Prof. d-r R.

Kabaktchieva- 2014
 In 1890 W. D. Miller, an American dentist teaching
in Germany, published his chemico-parasitic
theory of caries

Miller believed that extraction of the lime salts from

the teeth was a result of bacterial acidogenesis

It was the first step in dental decay

Miller's
work failed to identify
dental plaque as the source of the
bacteria and the bacterial acids
G. V. Black, described the
gelatinous microbial plaque
as the source of the acids.
 Dental caries is a multifactorial disease
process, often represented by the
interlocking circles

Influence of MO, carbohydrates

over time
 (1) There must be a
For caries to
susceptible tooth and host;
develop,
4 conditions
(2) Cariogenic
must occur
microorganisms must be
simultaneously:
present in a sufficient
quantity;

(3) There must be frequent

excessive consumption of
refined carbohydrates;

(4) This process must occur

over a sufficiently long
period of time.
 When a tooth covered with cariogenic bacteria
is exposed to a suitable substrate, such as a

refined carbohydrate, = the bacteria

produce acid.

If these conditions persist over a sufficiently long

period of time
an incipient lesion
develops
 The incipient lesion is the initial stage of
tooth decay that has not penetrated the
outer surface of the tooth.

The lesion looks like a white spot on the

enamel.
incipient lesion
caries
Physical and Microscopic Features of
Incipient Caries
The incipient lesion in her earliest stage, is
characterized by histological changes of
the enamel

These changes include demineralization

which represents the loss of

calcium and phosphate and
other ions from the enamel
Physical and Microscopic Features of Incipient Caries

The second stage includes the progress of

demineralization
toward the dentinoenamel
junction (DEJ),

then continues into the

dentin.

The final phase of caries development is the

development of the open or visible lesion
that is actually a really cavitation

We can also say overt, or frank, lesion

 The early identification of the incipient
lesion is extremely important,
because it is during this stage that the
carious process
can be arrested or reversed!!!
 The incipient lesion is macroscopically visible
on the tooth surface by the appearance of an
area of opacity, the white spot lesion.

At
this earliest clinically visible stage,
the subsurface demineralization at the
microscopic level is well established.
 The incipient lesion has been extensively
studied and is best described by
Silverstone.

he observations of the incipient lesion

have been based on the use of a polarizing
microscope.
 This microscope permits precise
measurements of the
amount of
space, called pore space,
which exists in normal enamel and
to a greater extent in enamel defects.
 If demineralization progresses

more pore space occurs;

in contrast, during remineralization,

less pore space is

present.
Direct Connection of the Bacterial Biofilm to the
Body of the Lesion

Tooth enamel is composed of

interlocking structures called
enamel rods, which contain
billions of crystals.
The pores present between
the crystals and the rods
form a network of
channels that allow
diffusion of fluid, ions
and small molecules
The striae of Retzius extend this network
into deeper layers of the enamel.

This diffusion remineralization of the

tooth throughout its life
network
allows:

plaque acids to enter

The the interior enamel,
channels causing
also allow demineralization.
 the initial attack may
In be on the ends of
demineralization the enamel rods,
of the surface
between the rods
enamel:
or both.

widening of the areas

Result from between adjacent rods
this: (inter-rod space)
 When conditions
are optimum

ragged interface 1. by the body

between surface and 2. through
defenses, such 3. By reduction
preventive
subsurface as calcium and of fermentable
strategies ,
phosphate and carbohydrates
such as fluoride
can be other ions from
therapy
in the diet.
the saliva,
remineralized:
Reaching the enamel-dentin border,
whether any liquid causes
demineralization or remineralization
can move in 3 directions:

1-2. along the hypomineralized

EDJ in both direction move
lateralli

3. into the dentinal tubules to the

pulp chamber
Diagram of a trichotomized
lesion (go in three directions )
attributable to diffusion of
acids:
-in both directions under the
enamel
- directly into the body of the
lesion in the dentin.
T, translucent zone;
B, body of the lesion;
R, reactionary dentin;
P, pulp.
(From Silverstone L. M., & Hicks, M. J.
(1985).
- ,
-
The
-
speed of progression of the caries
front depends on such factors as:

ion
concentration,

pH,
-all of them
continually
saliva flow changing.

buffering actions
Any chemical changes in the plaque
can soon be reflected throughout
the enamel and dentin as part of the
incipient lesion.
The pores The initial acid attack
allow preferentially :
dissolves the
plaque magnesium and
acids to be carbonate ions,

directed followed by removal of:

directly to the less-soluble

calcium,
the phosphate, and
subsurface other ions that are
part of the crystal.
region.
 The undermined surface zone
collapses.

Atthe same time, the more

soluble proteins are lost from
the subsurface matrix.
Cariogenic Bacteria
As a general rule, the cariogenic bacteria
metabolize sugars to produce the energy
required for their growth and reproduction.

The byproducts of this metabolism are acids,

which are released into the plaque fluid.

The damage caused by MS is mainly caused

by lactic acid, although other acids, such as
butyric and propionic, are present within the
plaque.
Measuring Plaque pH, the
Stephan Curve
There is a continuous pH change in
the plaque every time food is consumed.

There is an almost immediate drop in pH

when sugar or sugary snacks are eaten,
followed by a longer recovery period
than when other foods are eaten.
 This drop-and-recovery curve has been termed
the Stephan curve;

Different individuals have different capabilities

to buffer acid production (see next fig.);

Studies have identified foods that are

accompanied by a drop the critical pH of 5.5 to
5.0,
such as dried fruits,
white bread, cereals,
starchy foods
Fig. Stephan curves. These curves show the typical plaque pH response
to an oral glucose rinse . An immediate fall in the pH is followed by a
gradual return to resting values after about 40 minutes.
The upper curve was obtained from milk and the lower one from an apple-
drink, showing a large difference in the acidogenicity of these two drinks.
The Relationship of Saturation to pH

The concentration of calcium and phosphate

ions in the plaque fluid bathing the tooth at
the plaque-tooth interface is extremely
important because these are the same
elements that compose the
hydroxyapatite crystal found in the
enamel.

If the fluid adjacent to the tooth is

supersaturated with calcium and phosphate
ions at a given pH,
the enamel cannot undergo demineralization.
 The saliva in contact with the teeth is
normally supersaturated with calcium and
phosphate, compared with the levels of these
minerals in enamel.

The bacterial plaque can concentrate

these ions to an even greater extent.

For instance, the number of calcium and

phosphate ions in plaque is 3 times
greater than the number in the saliva.
This increased concentration is of
practical importance because
calcium and phosphate levels tend
to be inversely related to the caries
score.
 Asthe pH drops in an acid attack,
the level of supersaturation also
drops, and the risk of
demineralization increases.

There is no exact pH at which

demineralization begins, only a
general range of 5.5 to 5.0.
 Demineralization is a function of both:
- a drop in pH ,
- the length of time that the enamel surface is
exposed to the acidic environment.
Different plaques have:
- different initial pHs,
- different buffering potentials,
- different concentrations of calcium and
phosphate in different parts of the mouth.
A change in any of these variables
results in a different level of supersaturation in the
tooth environment.
Demineralization and
Remineralization Principles
Demineralization is caused by plaque acids,
which dissolve the tooth minerals making up
the basic calcium, phosphate, and hydroxyl
crystals of the enamel, dentin, and cementum.

Remineralization, requires the availability of

the same ions, preferably with fluoride as a
catalyst to reconstruct the missing or damaged
rods, a process that ten Cate called non-
restorative repair.
 The crystals and fluoride
compound of most dental interest
in the demineralization and
remineralization process are:

- hydroxyapatite (HAP),
- fluorhydroxyapatite (FHA),
- calcium fluoride (CaF2).
Enamel mineral
Themineral of enamel is a salt
formed from calcium phosphates.

Basic
calcium phosphate in
enamel is hydroxyapatite.
Enamel mineral
Apatite - a mineral with chemical
formula
10(4)6 (F, OH)2

FHA- Ca10(PO4)6(F,OH)2
FA Ca10(PO4)6 F2
Enamel mineral
Other calcium phosphates:

Brushite - 4.2 2,
-tricalcium phosphate- 3( 4) 2
Octacalcium phosphate-
8( 4) 4( 4) 2.5 2.
 Dissociation equilibrium of hydroxyapatite

in liquid
medium
undergoes
electrolytic
dissociation HA dissociates to :
10 calcium ions
6 trivalent phosphate ions
2 hydroxide ions
10( 4) 6 ()2 10 2+ + 643- +
2 -
 Calcium and phosphate ions from the
enamel get into plaque :
- serve for buffering of the medium;

- if the environment is alkaline the iones can

reenter in enamel;

- part of the ions get into the saliva,

Processes of de-and remineralization of enamel in the oral environment

Between enamel and saliva is situated the

plaque biofilm

Ions entering the food diffuse plaque and

saturate it;
Within each eating into the plate enter acid,
and other acids are formed from microbial
metabolism.
Dissociation equilibrium of plaque acids

The acid is salt, and also in the liquid medium as well

as the crystal starts to dissociate.

hydrogen ions + acid anions

The active part of an acid is the hydrogen ion,
and its strength is dependent on the quantity
thereof.
The carious process is a
process of acid
demineralization
When in the solution around HA acid is
dissociate , begins the active effect of
hydrogen ions;
The hydrogen ions pass into the enamel
and move in competitive reaction with
calcium.
The hydrogen ions move into contact with the
hydroxyapatite and combined with the phosphate and
hydroxide ions of the crystal
form a monohydrogen phosphate ion (42+) and
(2).

They quickly leave the crystal and move in solution

10( 4) 6() 2 2+ + 6 43- + -
+

42+ 20
+
monohydrogen phosphate
2 4-
dihydrogen phosphate ion
 Processes of de-and remineralization of enamel in
the oral environment

Enamel constantly washind from saliva.

The concentration of Ca2 + and PO4 ions in the

saliva varies - under normal conditions - 1,5 mmol /
l.

At neutral pH in the mouth the amount of Ca2 +

and PO4 ions is sufficient to saturate the medium.

These conditions provide balance in the process of

de-and remineralization and no significant ion
motion.
Processes of de-and remineralization of enamel in the oral environment

By acidification of the medium saturation with inherent

apatite ions decreased sharply

Starts quickly extracting of ions from enamel for her

saturation.

Critical pH = 5,5 - direction of movement of the ions only

in the direction from the enamel to the solution
performed only under demineralization

Performed only process of demineralization

By dissolving apatite:
over the enamel in the solution increases the concentration of Ca 2 +,
Mg2 + PO 43 -, HPO4 -, CO 32 - / HCO 3 - ions. + Ions from saliva

as a result of the action of saliva begins alkalization of the

medium

ions are directed to the enamel, enter it and precipitate to:

- dicalcium phosphate dihydrate (DCPD) or
oktakaltsiev phosphate (OCP)

in a favorable environment, they pass into the hydroxyapatite and,

in the presence of fluoride ions to fluorhidroksiapatit
Thus is realize the remineralization of tooth enamel
 The long-term exposure of teeth to low
concentrations of fluoride (as found in
fluoridated water) results in the gradual
incorporation of fluoride into the existing
hydroxyapatite (HAP) crystals to form
fluorhydroxyapatite (FHA), which is more
resistant to acid damage.

 Conversely, a higher concentration of
fluoride (as occurs with the use of topical
fluoride applications, fluoride dentifrices,
foams, and varnishes, etc.) results in the
formation of surface globules of CaF2
(as seen in electron microscope images).

If phosphates and proteins of the saliva

coat these globules, the globules become
more insoluble.

When the fluoride is incorporated into
HAP to form FHA, it is said to be firmly
bound,

Fluoride in the form of CaF2, is loosely

bound and adsorbed onto the surface of
HAP and FHA crystals.
The Relationship between HAP, FHA,
and CaF2
After an attack by plaque acid(s),
- CaF2 dissolves first,
- followed in sequence by HAP,
- and finally, FHA (with its fluoride substitutions).
-
As the attack continues, the dissociated ions
increase the saturation level of the immediate
fluid , sufficiently to slow crystal dissolution and
eventually arrest further solution of the
crystals.
 As the pH begins to return to normal, crystals
begin to re-form from the complex pool of
dissolved ions;
- some as HAP,
- some as FHA
(with many of the fluoride ions coming from the
previous CaF2).
 Any deficiencies are
subsequently replaced, in time,
by calcium, phosphate, and
fluoride from sources such as the
saliva, water, and toothpastes.
 The system breaks down
(state of equilibrium -homeostasis)
when the attacks are too frequent
and too prolonged.
 end