Dental Caries

Dental Caries
• Caries is an infectious microbial disease that
results in irreversible localized dissolution and
destruction of calcified tissue of teeth.
• The bacteria in oral cavity produced enzymes to
act on fermentable carbohydrates to produce
acid. These acids react with enamel leading to
dental caries as a result of demineralization.
• This is a multifactorial disease requiring presence
of host, cariogenic micro flora and diet
conductive to enamel demineralization.
Bacteria Enzyme + Fermentable Carbohydrate= Acid
Acid + Enamel = Demineralization (Dental
Caries)

• There is an alarming rate of increase in prevalence of

dental caries in developing countries.
• It is considered as a disease of modern civilization
since pre historic man rarely suffered from this form
of tooth destruction.
• Mainly the introduction of sucrose into the modern
diet has resulted in this trend. The use of refined
carbohydrate foods has increased more rapidly in
these countries than the knowledge of oral hygiene
and increase in dental man power.
 ECONOMIC IMPLICATIONS OF DENTAL CARIES
There is a striking relationship b/w family
income, education and % of persons visiting
the dentist. Those with less income visited
the dentist less no. of times per year than
those of high income people . Same is true
with education, more educated people make
more visits to dentist than those with less
education.
ETIOLOGICAL FACTORS IN DENTAL CARIES

There is interplay of three principle factors:

1. Host (teeth, saliva etc)
2. Microflora
3. Substrate (Diet)
4. Time
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 RISK FACTORS

A. TOOTH
Composition
Morphologic characteristics,
Position
B. SALIVA
Composition,
pH,
Quantity,
Viscosity,
Anti bacterial factors.
C. MICROFLORA

D. DIET
DEMOGRAPHIC RISK FACTORS
AGE
SOCIOECONOMIC STATUS
RACE
ETHNICITY
GENDER
Also influence the caries development.
SALIVA:
The teeth are in constant contact and
bathed in saliva. One of the most important
functions of saliva with respect to caries is
its role in removal of bacteria and food
debris from mouth. It is reported that calcium
phosphorus content is low in caries active
persons. The enzyme ptyalin or amylase in
saliva is responsible for degradation of
Starches.
pH of SALIVA:
pH of saliva is determined mainly by the
bicarbonate concentration. The saliva Ph
increases with flow rate. Saliva may be
slightly acidic at unstimulated flow rate, but
may reach Ph 7.8 at high flow rate. As it is
exposed to atmosphere, CO2 will diffuses
out and pH will rise often to 9.
Quantity daily secreted : 700-800 ml/day
VISCOSITY OF SALIVA:
A high caries incidence is associated with a
thick mucinous saliva. Viscosity of saliva is
largely due to mucin content.
COMPOSITION
CALCIUM and PHOSPHORUS:
The quantity of calcium and phosphorus is inversely
related to the rate of flow. Its quantity is less in case
of caries active individuals.
AMMONIA:
The quantity of ammonia decreases, caries activity
increases, because ammonia retards plaque
formation and neutralizes acid.
 UREA
Urea gets hydrolyzed to ammonium carbonate by urease
which has neutralizing affect.
PTYALIN and AMYLASE
Help in degradation of starches.
ANTIBACTERIAL COMPONENT:
Lactoperoxidase:
Participate in killing of microorganism.
High affinity for enamel surface and limit early microbial
colonization of tooth surface.
Lysozyme:
Small highly positive enzyme that catalyze the degradation of
negatively charged peptidoglycan of microbial wall.
Low pH interfere with binding capacity of lysozyme.
• Lactoferrin:
• Iron binding basic protein found in saliva, bind and limit
the free iron.
• Iron is essential for microbial growth
• IgA:
• Predominant immunoglobulin present in saliva.
• It inhibits adherence and prevents colonization of
mucosal surface and teeth by organisms facilitating their
disposal by swallowing.
ROLE OF MICROFLORA:
A variety of microbial factors have been
associated with caries activity. Various
observations indicate a causal relationship
between streptococcus and the
development of the early carious lesion of
enamel.
Lactobacilli, however seem to be associated
with dentinal caries and Actinomyces strains
with root surface caries. ‘‘Micro organisms
are a pre requisite for caries initiations’’
DIET:
The role of diet and nutritional factors
deserves special consideration because of
difference in caries incidence of various
populations, Physical properties of food,
particularly those that improve the cleansing
action and reduce retention of food within
the oral cavity and increase saliva flow, are
to be encouraged in everyday diet.
The primitive man had strong jaws and teeth
less caries incidence as compared modern
man because the primitive man’s diet
consisted of great deal of roughage while
the modern man diet is of soft refined foods
which tends to cling tenaciously to the teeth
and are not removed because of the general
lack of roughage.
 Role of Acid
• The enzymatic break down of carbohydrates
results in formation of acid chiefly lactic acid.
• Localization of acid in dental plaque serves a
major role in dental caries.
• Carbohydrates + Enzymes = Lactic acid.
 Pathophysiology of Dental Caries
S. mutans and lactobacilli metabolize sucrose and
other substrates
Lactic acid production

Acid from plaque overcome buffering capacity of

salivary bicarbonates

Lowered pH 5.5 for 20-25 min

Tooth mineral act as buffer and lose calcium and

Phosphate ion into plaque
 Buffering capacity maintain pH at 5

At this pH surface remain intact and subsurface

mineral is lost and initial carious lesion occur
(Incipient caries)
Incipient lesion can be reversed by remineralization
 STUDIES
• Vipeholm Study:
• Conducted by Gustafsson et. al in 1954 in Sweden.
• Experimental study
• It was investigation of 436 adult inmates of mental institution
at Vipeholm Hospital near Lund, Sweden.
• Study Findings:
• Increase in carbohydrate increase the level of caries.
• Risk of caries is greater if food is retained on tooth.
• Risk of caries is greater if sugar consumed between the
meals.
• Increase caries activity rapidly disappears upon with drawl of
sugar rich foods.
• High concentration of sugar in solution and its prolonged
retention on tooth surface lead to increase caries activity.
• The clearance time of sugar correlates closely with caries
activity.
• This study shows that physical form of carbohydrates is much
more important in cariogenicity than total amount of sugar
ingested.

The experimental design divided the inmates into 7 groups.

• Control Group: Nutritious diet, but contained little sugar with no
provision for between meals snacks.
• A Sucrose Group: (300 mg of sucrose given in solution)
• A bread Group: ( 345 gms of sweet bread containing 50 gms sugar
daily )
• A Chocolate Group: ( 65 gms of milk chocolate daily b/w meals)
• A Caramel Group: ( 22 caramels = 70 gms of sugar b/w meals )
• An 8 toffee Froup: (8 sticky toffees = 60 gms of sugar daily )
• A 24 toffee Group: ( 24 sticky toffees = 120 gms of sugar daily )
• Hopewood House Study:
• Conducted by Sullivan in 1958.
• Longitudinal study
• Study findings:
• The children oral hygiene was poor and gingivitis was
prevalent in 75% of them.
• In institutionalized children, at least dental caries can be
reduced by diet, without beneficial effects of fluoride
and in the presence of unfavorable oral hygiene.
• Turku Sugar Study:
• Conducted by Scheinin Makinen et al in 1975.
• Study findings:
• Dramatic reduction in the incidence of dental caries was
found after 2 years of xylitol consumption.
• Fructose was as cariogenic as sucrose for the first 12
months but become less at the end of 24 months.
• It was found out that chewing of xylitol gum between
meals produced anticariogenic effect.
• Seventh Day Adventist Children Study:
• The seven day Adventist had certain restrictions in their
diet which include the limitations of
• Sugar sticky elements
• Highly refined starches
• Between meal snacking

• All the studies showed that the level of dental caries

was much lower in seven day Adventist group compared
to the other children.
 Early Child Hood Caries
• Also known as nursing caries and as baby bottle tooth
decay.
• ECC is a distressing syndrome.
• Most common in primary maxillary incisors of infants,
typically 1-3 years old.
• Rapidly spreading, difficult and expensive to treat.
• ECC is caused by prolonged infant feeding by bottle,
holding of sweetened liquids in contact with child teeth
for hours is a prime causative factor.
• Prevention is based largely on education.
Early Childhood Caries
 ROOT CARIES
• Caries that begins on cemental root surface
below the cementoenamel margin.
• It is found only where loss of periodontal
attachment has led to exposure of roots to
oral environment.
• Other actors which can contribute towards
root caries are socioeconomic status, years of
education, number of teeth remaining, use of
dental services, oral hygiene levels, and
preventive behavior.
Root Caries
• Use of medication is important risk factor
among elderly.
• Medication can cause xerostomia which is
known as major risk factor for caries.
• Smokers exhibit more root caries as compared
to non smokers.
• Root caries is more common in low
fluoridated areas.
 METHODS OF CARIES CONTROL

Can be classified into 3 general types;

1. Chemical Measures
2. Mechanical Measures
3. Nutritional Measures
 Chemical Measures
• Substances which alter the tooth surface or
tooth structure.
• Fluorides, iodides, bis-biguanides, silver nitrate,
zinc chloride and potassium ferrocyanide.
• Substances interfere with carbohydrates
degradation through enzymatic alterations.
• Vitamin K , sarcoside
• Substances interfere with bacterial growth and
metabolism.
• Urea and ammonia compounds, chlorophyll,
nitrofurans, antibiotics, caries vaccine.
 Mechanical Measures for Dental Caries Control
• Mechanical measures refers to procedures specifically
designed for and aimed at removal of dental plaque
from tooth surface.
• Method:
• Prophylaxis
• Tooth bushing
• Mouth rinse
• Use of dental floss and tooth picks
• Incorporation of detergent food in diet
• Pits and fissure sealants
 Nutritional Measure
• The chief nutritional measures for controlling dental
caries is the restriction of refined carbohydrates intake.
• Reduce the consumption of sugar containing food and
drinks and limit their consumption to meal time.
• Avoid sugar containing food and drinks close to bed
time.
• Encourage the use of food such as cheese and sugar free
gums after meals to neutralize the acidogenic effect of
dietary sugars.
• Encourage mothers not to add any drink or food to a
baby’s bottle, except formula milk, expressed breast,
milk, cow’s milk or water.
• When a structured meal plan is not followed, limit the
consumption of sugary foods to 3–4 times a day.
 Caries Susceptibility of Individual
Teeth
• Upper and lower fist molar 95%
• Upper and lower second molar 75%
• Upper second bicuspid 45%
• Upper first bicuspid 35%
• Lower second bicuspid 35%
• Upper central and lateral incisor 30%
• Upper cuspids and lower 1st bicuspids 10%
• Lower central and lateral incisors 3%
• Lower cuspids 3%
• Patients vary in their susceptibility to caries
process and in managing dental caries. There is
either a mild or a moderate challenge to caries
attack, usually affecting deep pits and fissures
and proximal surfaces.
• Rampant caries
• Sudden rapid destruction of many teeth,
affecting surfaces that considered relatively
immune to caries attack.
• Nursing caries
• Caused by prolonged Brest or bottle feeding,
especially during night.
• Recurrent or Secondary Caries
Seen in the margins of an old restored area.
• Arrested Caries
Re mineralized carious lesion.
 Theories of Caries
• Endogenous Theories:
• Humoral Theory
• The four elemental humors of the body were
blood, phlegm, black bile, and yellow bile.
• According to Galen, the ancient Greek
physician and philosopher “ dental caries is
produced by internal action of acid and
corroding humors”.
• Vital Theory
• The vital theory of tooth decay was advanced
towards the end of the 18th centaury which
postulated that tooth decay originated like
bone gangrene from with in the tooth itself.
 Exogenous Theories
• 1) Chemical acid Theory
• Appeared in 17-18th centaury.
• Proposed that teeth were destroyed by the acids
formed in oral cavity.
• Robertson (1835) proposed that dental decay
was caused by acid formed by fermentation of
food particles around the teeth.
• 2) Parasitic Theory:
• Dubos (1954) postulated that microorganisms can
have toxic effect on tissues.
• ANTON VAN LEEUWENHOCK (1632-1723)
indicated that microorganisms were associated
with the carious process.
• In 1843, ERDL described filamentous parasites in
membrane removed from the teeth.
• FICINUS in 1847, a physician also observed
filamentous organisms in the enamel cuticle.
• 3) Millers Chemoparasytic Theory
• Proposed by W.D. MILLER in 1890.
• Made significant observation that many organisms
can produce acid from fermentation of sugar and
showed that several oral microorganisms have this
property and lactic acid is one of the major acid
formed.
• Also showed that extracted teeth can be
demineralized by incubation in mixture of bread and
sugar with human saliva.
• William (1897) recognize the fact that bacteria
adhere film to tooth surfaces, producing gelatinous
film that might localize the acid to the surface of the
tooth.
• STEPHAN showed that within 2-4 min of
rinsing with a solution of glucose or sucrose
plaque PH is reduced from about 6.5-5 and
gradually returns to original value with in 40
min. Graphically plotted as Stephens curve.
• 4) Proteolysis Theory:
• Gottileb (1944) suggested that the initial attack on
enamel might be the destruction of organic material
rather than demineralization by acid.
• According to this theory the organic matrix would be
attacked before the mineral phase of the enamel.
• The proteolytic enzymes liberated by oral bacteria
destroyed the organic matrix of enamel, loosening
the appetite crystals.
• PINCUS (1949) extend the concept by proposing that
sulfates of gram negative bacillis hydrolyze the
sulfated mucosubstances of the matrix, liberating
sulfuric acid which then dissolves the mineral.
• However, areas of enamel with a relatively high
organic content do not show a greater
susceptibility to caries. It has also not been
possible to stimulate caries in vitro with
proteolytic agents.
• Proteolysis Chelation Theory
• Originated by Schartz and Martin in 1955.
• It proposes that some of the products of bacterial
action on enamel, dentin and food and salivary
constituents can form chelates with calcium.
• Since chelates can be formed at neutral or alkaline
PH, the theory suggested that demineralization of
enamel could arise without acid formation.
• Jenkins and Dawes state that saliva and plaque do
not contain substances in sufficient concentration to
chelate calcium in detectable amounts from enamel.
Chelation plays a minor role in the established lesion.
• Sucrose Chelation Theory
• EGGERS-LURA (1967) proposed that sucrose itself
and not the acid derived from it can cause
dissolution of enamel by forming unionized calcium
substrates.
• The theory is that calcium saccharides and calcium
complexing intermediaries requires inorganic
phosphate which is subsequently removed from the
enamel by phosphorylating enzymes.
• However, since saliva is an abundant source of
inorganic phosphates for bacterial utilization, it is
highly improbable that depletion of phosphate in
plaque by oral microbial metabolism results in
phosphate withdrawal from enamel.
• 5) Auto Immune Theory
• Burch & Jackson (1966) analyzed caries
epidemiologic data and suggested that genes
partly inherited and partly mutational and
determine whether a site on a tooth is at risk.
 Role of Carbohydrates
• Cariogenic carbohydrates are dietary in origin.
• Sticky solid carbohydrates are more
cariogenic.
• Cariogenicity varies with
• Frequency of ingestion
• Physical form
• Chemical composition
• Routes of administration and presence of
other food constituents
• Types of Sugars:
• Intrinsic Sugars: Sugars Integrated into cellular
structure of Food.
• Extrinsic Sugar: Present in free form or added to
food.
• Extrinsic sugars are potentially more cariogenic.
• Non milk extrinsic sugars (NMES) are potentially
damaging to dental health and all added sugars
in syrups, fruit juices and honey.
• Monosaccharide's (Glucose, fructose, galactose)
(Cariogenic)
• Disaccharides (sucrose, lactose, maltose)
(Cariogenic)
• Polysaccharides (starch, glycogen)
• Oligosaccharides (Found in sugar free chewable
vitamin and yogurts)
• Maltodextrins ( Tasteless oligosaccharides that
are used to increase the energy content of food
without increasing the sweetness)
 Non Cariogenic, Non Sugar Sweetener
• Mannitol (Sugar alcohols)
• Sorbitol (Sugar alcohols) (Low cariogenic effect)
• Xylitol : Cannot be metabolized by cariogenic bacteria and
can maintain pH
Anticariogenic effect because it can promote
remineralization.
• Lactitol
• Isomalt
• Hydrogenated glucose syrup
• Saccharin
• Aspartame (NutraSweet, Canderel)
• Acesulfame
• Thaumatin
• Maltitol
 Foods and drinks with low potential
for dental caries
• Low/no caries risk
• Bread (sandwiches, toast, crumpets and pitta bread)
• Pasta, rice and starchy staple foods
• Unsweetened or artificially sweetened yogurt
• Low-sugar breakfast cereals (e.g. shredded wheat)
• Sugar-free confectionery
• Fresh fruit (whole and not juices)
• Water
• Sugar-free drinks
 Possible Anti-Cariogenic Effect
• Milk
• Cheese
• Peanuts
• Sugar-free chewing gum
• Fibrous foods (e.g. raw vegetables)
• Xylitol sweeteners, gum and mints
• Tea (unsweetened)
 Highly Cariogenic Food
• Sugar and chocolate confectionery
• Cakes and biscuits
• Buns, pastries, fruit pies
• Sponge puddings and other puddings
• Table sugar
• Sugared breakfast cereals
• Jams, preserves, honey
• Ice cream
• Fruit in syrup
• Fresh fruit juices
• Sugared soft drinks
• Sugared, milk-based beverages
• Sugar-containing alcoholic beverages