Definition

• Progressive
• Bacterial damage
of hard tooth structure exposed to oral
enviroment
Etiology
Multifactorial disease
Host
Susceptible
teeth
saliva
Substrate Plaque
(fermentable caries Microrganisms
CHO)

Time
A. Susceptible tooth
1-position
2-Morphology
3- Structure

• Enamel hypoplasia
or hypocalcification
→ has no effect on
caries initiation but
rapid progression
• Newly erupted
teeth are more
susceptible to caries
4- Fluoride
has a cariostatic effect
• ↓demineralization
(fluoroapatite)
• ↑ remineralization
• Inhibition of bacterial
enzymes & thus
bacterial activities
Sources are drinking
water, tea, seafood
and therapy
5- genetic factors
• Tooth morphology
Enviromental factors
• Food habbits
• Dental care
• socioeconomic status
saliva
• Formation of enamel
pellicle
• Cleansing effect
• Salivary buffers
(bicarbonates) neutralize
the acidity
• Inorganic components→
promote remineralization
• Secretory immunoglobulin
A → killing of bacteria,
prevent adherence to
tooth surface & inhibit
bacterial activity
• Lyzozymes, peroxides and
lactoferrin → direct anti
bacterial action
B. Carbohydrates

• CHO
→ acted upon in the
oral cavity
• Proteins & fats
→undergo little
change in oral
cavity
Factors affecting cariogenicity of
CHO
1. Type of CHO
Monosaccaharides & polysaccharides →
less cariogenic
Disaccaharides → most cariogenic
 Sucrose
Is the arch
criminal of
dental caries
• Low molecular weight → pass easily
into dental plaque
invertase
• Sucrose fructose+ glucose
hydrolysis

Fructokinase glucokinase
glycolsis

Energy + H2O + organic acids

Pyruvic acid Lactic acid

• It’s the cheapest & commenest in use

 • Sucrose
(glucose + fructose)
fructosyltransferase
glucosyltransferase

polymerization

Dextran Levan
1. Glucose polymer 1. fructose polymer
2. Extracellular 2. Extracellular
polysaccharide polysaccharide
3. H2O insoluble 3. H2O soluble
4. Adhesive 4. Less adhesive
5. Main bulk of 5. A store for CHO
dental plaque
2. Total amount of CHO
↑ caries activity
3. Frequency
↑ caries activity
4. Local effect
5. Consistency
Sticky
6. Refinement
Treatment of CHO to obtain
whiter-sweeter-improved
flavor-removal of fibrous
content
Xylitol ≠ honey
 Vipeholm experiment
by Gustafson in Sweden
Aim: to show the effect of total
amount, frequency and texture of
CHO.
400 patients in a mental hospital were
divided into 7 groups
DMF was measuerd before the
experiment
 Control
group (Basic
low CHO
diet + fat)

2 groups 4 groups
(Basic low (Basic low
CHO diet + CHO diet +
sugar at sugar
meal time) between
meal time)
In Sweetened toffee chocolate
solution bread
caramel
 DMF was measured after 5 years &
a diagram was drawn

Observation: ↑↑ caries activity with sticky

CHO (toffee & caramel between meals)

Conclusion: frequency & texture of CHO are

more effective than total amount
Microorganisms
Miller’s experiment
Saliva
(m.o.)+
fermentable
CHO

Tooth has
Tooth doesn’t
shown caries
show caries
like lesions
like lesions

heat
Orland’s experiments
(54)
They obtained germ free animals by
cesearian sectioning of pregnant rats
under complete aseptic conditions

Rats divided into 2 groups

Grow in aseptic live in containers in
incubators & eat air & eat nonsterile
completely aseptic food
cariogenic food

No caries caries
 (55)
Gnotobiotes (known life controlled flora)

• Gnotobiotic animals: are germ free animals

to which a single known strain of m.o. is
introduced to its oral activity
The most potent types
responsible for caries production
• Mutant streptococci
1. Streptococcus mutans
2. Streptococcus
sorbinus & other 5
groups
• Lactobacilli (pioneers
in dentin caries)
• Actinomyces viscousus
(root surface caries)
Essential features of cariogenic
bacteria
• Acidogenic property act upon
fermentable CHO → organic acids
 invertase
• Sucrose fructose+ glucose
hydrolysis

Fructokinase glucokinase
glycolsis

Energy + H2O + organic acids

Pyruvic acid Lactic acid

• Aciduric property M.O. can live, grow,
flourish in acidic medium
• Formation of intracellular
polysaccarides amylopectin (made up of
glucose units & used by m.o. at time of
CHO deficiency)
• Formation of abundant extracellular
polysaccarides
 • Sucrose
(glucose + fructose)
fructosyltransferase
glucosyltransferase

polymerization

Dextran Levan
1. Glucose polymer 1. fructose polymer
2. Extracellular 2. Extracellular
polysaccharide polysaccharide
3. H2O insoluble 3. H2O soluble
4. Adhesive 4. Less adhesive
5. Main bulk of 5. A store for CHO
dental plaque
• M.o. have attachement mechanism for
firm adhesion to tooth surface
• Proteolytic property having
proteolytic enzymes that is capable
of digestion of protein matrix of
tooth
 Dental plaque

• Definition: It is tenaciously adherent

bacterial structure formed on the tooth
surface (biofilm)
Mechanism of formation

1. Acquired enamel pellicle it is acellular,

structurless, bacteria free film of salivary
glycoproteins. Its thickness is about 0.3-
1μ. Formed immediately after thorough
tooth brushing
 2. Initial community
• Colonization phase (8)
Pioneer m.o (sanguis, • Growth phase (8-48)
oralis, mitis) → Rapid growth of
proteolytic enzymes pioneer bacteria
→digest protein coat forming colonies →
around m.o & some monolayer of m.o is
sites on tooth surface formed →
→ exposure of charges further bacterial
on bacteria & tooth
proliferation in
surface →
vertical ┴ direction
so attachment of m.o is
achieved
3. Intermediate community
Ingress & proliferation of secondary invadors (s
mutans) which have two effects →
1. Fermentation of sucrose & production of
organic acids → ↓s. sanguis & veillonella
flourishes
2. Synthesis of extracellular polysaccharides &
proliferation of m.o & shifting in microbiota →
deepest layer (anaerobic), mid layer (facultative)
& superficial (aerobic)
4. Mature community

1. plaque matures →
2. filamentous organisms proliferate →
3. they are arranged // to each other & ┴ to
tooth surface
Acid production in d. plaque
(Stephen’s curve)
• Aim: is to study the change in pH of plaque after
CHO intake
• Measuring the resting pH by putting an electrode
in contact with plaque & the other electrode in the
floor of the mouth
• Resting pH: is the pH of an individual at least 1
hour after the last meal when there is no f. CHO
consumed
• Patients → rinse their mouth by 25 ml 10 %
glucose for 10 seconds
• pH changes measured frequently & a curve was
plotted
 • Slow return in pH
• Metabolism of
• Rapid drop in pH after residual sugar d.
CHO intake plaque
• Rapid diffusion of • Breakdown of
sugar through dental reserve
plaque polysaccharides
• Activity of large no. • Diffusion limiting
of bacteria & enzymes membrane of d.
→ acid production plaque
• Diffusion limiting membrane:
Delayed diffusion of acid outwards &
salivary buffers inwards
Biochemical reactions in d.
plaque
1. Acid production
2. Dextran & levan formation
3. Amylopectin formation
4. Demineralization
5. remineralization
 Demineralization
Bacteria act on sucrose producing weak
acids

Weak acid is partially ionized into H+

and R-COO-

H+ accumulated in plaque moves toward

tooth structure displacing ca++

Accumulated ca++ moves outside by

concentration gradient and binds with
R-COO-
 Demineralization
Accumulated ca++ moves outside by
concentration gradient and binds with R-COO-

Available unbonded ca++ reduces and so the

process continues

Removing plaque that allows the tooth to

come in contact with saliva (supersaturated
with minerals) reverses the process and
remineralization starts