaccharide organic acid
Frequency of eating
Oral clearance
Effective concentration of Sucrose
Frequent eating - Acid
No acid formation
• Cannot directly serve as substrate .
• Two varieties of Starch – Cooked Starches and Uncooked Starches
• Cooked Starches Ex : Rice , Potatoes and Bread -cariogenic.
• Uncooked Starches – Virtually non cariogenic.
• Untreated Starchy foods – Lower caries promoting potential.
• Addition of sugars – Increases cariogenicity.
• Less refined Starchy foods – Protect teeth.
• Gross protein deficiencies are rare
• Adding of Casein to diet – Significantly less caries
susceptibility
• Amount and quality of protein – Important factors.
• Ayad et al 2000 – There is no direct evidence.
 Williams et al 1982 – Certain fatty acids , antimicrobial action.
 Deficiency of essential fatty acids in man – rare.
 Oleic and lenolic fatty acids – bactericidal activity.
 Oleic acid – protection against decalcification.
 Cheese – Remineralization and Neutralizes acids.
FAT AND DENTAL CARIES
The mechanisms whereby fats act to reduce dental caries.
 Coating of tooth surface with a oily substance.
 Prevent fermentable sugar from being reduced to acids.
 May interfere with the growth of cariogenic bacteria.
 Increased dietary fat – Decrease the amount of dietary
fermentable carbohydrate.
Vitamin D
 Enamel hypoplasia – Most common abnormality.
 Linear enamel hypoplasia –specific type of enamel hypoplasia.
 Nikiforuk et al 1979, Hypocalcaemia – Enamel Hypoplasia.
Enamel Hypoplasia and Caries.
 Mellanby 1936 – Enamel hypoplasia and caries susceptibility.
 Other Vitamins and Dental Caries.
 Gustafson et al 1963 – Level of calcium in the diet is a
determining factor.
 Phosphate – Locally Cariostatic.
 Local effect P+ is due to :
Reduce the rate of dissolution
Redeposit CaPo4
Buffer organic acids
Desorb proteins
Minerals that may inhibit or promote caries :
• Strongly cariostatic : Fl , P.
• Mildly cariostatic : Mb , Sr, Ca, B, Li , Au , Cu.
• Promoting elements : Se, Mg , Cd , Pl , Pb , Si.
• Caries inert : Ba, Al , Ni ,Fe ,Ti.
• Doubtful : Be, Co , Mn , Sn , Zn , Br, I.
TRACE ELEMENTS AND DENTAL CARIES
• DAIRY PRODUCTS.
• SUGAR SUBSTITUTES AND ALTERNATIVE
SWEETNERS.
• PLANT FOODS.
• OTHER FOODS.
Milk and dental caries
• Substantial source of sugars in the diet of young
children.
• Lactose – Less acidogenic.
• Phosphorus, Calcium and Casein – demineralization .
• Animal studies – Anti cariogenic.
• Human breast milk – Higher lactose but Lower P and Ca
Polyphenols
• Polyphenols such as tannins in cocoa, coffee, tea, and
many fruit juices may reduce the cariogenic potential of
foods.
• In vitro experiments have shown that these polyphenolic
compounds may interfere with glucosyltransferase activity
of mutans streptococci, which may reduce plaque
formation
Caries Prevention
1
Reduce the
pathogenic
potential of
dental plaque
2
Increase the
resistance of
tooth
structure to
caries attack
3
Augment
salivary
factors
Walsh, 2004
Reduce the pathogenic potential of dental plaque
Mechanical plaque control1
Chemotherapeutic method2
Food intake restriction3
Replacement sweetener4
Sugar frequency reduction5
Augment salivary factors
Sugar free chewing gum1
Supportive life style2
Elevate salivary quality3
Increase saliva mineralization4
Enhance F in saliva5
Increase tooth structure resistance to caries attack
Community fluoride program1
Professional fluoride2
Self application fluoride3
Sealant4
Enamel treatment5
Mode of
Action
Bactericide
Crystallize
Remineralize
Conclusion
References
16 diet and dental caries

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16 diet and dental caries

  • 3. Contents • Introduction • Definitions • Classifications of food • Studies on relation to diet and caries • Pathogenesis of caries • Conclusion • References
  • 4. • Every part of the body is derived from nutrients contained in the diet. The nutrients form an essential and continuing component in the complex process of maintaining optimal health throughout life. • Diet plays a major in development of dental caries.
  • 5. • A dynamic relation exists between sugars and oral health. • Diet affects the integrity of the teeth; quantity, pH, and composition of the saliva; and plaque pH. • Sugars and other fermentable carbohydrates, after being hydrolyzed by salivary amylase, provide substrate for the actions of oral bacteria, which in turn lower plaque and salivary pH. • The resultant action is the beginning of tooth demineralization
  • 6. Food- Any substance which when taken into the body or an organ may be used either to supply energy or build a tissue.
  • 7. • Diet refers to the local action of the foods in oral tissues and encompasses the composition of the food, its consistency pattern and frequency of eating. It encompasses the food that is eaten regardless of its fate and exerts local/direct effect upon the dentition. Nizel (1989): Diet is the total oral intake of a substance that provides nourishment. DIET- Diet is defined as the types and amounts of food eaten daily by an individual. (FDI, 1994)
  • 8. NUTRITION-It is defined as the sum of the processes by which an individual takes and utilizes food (FDI,1994) NUTRITION-It is defined as the sum of the processes by which an individual takes and utilizes food (FDI,1994) W.H.O: Nutrition is the science of food and its relationship to health. It is concerned primarily with the part played by the nutrient in body growth, development & maintenance
  • 9. • Nutrition differs from diet. In that it deals with those elements of food that are absorbed through the intestinal tract and enter into metabolic processes in the body in the formation and replacement of the tissue. It exerts systemic effects upon the dentition via the pulpal blood supply and the saliva.
  • 10. • BALANCED DIET: Def: A balanced diet is one in which each nutrient from each food group in recommended servings is present for the optimal functioning of the human. • It contains variety of foods in such quantities and proportions that the need for energy, amino acids, vitamins, minerals, fats, carbohydrates, and other nutrients is adequately met for maintaining health, vitality and general well-being and also makes a small provision for extra nutrients to withstand short duration of leanness.
  • 11. DENTAL CARIES Def: Dental caries is an irreversible microbial disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic portion and destruction of the organic portion substance of the tooth, which often leads to cavitations. (Shafer’s)
  • 12. CLASSIFICATION OF FOODS By origin: • Foods of animal origin • Foods of vegetable origin By chemical origin: • Proteins, fats, carbohydrates, vitamins, minerals By predominant function: • Body building foods – milk, meat, poultry • Energy-giving foods – cereals, sugars, roots • Protective foods – vegetables, fruits, milk
  • 13. By nutritive value: Cereals and millets, pulses, vegetables, nuts and oilseeds, fruits, animal foods, fats and oils, sugars and jiggery.
  • 14.
  • 15. FOOD GUIDE PYRAMID • The food guide pyramid can help to choose a variety of foods to help achieve a balanced diet. Selecting foods from each group will provide the many nutrients needed by the body. • The dietary goals (prudent diet) recommended by the expert committees of WHO are: • Dietary fat should be limited to 15-20% of total daily diet. • Saturated fats – not more than 10% of total energy intake • Excessive consumption of refined carbohydrate to be avoided • Salt intake reduced to not more than 5gm/day • Protein – 10-15% of daily intake • Reduced consumption of colas, ketchups and other foods that supply empty calories
  • 16.
  • 17. Studies providing evidence for the relationship between diet and dental caries CONCEPT OF NOBLE SAVAGE: • Developed during later part of the 18th century. • An understandable development from this ideal was the belief that the apparent freedom from caries enjoyed by so called primitive races should be attributed to the natural diet on which they existed. • Eating hard, fibrous, unprocessed food to better development of the jaws and teeth helped to clear the food debris from the teeth. • Humans started eating soft processed food, highly fermentable carbohydrate which did not properly exercise the masticatory apparatus and lead to dental decay.
  • 18. • WALLACE-1902, was a firm proponent of cleansing foods, stated that the accumulation of fermentable carbohydrate were the cause of caries and that such deposits could be removed by eating hard and fibrous foods(cleansing/detersive foods) • PICKERILL – 1923, stated that if a meal was finished with a salivary stimulant like apple, the mouth would be kept free of fermentation both by physical cleansing effect of fibrous food and also because of induced salivary flow.
  • 19. OBSERVATIONAL STUDIES 1.) EPIDEMOLOGICAL OBSERVATION: • Modern diet v/s primitive diet • Caries prevalence of ancient Hawaiians was extremely low in contrast to the present scenario • Dental caries incidence in native population – Australian Aborigines, Bantu tribes of South Africa, the New Zealand Maoris, The Eskimos were low before introduction of modern
  • 20. 2). WORLD WAR II STUDIES: • Toverud 1957 Scandinavian countries: • Decrease in dental caries among 7 and 8 years old children about 1-3 years after reduction in sugar intake. • Caries rates increased 12 years after rise of sucrose in postwar diets in children
  • 22. • 80 children – entered soon after birth • Duration – 12 years (1947-1962) • Diet – lacto vegetarian • Whole meat flour - brad, biscuits • Strictly vegetarian, restriction of refined carbohydrate • Vitamin supplements and fluoride concentration of water is very less • Oral hygiene was virtually absent At the end of 12 years, 13 year children represented: • Mean DMFT – 1.6, while of general population – 10.7 • 53% of hopewood house population is caries free while only 0.4% of state school children were caries free
  • 23. VIPEHOLM STUDY – GUSTAFFSON (1954) Vipeholm Hospital, Lund(Sweden) - an institution for mentally defective individuals.
  • 24. • Duration: 5 year study • The 436 patients involved in this study were divided into 6 • control groups. They were as follows: • Sucrose group (300gm) • Bread group (345gm) • Chocolate group (65gm) • Caramel group (22 – 70gm) • 8 toffee group (60gm) • 24 toffee group (120gm)
  • 25. CONCLUSION Increase in carb – increase dc
  • 26. RISK OF CARIES – GREATER – FOOD RETAINED ON THE SURFACE
  • 27. TURKU SUGAR STUDY – SCHEININ, MAKINEN (1975) • STUDY PERIOD = 2 years; n = 125 SUCROSE N = 35 FRUCTOSE N = 38 XYLITOL N = 52
  • 28. • Location – Turku, Finland • Aim: to compare the cariogenicity of sucrose, fructose and xylitol as xylitol is a sweet substance not metabolized by plaque microorganisms. • Mean age of subjects: 27.6 yrs Findings: • After one year: sucrose and fructose are equal cariogenic whereas xylitol produced almost no caries • After 2 years: caries had continued to increase in sucrose group but remained unchanged in the fructose group whereas xylitol produced almost no caries.
  • 29. SEVENTH DAY ADVENTIST CHILDREN STUDY • Limitation of sugar sticky elements, highly refined starches, between meal snacking. Level of DC was much lower.
  • 30. Plaque pH studies • Measures acidogenic potential • Four methods: • Metal probes (which can be inserted in situ into plaque) • Glass probes • Miniature glass electrodes (built into partial dentures that stays in the mouth for several days to enable plaque to grow on surface) • Harvesting method: most accepted (removing small samples of plaque from selected tooth and measuring pH outside the mouth)
  • 31. • Stephen (1940, 1944) – demonstrated the relationship between sugar exposure resulting in the acidification of dental plaque and caries experience. • These studies have been used to rank the acidogenecity of snack foods • Boiled sweets: lowest plaque pH • Sweetened tea and coffee: low pH • Foods sweetened with nonsugar sweeteners (e.g. sugar free chewing gum {pH-6.8}, diabetic chocolate sweetened with sorbitol) and salivary stimulants {peanuts}:high pH
  • 32. Survey of dietary habits in children AVAILABILITY OF SWEET AND CANDY: • Fanning et al • Examined 1226-found fewer DMFS where sweets are not available • Study on south Australian children • Frequent users of canteen sweets had high caries • Infrequent users had less • Dentist children had better oral health than others
  • 33. SPECIAL POPULATION GROUP: • NURSING BOTTLE CARIES • Jacobi found the relation between the practice of feeding infants with sucrose containing beverages and milk at bedtime • Lactose is responsible Added sugar or sugar dipped pacifier at bedtime – • Breast feeding – primary dentition 8 in infants • 7.2% lactose by wt in human milk: 4.5% in bovine
  • 34. • CEREAL STUDIES Sugar coated cereal – highly cariogenic • Eating sucrose during mealtime as a part of diet does not increase dental caries – swallowed before the sweetness is extracted – increased salivation during meal time removes dissolved sugar. • Buffering capacity of milk proteins or high phosphate content • Shaw suggested that amount of presweetened cereal is less than total amount ingested daily • Still controversy exists regarding cariogenicity of cereal
  • 35. HEREDITARY FRUCTOSE INTOLERANCE • Caused by reduced level of fructose • Person learns to avoid food containing fructose or sucrose • Dental caries in theses is extremely low • Siblings of theses showed similar incidence of caries
  • 36. INDIVIDUAL RISK • Persons in bakery and candy factories showed higher incidence of caries than the workers in textile industries. • Employees in chocolate factory showed more caries than person in shipyard. • Sugarcane workers had more caries incidence than workers in textile industry.
  • 37.
  • 38. Major Factors in the Dental Caries Process • Dietary factors must be modified to reduce the risk of caries. Dietary recommendations need to address the following dietary factors: – Frequency of eating meals and snacks – Oral retentiveness of foods (sticky, chewy, starchy) – Sequence of food consumption – Amount of fermentable carbohydrate consumed – Sugar or acid concentration of the food or drink item – Physical form of the carbohydrate – Proximity of eating to bedtime
  • 39. Important factors in caries determination
  • 41. – Liquids include fruit juice, soda, sports drinks, energy drinks, liquid medications • An acidic medium that further demineralizes the tooth • Diet soft drinks contain added citric and phosphoric acids – Retentive CHOs include bakery items, crackers, potato chips, pretzels – Slowly dissolving CHOs include antacids, cough drops, breath mints Physical form
  • 42. – Linear relationship between caries rate and number of meals and/or snacks consumed • Each time a food containing carbohydrates is eaten, the salivary pH drops below the critical level for approximately 40 minutes • Enamel demineralization occurs • Acid exposure is additive throughout the day • Eventually demineralization progresses to the point at which decay may be detected clinically • The calcium and phosphorus in saliva need time to remineralize the tooth between meals/snacks Frequency of intake
  • 43. – Amount of acid is reduced if a fermentable carbohydrate food is eaten before or between other non cariogenic foods • Dairy products, such as cheese, reduce demineralization of the tooth and help buffer acids produced by the bacteria • Sialagogues, like sugar-free chewing gum, stimulate the saliva and promote buffering of acids produced by bacteria and aid in oral clearance of the food • Coffee with sugar after a meal decreases pH which increases cariogenicity Timing and sequence in a meal
  • 44. Food constituents  The four carbohydrates starch, sucrose, fructose and glucose comprise the greatest proportion of food consumed by man.  Starch is not cariogenic in humans.  Glucose & fructose are minor constituents of human foods as they are present only in dried fruits, honey and milk
  • 45. Natural versus processed food  Saliva incubated with refined food cause a greater dissolution of enamel than when incubated with unrefined foods.  Mixtures that included bran, wheat germ and unrefined treacle contained protective factors
  • 46. Acidity of foods  Natural foods such as lemons, apples, fruit juices and carbonated beverages are sufficiently acidic when in prolong contact with tooth.  Habitual use of these foods and beverages may cause etching of enamel with cavitation
  • 47. Cariogenic vs. Cariostatic • Cariogenic: containing fermentable carbohydrates that can cause a decrease in salivary pH to <5.5 and demineralization when in contact with microorganisms in the mouth; promoting caries development • Cariostatic: not metabolized by microorganisms in plaque to cause a drop in salivary pH to <5.5
  • 48. Cariogenic Foods • Promote formation of caries • Fermentable carbohydrates, those that can be broken down by salivary amylase • Result in lower mouth pH • Include crackers, chips, pretzels, cereals, breads, fruits, sugars, sweets, desserts
  • 49. Cariostatic Foods • Foods that do not contribute to decay • Do not cause a drop in salivary pH • Includes protein foods, eggs, fish, meat and poultry; most vegetables, fats, sugarless gums
  • 50. Anti cariogenic Foods • Prevent plaque from recognizing an acidogenic food when it is eaten first • May increase salivation or have antimicrobial activity • Includes xylitol (sweetener in sugarless gum) and cheeses
  • 51. ETIOLOGY OF DENTAL CARIES • Dental caries is a multifactorial disease. According to the current concepts, mainly four factors are responsible for the causation of the dental caries. i.e. Diet Bacteria Susceptible tooth surface Time
  • 52. EFFECTS OF NUTRTION ON DENTAL CARIES
  • 53. PRE-ERUPTIVE EFFECTS • Mineral malnutrition may be due to inadequate quantities of calcium, phosphorus and iron. • In deciduous teeth the dental dysplasias caused are Odontoclasia Yellow teeth Infantile melanodontia Lesion cauque: it occurs due to deficiency of vitamin A or neonatal infection Pulpal stone formation: due to L- ascorbic acid
  • 55.
  • 56. Role of vitamin D in maintaining dental health
  • 57. MULTI-FACTORIAL PROCESS • Involves the interaction of host factors (tooth surface, saliva, acquired pellicle), diet, and dental plaque (biofilm). • Caries does not occur in the absence of either plaque or dietary fermentable carbohydrates. • Therefore, caries must be considered a dietobacterial disease. • Dental caries can be conceptualized as an interaction between genetic and environmental factors, in which the biopsychosocial components are expressed in a highly complex, interactive manner.
  • 59. Diet and dental caries
  • 60.
  • 61. 1 2 3 4 Prediction based on socio- economic status, oral hygiene and dietary factors Prediction based on behavioral factors Prediction based on past caries experience Prediction based on salivary factors and microbial colonization Messer, 2000
  • 63. • Low indices of socioeconomic status (SES) have been associated with elevations in caries, although the extent to which this indicator may simply reflect previous correlates is unknown • Low SES is also associated with reduced access to care, reduced oral health aspirations, low self efficacy, and health behaviors that may be enhance caries risk NIH 2002
  • 64. Multifactorial disease External (environmental factors) Internal (endogenous factors) Four factors HOST MICROFLORA SUBSTRATE OR DIET TIME Microorganisms Substrate Time Host & teeth CURRENT CONCEPTS OF CARIES ETIOLOGY
  • 65. ENAMEL PELLICLE + BACTERIA PLAQUE FORMATION PLAQUE BACTERIA + FERMENTABLE CARBOHYDRATE ( FOOD) ACID PRODUCTION DEMINERALISATION AND DISSOLUTION OF INORGANIC AND ORGANIC STRUCTURES OF TOOTH DENTAL CARIES PATHOGENESIS OF CARIES
  • 66. • Factors that proved in cross-sectional studies, to be significantly associated with increased prevalence of specific disease – Risk indicators (RIs) • Factors that have proved, in well- controlled prospective studies, to increase significantly the risk of onset or progression of a specific disease- Risk factors (RFs) and Prognostic risk factors (PRFs)
  • 67. Education Social class Incom e Knowledge Attitude Behaviour Fluoride Diet composition frequency Microbial Species Buffer capacity Sugar Clearance rate Saliva (flow rate) Saliva (composition) Time Tooth Tooth Among external modifying RIs, RFs, and PRFs, for dental caries are… Fermentable carbohydrates Poor socioeconomic statue Systemic disease Medication that impairs salivary function Irregular dental care habits
  • 68. METHODS TO MEASURE THE CARIOGENIC POTENTIAL – In vitro caries models – In vivo/ In vitro caries models – Adhesiveness of foods – Plaque PH measurements ASSESSMENT OF CARIOGENIC POTENTIAL OF FOOD STUFFS
  • 69. • Food consumption and dietary habits – favorable and unfavorable • Influence the type and proportions of specific cariogenic microorganisms found in the dental plaque • Sequence of eating pattern • Ideal test: should include host and micro flora as well as substrate- combination of tests
  • 70. Currently accepting methods: pH measurements and animal testing ( control –sucrose) – No cariogenic potential: do not lower plaque pH significantly – Low cariogenic potential: causes less than 40% of the caries – High cariogenic potential: similar to positive control group Large group fall into an intermediate category between low and high – becos of overlap of standard deviation
  • 71. • Food is mixed with an inoculum of salivary flora- amount of acid formed • Adhesiveness of food • Enamel demineralization • Production of titratable acid an artificial mouth Limitation – – Remote from the real life. – Salivary flow – Salivary flora is not representative of the plaque microbes
  • 72. • Two tests ICT and IPT • Intraoral Caries Test – Enamel hardness. • Iodine Permeability Test – Permeability. • Bovine enamel block mounted on the prosthesis – worn intraorally • Limitation – Food only in solution and Patient compliance.
  • 73. • Cohesion: tendency of food to stick itself • Adhesion: pressure applied to food – inter proximal and occlusal sites : masticatory stress • Adhesiveness: firm attachment between the food and the tooth surface • Tackiness : ability of food to stick to the tooth when minimal force is involved
  • 74. • Adhesion test : tensile force required to break a bound between mixtures of food and saliva and the enamel surface of the teeth • High adhesiveness : corn flakes and milk, sugar coated flakes, toffee, chocolate, plain cake, tomato, apple etc
  • 75. Methods – – Sampling – Touch electrode – Built-in electrodes • Sampling : plaque is removed from the teeth at intervals after ingestion of the test food limitations: plaque is disturbed pooling of different sites measurements is intermittent
  • 76. • Microelectrodes placed with in plaque on the tooth surface at intervals after food ingestion • Direct reading of pH • Antimony and glass electrode- Limitations: – Disrupts the plaque structure – Outer surface of plaque pH
  • 77. • Miniature electrode built in to prosthesis • pH readings taken continuously by either wire or radio telemetry • Previously glass electrode- slow response(30 sec) • Hydrogen ion sensitive field transistor Extremely small : 1mm2 -si3N4 – Low electric resistance – Rapid response time (10sec) • Indwelling bimetallic ( palladium/ palladium oxide)- versatile
  • 78. • Criticism: – Pattern and sequence of food intake – influence plaque pH – used in small no. of persons – Permutations of sequence and frequency intake - impossible
  • 79. Swiss Office of Health – Plaque pH below 5.7 during and up to 30 min • “Safe for teeth” or Zahnschonend • Labeling the product: non cariogenic (nicht kariogen)
  • 80. STEPHEN CURVESTEPHEN CURVE • First described by Robert Stephen in 1943 • Stephen curve is a graph plotted on pH level against time • This graph will show the food intake will reduce pH level in the mouth to a level bad for teeth and then rises again with time • Stephen curve shows how the pH level at neutral in the mouth is 7 and every time it drops below 5.5 and is seemed to be critical and acid attack happens • First described by Robert Stephen in 1943 • Stephen curve is a graph plotted on pH level against time • This graph will show the food intake will reduce pH level in the mouth to a level bad for teeth and then rises again with time • Stephen curve shows how the pH level at neutral in the mouth is 7 and every time it drops below 5.5 and is seemed to be critical and acid attack happens
  • 81.
  • 82. PRINCIPLE OF STEPHEN CURVE PRINCIPLE OF STEPHEN CURVE • To assess the cariogenecity of different foods • Represents the change of plaque pH over a period of time SIGNIFICANCE OF RESEARCH: • Frequency of food intake is important which determines cariogenecity • Total amount of food intake is not important • To assess the cariogenecity of different foods • Represents the change of plaque pH over a period of time SIGNIFICANCE OF RESEARCH: • Frequency of food intake is important which determines cariogenecity • Total amount of food intake is not important
  • 83. PRINCIPLE OF STEPHEN CURVEPRINCIPLE OF STEPHEN CURVE • Relationship of food intake with PH level with respect to time
  • 84. GRAPH DESCRIPTIONGRAPH DESCRIPTION • The graph shows a pH below the critical level of 5.5 at which demineralization of enamel occurs following the intake of fermentable carbohydrates, acids and liquids • After consumption, there is an elimination of acid, and return to normal saliva or plaque PH, at which repair of any destruction of enamel structure takes place (remineralization) • The graph shows a pH below the critical level of 5.5 at which demineralization of enamel occurs following the intake of fermentable carbohydrates, acids and liquids • After consumption, there is an elimination of acid, and return to normal saliva or plaque PH, at which repair of any destruction of enamel structure takes place (remineralization)
  • 85. CRITICAL pHCRITICAL pH Critical pH: • The critical pH is the pH below which enamel will begin to dissolve • For enamel, critical pH is between 4.5-5.5 moles/L Critical pH: • The critical pH is the pH below which enamel will begin to dissolve • For enamel, critical pH is between 4.5-5.5 moles/L
  • 86. STEPHEN CURVESTEPHEN CURVE •Gradually over the following 30 minutes, the PH of the mouth begins to return neutrality and dissolving of enamel stops and products of saliva can begin to remineralize any dissolved enamel •Gradually over the following 30 minutes, the PH of the mouth begins to return neutrality and dissolving of enamel stops and products of saliva can begin to remineralize any dissolved enamel
  • 88. Mutan streptococci Ecological Plaque Lactobacilli Association of Lactobacilli and dental caries. Association of Lactobacilli and fermentable carbohydrates. Innoculation of S.mutans shows higher caries activity. High acid production activity of S.mutans Other oral bacteria are sufficiently acidogenic. Adherence of plaque without mutan streptococci.
  • 89. Xerostomia subjective report of oral dryness related to gender Salivary Flow Rate Hyposalivation Objective salivary flow rate that is under 0.1 or 0.16 ml/min (or 0.1 ml/min; relate to medication and systemic disease Tanathipanont & Korwanich, 2008
  • 90. Lenander-Lumikari & Loimaranta, 2000 Buffer Capacity
  • 91. • Effects of Carbohydrates. • Effects of Proteins. • Effects of fats. • Effects of Vitamins. • Effects of Calcium and Phosphorus. • Effects of Trace elements
  • 92. • Types of sugars and uses • Classification of sugars • Sucrose a unique substrate for cariogenic flora • Factors affecting cariogenecity of Sucrose in diet • Starches and dental caries
  • 93. Types of sugar • Raw sugar , Turbinado sugar ,White granulated refined sugar, Corn syrup , Honey Sugar manufacture’s : – Blended sugar. – Pure invert sugar. – Common invert sugar Uses of sugars : – Sweetening agent – Flavor blender and modifier – Texture and bodying agent – Dispersing/ lubricating agent.
  • 94. Total Sugars Intrinsic Sugars Extrinsic Sugars Milk Sugars Non Milk Extrinsic Sugars ( NMES) Classifications of Sugars –
  • 95.
  • 96. saliva Plaque micro organisms starches sucrose sucrose Energy + Organic acids glycogen Sucrose phosphate Glucose fructose Sucrose phosphateSoluble polysaccharides Glucose/fructose Insoluble polysaccharides extracellular intracellular polysaccharides Bacterial capsuleMaltose Glucose Lactose fructose PTS
  • 97. b) Newbrun 1982- S- shaped curve c) Woodward and walker 1994- linear d) Zero 2004- individuals with good oral hygiene and regular fl exposure, higher level of sugar can be tolerated
  • 98. • Smooth surface caries- biochemical ground depends on growth of dental plaque St. Mutans - Synthesize dextrans /glucans and levans. – Glucans: insoluble ,serve as structural Components of the plaque matrix- gluing certain bacteria to the tooth – Levans – soluble, serve as transient reserves of fermentable carbohydrates- prolonging duration of acid production
  • 99. • Polysaccharide built: glucose units are transferred from sucrose to the active sites of enzyme- to growing chain • Enzymes : Sugar 1- phosphate, nucleosidediphosphate- sugar: transfer glucose/ fructose units directly to growing polymer. • Enzymes conserves: high energy( dihemiacetals) btn two C1 of glucose and C2 of fructose ( 6600Cal/ Mol)
  • 100. Streptococcus sanguis and S.mutans: – Glucosyl 1- transferases- Plaque matrix material – Fructosyl transferses- Organic acids. Clinical relevance – Highly specific for sucrose – Broad pH optimum 5.2 to 7 coinciding with pH range of dental plaque – Sucrose is not required : formation of above enzymes
  • 101. n C12H22O11 (C6H10O5)n + n C6H12O6 sucrose glucan fructose polysaccharide organic acid
  • 102. Frequency of eating Oral clearance Effective concentration of Sucrose
  • 103. Frequent eating - Acid No acid formation
  • 104. • Cannot directly serve as substrate . • Two varieties of Starch – Cooked Starches and Uncooked Starches • Cooked Starches Ex : Rice , Potatoes and Bread -cariogenic. • Uncooked Starches – Virtually non cariogenic. • Untreated Starchy foods – Lower caries promoting potential. • Addition of sugars – Increases cariogenicity. • Less refined Starchy foods – Protect teeth.
  • 105. • Gross protein deficiencies are rare • Adding of Casein to diet – Significantly less caries susceptibility • Amount and quality of protein – Important factors. • Ayad et al 2000 – There is no direct evidence.
  • 106.  Williams et al 1982 – Certain fatty acids , antimicrobial action.  Deficiency of essential fatty acids in man – rare.  Oleic and lenolic fatty acids – bactericidal activity.  Oleic acid – protection against decalcification.  Cheese – Remineralization and Neutralizes acids. FAT AND DENTAL CARIES
  • 107. The mechanisms whereby fats act to reduce dental caries.  Coating of tooth surface with a oily substance.  Prevent fermentable sugar from being reduced to acids.  May interfere with the growth of cariogenic bacteria.  Increased dietary fat – Decrease the amount of dietary fermentable carbohydrate.
  • 108. Vitamin D  Enamel hypoplasia – Most common abnormality.  Linear enamel hypoplasia –specific type of enamel hypoplasia.  Nikiforuk et al 1979, Hypocalcaemia – Enamel Hypoplasia. Enamel Hypoplasia and Caries.  Mellanby 1936 – Enamel hypoplasia and caries susceptibility.  Other Vitamins and Dental Caries.
  • 109.  Gustafson et al 1963 – Level of calcium in the diet is a determining factor.  Phosphate – Locally Cariostatic.  Local effect P+ is due to : Reduce the rate of dissolution Redeposit CaPo4 Buffer organic acids Desorb proteins
  • 110. Minerals that may inhibit or promote caries : • Strongly cariostatic : Fl , P. • Mildly cariostatic : Mb , Sr, Ca, B, Li , Au , Cu. • Promoting elements : Se, Mg , Cd , Pl , Pb , Si. • Caries inert : Ba, Al , Ni ,Fe ,Ti. • Doubtful : Be, Co , Mn , Sn , Zn , Br, I. TRACE ELEMENTS AND DENTAL CARIES
  • 111. • DAIRY PRODUCTS. • SUGAR SUBSTITUTES AND ALTERNATIVE SWEETNERS. • PLANT FOODS. • OTHER FOODS.
  • 112. Milk and dental caries • Substantial source of sugars in the diet of young children. • Lactose – Less acidogenic. • Phosphorus, Calcium and Casein – demineralization . • Animal studies – Anti cariogenic. • Human breast milk – Higher lactose but Lower P and Ca
  • 113. Polyphenols • Polyphenols such as tannins in cocoa, coffee, tea, and many fruit juices may reduce the cariogenic potential of foods. • In vitro experiments have shown that these polyphenolic compounds may interfere with glucosyltransferase activity of mutans streptococci, which may reduce plaque formation
  • 114. Caries Prevention 1 Reduce the pathogenic potential of dental plaque 2 Increase the resistance of tooth structure to caries attack 3 Augment salivary factors Walsh, 2004
  • 115. Reduce the pathogenic potential of dental plaque Mechanical plaque control1 Chemotherapeutic method2 Food intake restriction3 Replacement sweetener4 Sugar frequency reduction5
  • 116. Augment salivary factors Sugar free chewing gum1 Supportive life style2 Elevate salivary quality3 Increase saliva mineralization4 Enhance F in saliva5
  • 117. Increase tooth structure resistance to caries attack Community fluoride program1 Professional fluoride2 Self application fluoride3 Sealant4 Enamel treatment5

Editor's Notes

  1. The relation between sugars and oral health is dynamic. Although sugars, both naturally occurring and added, and fermentable carbohydrates stimulate bacteria to produce acid and lower the pH, several dietary factors affect the caries risk associated with fermentable carbohydrates. Sugars and oral health are integrally related. Dietary guidelines for the prevention and management of dental caries provide a framework for consumers and health professionals to use in managing the intake of sugars.