De - Remineralization Seminar

Introduction and History
INTRODUCTION AND by oral bacteria. This theory
HISTORY highlights the interaction between

mineral content of teeth and the
carious process.
A mineral is any naturally
occurring, inorganic solid consisting
For many years, dental caries
of either a single element or
was considered as a progressive
compound having a definite chemical
dimineralization of enamel apatite
composition and a distinctive internal
followed by degradation of dentin.
crystal structure.
Originally, bacteria was considered
E.g.: Naturally occurring elements
the only causative factor for dental
like gold, silver, copper,
caries. However, the present concept
identifies caries as a dynamic process
Naturally occurring compounds
which can be conceptualized as an
like Bauxite Al 2 O 3 .xH 2 O,
imbalance between mineral loss called
Haematite Fe 2 O 3 ,
demineralization and mineral gain
Magnetite Fe 3 O 4 ,
called remineralization.
Galena PbS.
The phenomenon of reminerali-

Teeth are highly mineralized
zation was first described by Head in
tissues of the body containing
1909. It is now recognized that dental
biological apatite as the mineral.
hard tissues are constantly undergoing
Biological apatite is a calcium
cycles of demineralization during
phosphate salt where some of the
periods when pH is low, followed by
phosphates are replaced by hydroxyl
repair when conditions favor
groups to give formula
remineralization leading to variations
Ca 1 0 (PO 4 ) 6 (OH) 2 .
in mineral status of teeth many times
In 1890, Miller gave the a day. Ultimately the net loss of
“chemoparasitic theory” according to mineral determines the progressive
which caries is brought about by acid nature of carious lesion. The
dissolution of mineral phase of teeth, widespread use of fluoride has
the acid being produced by increased the rate of remineralization
metabolism of dietary carbohydrates and has dramatically reduced the
De Re Mineralization 1
Introduction and History
prevalence of dental caries and rate of

progression of carious lesion.
This library dissertation

highlights the basic concept of
de-re mineralization phenomenon and
the various factors influencing them.
Composition of Dental Hard Tissues
COMPOSITION OF DENTAL potassium, sodium and fluoride are
HARD TISSUES also present as described below.
Mineral composition in weight (%) 2 8

Principle hard tissues of tooth are
Ion Weight %

Enamel
Calcium 33.6–39.4

Dentin
Phosphorous 16.1–18.0

Cementum
Carbonate 1.95–3.66
Magnesium 0.25–0.56
ENAMEL
Sodium 0.25–0.90
Dental enamel is one of the
Potassium 0.05–0.30
highly mineralized systems known to
Chlorine 0.19
us. With its unusual chemical
Fluorine 0.006–0.3
composition and highly ordered
structure, it is the densest material in
ORGANIC COMPONENT
the vertebrate system.
Developing enamel
Two groups of proteins 
Composition
Amelogenins 90%
By weight By volume
Non-amelogenins 10%
Inorganic material Inorganic material
Amelogenins are rich in amino
96% 89%
acid Proline.
Organic material Organic material
1% 2% Non-amelogenins called ename-
Water Water lins are rich in Glycine and Aspartic

acid.
3% 9%
Mature enamel
Inorganic component Amelogenins are removed
The inorganic material is during enamel’s development although
mainly calcium phosphate in the form small amounts of degradation products
of hydroxyapatite crystals. Small of amelogenins (tyrosine rich
amounts of carbonate, magnesium, amelogenin polypeptide) and non
amelogenin proteins persist in fully 

Orderly arranged with elongated
mineralized tissue. plates of hexagonal cross-
section
Levels of structure in dental enamel 
Length of crystal 1000–
The organization of the mineral
10,000A 0
in dental enamel follows a hierarchy 
Width of crystal 300–400A 0
of structural levels from macroscopic 
Thickness of crystal 100–400A 0
down to atomic.

The largest structural elements 300 – 400A0
encountered are the rods or 100 – 400A0

prisms. Enamel is composed of
1,000 – 10,000A0
densely packed and interwined
assembly of rods that extend
from the enamel dentin junction
towards the outer surface.
-
Length of rods–3mm
-
Thickness of rods–10,000A 0

The rods are composed of
Fig 2.1: Hydroxyapatite Crystal
millions of small, elongated
hydroxyapatite crystals (length
Structure of enamel rods
of order of 1000A 0 ) arranged in
Each rod is an elongated
characteristic pattern within the
assembly of millions of crystallites
rods.
laid end to end and packed into a

Each crystal in turn is
staggered bundle many crystallites
composed of thousands of
thick.
subunits called unit cells
(dimensions of order of 10A 0 )
Rod diameter 4-6 m/40,000–60,000A 0
which are stacked together like
Rod length – 1-3mm
building blocks. 
Crystal along the central axis of
Internal structure of unit cell is
rod run parallel to the
highly ordered arrangement of atoms.
longitudinal axis of rods.
Properties of Hydroxyapatite crystal

Crystals flare laterally to an ground sections, when the
increasing degree as they inorganic components are
approach the rod periphery (Fi g removed.
2.2)
Fig 2.3: Fish scale appearance of

enamel rods

The rod sheath is significant
around three-fourth of
Fig 2.2: Flaring of crystal in enamel
circumference of rod. The
rods
portion of inter-rod region
located directly cervical to

The inter rod region is an area
particular rod is not separated
surrounding each rod in which
by rod sheath because the
crystals are oriented in a
crystals there are confluent with
different direction from those
those making up the rod.
making up the rod (40 0 –60 0
deviation). The boundary where Formation of rod and interrod
crystals of rod meet those of enamel
inter rod region at sharp angles 
Differentiating ameloblasts
is known as rod sheath. from the inner enamel

These rod sheath contain more epithelium of dental organ
enamel proteins (organic secrete enamel matrix. As first
material) than other regions, as increment of enamel is laid,
crystals meeting at different ameloblasts move away from
angles cannot be packed tightly. dentin surface and each
This accounts for fish scale ameloblast forms a conical
appearance (Fi g 2.3) in etched projection into newly formed
enamel called TOMES Ameloblast

PROCESS.

When Tome’s process is
established secretion of enamel Tomes process
protein occurs from two sites.
a. Proximal site of Tomes
Proximal secretory site
process, close to junctional
complex, along with that Distal secretory site
from adjoining ameloblasts
result in formation of
enamel matrix wall. These Fig 2.4: Formation of rod and
walls enclose a pit into interrod enamel
which Tomes process fits 5 6 .
b. Secretion from distal Direction of enamel rods
secretory site, later fills this 
The rods follow indulating
pit with matrix. (Fi g 2.4) paths that span the distance

Crystals in the pit have a from the enamel-dentin junction
different orientation than those to the tooth surface.
in the walls of pit. This 
Length of rods is greater than
difference gives the structure to the thickness of enamel due to
enamel, with the walls oblique direction and wary
becoming inter-rod enamel and course of rods. In cervical
the pit becoming enamel rod. enamel, they have a straight

Each rod is formed by 1 course. These rods tend to be
ameloblast but 4 ameloblasts roughly perpendicular to both
contribute to inter-rod region. the enamel-dentin junction and
tooth surface.

Diameter of rods increases from
dentio-enamel junction towards
the surface of enamel at ratio of
1:2 as outer surface of enamel
is greater than dentinal surface.
Crystal structure of Hydroxyapatite atoms both from the hydroxyl groups

Each hydroxyapatite crystal is and phosphate groups. Phosphate
composed of thousands of subunits groups occupy the bulk of the space
called unit cells which are stacked between the calcium channels in the
together like building blocks. Internal structure.
structure of unit cell is a highly
The hydroxyl groups are lined
ordered arrangement of atoms.
up along the central axis of the
Arrangement of atoms in unit cell channels of calcium ions, forming
Each unit cell is divided into 3 columns running in the c-direction
axis a, b, c axis. Length of a and b Individual hydroxyl groups are
axis are equal. c axis corresponds to slightly displaced from the planes of
long axis of enamel crystal. The the calcium triangles and are oriented
hydroxyl groups in hydroxyapatite are with its hydrogen atom directed away
arranged in columns paralled to c axis from the triangle along the channel
that are surrounded by channels axis.
formed by triangles of calcium ions.
The hydroxyl groups are
arranged both above and below the
Two calcium triangles lie
planes of calcium triangles. This
perpendicular to the crystallographic c
orientation of hydroxyl groups varies
axis. One triangle is located ¼ the
in a random fashion in enamel crystal.
way up the c axis and the second one
is situates ¾ of the way along c.
Incremental lines
These triangles are twisted 180  Two types of incremental lines
relative to each other. The calcium are found in enamel as a result of the
triangles are repeated along c from phasic nature of the development of
unit cell to unit cell, resulting in tissue namely cross – striations and
cylindrical arrays of calcium ions striae of retzius.
running throughout the length of
crystals in the c direction. The Cross – striations
calcium ions that form the c-axis  These are short period markers
channels coordinates with the oxygen seen on each individual rod at
right angles to long axis of DENTIN

rods. Dentin provides the bulk and
 They represent daily increments general form of the tooth and is
of growth (circadian cycle) characterized as a hard tissue with
during enamel formation. tubules throughout its thickness.
 Enamel is formed at a rate of
4m/day. Therefore the interval Composition
between cross striations is By weight

Inorganic material - 70 %
being 2.5-7m, the lower values
Organic material - 20 %
being found near dentinoenamel
Water - 10 %
junction and surface enamel.
By volume
2. Straie of Retzius
Inorganic material - 45 %
These are long period marker
Organic material - 33 %
seen as irregularly spaced brown lines
Water - 22%
running obliquely across the enamel
from dentinoenamel junction. They
Inorganic component consists
mark the position of developing
mainly of hydroxyapatite, and the
enamel at weekly intervals and are 20-
organic phase is type I collagen with
80m apart. Seven cross–striations are
fractional inclusions of glycoproteins,
seen between consecutive Straie of
proteoglycans and phosphoproteins.
Retzius. Also, they may be formed as
a result of temporary constriction of PRIMARY DENTIN
Tomes process with an increase in It is of two types:
secretory phase forming interrod Mantle dentin
enamel. Mantle dentin is the name of
first formed dentin in the crown
The Striae of Retzius often
underlying the dentinoenamel
extend from dentinoenamel junction to
junction. It is thus the outer or most
the outer surface of enamel, where
peripheral part of the primary dentin
they end in shallow furrows known as
and is about 20µm thick. The fibrils
perikymata 7 .
formed in this zone are perpendicular
to the dentinoenamel junction, and the HISTOLOGY OF PRIMARY

organic matrix is composed of large DENTIN
collagen fibrils that are not present in Dentinal tubules
the rest of primary dentin Dentinal tubules extend through
(circumpulpal dentin). the entire thickness of the dentin from
the dentinoenamel junction to the pulp
Circumpulpal dentin
and takes the course taken by the
Circumpulpal dentin forms the
odontoblasts during dentinogenesis
remaining primary dentin or bulk of
i.e. S-shaped path. This S-shaped
the tooth. It is the circumpulpal
curvature is less pronounced in root
dentin that represents all of the dentin
dentin.
formed before root completion. The
The ratio between the outer and
collagen fibrils in circumpulpal dentin
inner surfaces of dentin is about 5:1.
are much smaller in diameter
Accordingly, the tubules are farther
(0.05µm) and are more closely packed
apart in the peripheral layers and are
together compared to the mantle
more closely packed near the pulp. In
dentin. The circumpulpal dentin may
addition, they are larger in diameter
contain slightly more mineral than
near the pulpal cavity (3 to 4µm) and
mantle dentin 6 5 . (Fi g 2.5)
smaller at their outer ends (1µm).
The ratio between the number of
tubules per unit area on the pulpal and
outer surfaces of the dentin is about
4:1. There are more tubules per unit
area in the crown than in root. The
dentinal tubules have lateral branches
throughout dentin, which are termed
canaliculi or microtubules which are
1µm or less in diameter. A few
dentinal tubules extend through the
dentinoenamel junction into the
Fig 2.5: Types of Primary Dentin
enamel for several millimeters. These
are termed enamel spindles.
Peritubular dentin mass within mature dentin. These

The dentin that immediately areas are prevalent in human teeth in
surrounds the dentinal tubules is which there has been a deficiency in
termed peritubular dentin. This dentin vitamin D or exposure to high levels
forms the walls of the tubules in all of fluoride at the time of dentin
but the dentin near the pulp. It is more formation (dentinogenesis). Inter-
highly mineralized (about 9 percent) globular dentin is seen most
than intertubular dentin. It is twice as frequently in the circumpulpal dentin,
thick in outer dentin (approximately where the pattern of mineralization is
0.75µm) than in inner dentin (0.4µm). largely globular. The dentinal tubules
By its growth, it constricts the pass uninterruptedly through inter-
dentinal tubules to a diameter of 1µm globular dentin, thus demonstrating
near the dentinoenamel junction. more defect of mineralization and not
of matrix formation 7 1 .
Intertubular dentin
Dentin located between the Predentin
dentinal tubules is called intertubular Predentin is a layer of variable
dentin. It represents the primary thickness (10 to 47µm) that lines the
secretory product of the odontoblasts innermost (pulpal) portion of the
and consists of a tightly interwoven dentin. It is unmineralized dentin
network of type I collagen fibrils in matrix and consists principally of
which apatite crystals are deposited. collagen, glycoproteins, and proteo-
Apatite crystals are generally oriented glycans.
with their long axis paralleling the
fibril.
Interglobular dentin
Interglobular dentin is the term
used to describe areas of
unmineralized or hypomineralized
dentin where globular zones of
mineralization (calcospherites) have
failed to fuse into a homogeneous
has been completed. This dentin

Dentinoenamel contains fewer and irregular tubules
Junction
than primary dentin. Secondary dentin
Mantle dentin is not formed uniformly and appears
Interglobular in greater amounts on the roof and

dentin floor of the coronal pulp chamber
leading to pulp recession and
Peritubular protecting the pulp from exposure in

dentin older teeth.
DEFENSIVE MECHANISMS OF PULP
Intertubular DENTIN ORGAN

dentin The pulp dentin organ may react
against any stimulation or irritation in
one of the following ways:
1. Healthy Reparative reaction
Odontoblast
process This is the most favorable
response, and it consists of
Predentin
stimulating the pulp dentin organ to
form sclerotic dentin and/or calcific
barriers.
a) If an irritation is mild, the
Odontoblast
odontoblasts can remain vital,
prompting Tomes fibers (which
are protoplasmic extentions of
odontoblasts) to form more
peritubular dentin peripherally.
Fig 2.6: Histology of Primary dentin
Such peritubular dentin is
highly calcified in contrast to
Secondary dentin
the remaining intertubular
It represents the continuing, but
dentin matrix and is called
much slower, deposition of dentin by
dentin sclerosis . This is the
the odontoblasts after root formation
first defensive mechanisms Eventually, the odontoblasts will pave

against irritation to the pulp over this reparative dentin, and start
dentin organ. the formation of normal secondary
b) If further irritation occurs, the dentin.
more peripheral dentinal tubules
will be completely obliterated Tertiary dentin has certain limitations:
by peritubular dentin, replacing a) It is not completely impervious
the ends of Tomes fibers. This like a calcific barrier.
is called a calcific barrier , b) It is less elastic than primary
which is second defensive dentin.
mechanism. c) Tertiary dentin is said to “age
the pulp" reducing its capacity
for further defensive action
2. Unhealthy reparative reaction
against further irritation as
If further irritation occurs, the
rapid formation of tertiary
odontoblasts will completely
dentin will lead to occupation
degenerate, leaving their protoplasmic
of part of the pulp chamber with
fibers in the dentin. As these fibers
tissues other than those
disintegrate the empty tubules are
normally responsible for further
filled with air leading to formation of
repair, metabolism and
dead tract and there is complete
innervation. Clinically if this
cessation in the formation of
reaction occurs as a result of
secondary dentin.
carious process, the restoration
of this tooth may not be
Then the undifferentiated
favorably received by pulp 4 6 .
mesenchymal cells and fibroblasts of
pulp assume the work of odontoblasts
Incremental Growth lines
and form a reparative, irregular type
Dentinogenesis proceeds rhy-
of dentin to seal itself off from the
thmically, with alternating phases of
irritation. This tertiary or reparative
activity and quiescence represented in
or reactive dentin deposition
formed dentin as incremental lines.
continues until they seal the dead
The organic matrix of dentin is
tract and counteract the irritation.
deposited at a daily rate of 4 µm. medium for the attachment of collagen

fibers that bind the tooth to
A five day rhythmic pattern
surrounding structures.
associated with the dentin deposition
at 20µm intervals is referred as Chemical composition
incremental lines of Von Ebner . On a dry weight basis,
They run at right angles to the dental cementum from fully formed
tubules. permanent teeth contains about 45%
to 50% inorganic substances and 50%
Some of the incremental lines to 55% organic material and water.
are accentuated because of
The inorganic portion consists
disturbances in the matrix and
mainly of calcium and phosphate in
mineralization process and are called
the form of hydroxypatite. The
as Contour lines of Owen. In the
organic portion of cementum consists
decidous teeth and in the first
primarily of type I collagen and
permanent molars where dentin is
protein polysaccharides (proteogly-
formed partly before and partly after
cans).
birth, the prenatal and postnatal
dentin are separated by and
Structure
accentuated contour line called the
With the light microscope two
neonatal line. This line reflects the
kinds of cementum can be
abrupt changes in environment that
differentiated: acellular and cellular.
occurs at birth. The neonatal line may
Acellular cementum do not
be a zone of hypocalcification.
incorporate cells, the spiderlike
cementocytes, whereas cellular
CEMENTUM
cementum contain such cells in their
Cementum is the mineralized
lacunae.
dental tissue covering the anatomic
roots of human teeth. It begins at the Acellular cementum may cover
cervical portion of the tooth at the the root dentin from the
cementoenamel junction and continues cementoenamel junction to the apex,
to the apex. Cementum furnishes a but it is often missing on the apical
third of the root. Here the cementum the apical half. Layers of acellular
may be entirely of the cellular type. and cellular cementum may alternate
Cementum is thinnest at the in almost any pattern. Acellular
cementoenamel junction (20 to 50 m) cementum can occasionally be found
and thickest toward the apex (150 to on the surface of cellular cementum.
200m). The apical foramen is Cellular cementum is frequently
surrounded by cementum. Sometimes formed on the surface of acellular
cementum extends to the inner wall of cementum, but it may comprise the
the dentin for a short distance and so entire thickness of apical cementum.
a lining of the root canal is formed. It is always thickest around the apex
and, by its growth, contributes to the
Cementocytes length of the root.
The cells incorporated into
cellular cementum, cementocytes, are Cementodentinal junction
similar to osteocytes. They lie in The dentin surface upon which
spaces designated as lacunae. A cementum is deposited is relatively
typical cementocyte has numerous cell smooth in permanent teeth. The
processes or canaliculi radiating from cementodentinal junction in deciduous
its cell body. These processes may teeth, however, is sometimes
branch, and they frequently scalloped.
anastomose with those of a
Since collagen fibrils of
neighbouring cell. Most of the
cementum and dentin intertwine at
processes are directed toward the
their interface in a very complex
periodontal surface of the cementum.
fashion, it is not possible to precisely
determine which fibrils are of dentinal
Location
and which are of cemental origin.
The location of acellular and
cellular cementum is not definite. As Sometimes dentin is separated
a general rule, however, acellular from cementum by a zone known as
cementum usually predominates on the intermediate cementum layer,
the coronal half of the root, whereas which does not exhibit characteristic
cellular cementum is more frequent on features of either dentin or cementum.
This layer is predominately seen in (Fi g2.7) . This occurs when the enamel
the apical two thirds of roots of epithelium degenerates at its cervical
molars and premolars and is only termination, permitting connective
rarely observed in incisors or tissue to come in direct contact with
deciduous teeth. It is believed that the enamel surface. Electron
this layer represents areas where cells microscopic evidence indicates that
of Hertwig’s epithelial sheath become when connective tissue cells, probably
trapped in a rapidly deposited dentin cementoblasts, come in contact with
or cementum matrix. enamel they produce a laminated,
electron-dense, reticular material
Cementoenamel junction
termed afibrillar cementum. Afibrillar
The relation between cementum
cementum is so named because it does
and enamel at the cervical region of
not possess collagen fibrils with a
teeth is variable.
64nm (640Å) periodicity. If such
afibrillar cementum remains in
In approximately 30% of all
contact with connective tissue cells
teeth, cementum meets the cervical
for a long enough time, fibrillar
end of enamel in a relatively sharp
cementum with characteristic collagen
line.
fibrils may subsequently be deposited
In about 10% of the teeth, on its surface; thus the thickness of
enamel and cementum do not meet. cementum that overlies enamel
Presumably this occurs when enamel increase.
epithelium in the cervical portion of
the root is delayed in its separation
from dentin. In such cases there is no
cementoenamel junction. Instead, a
zone of the root is devoid of
cementum and is, for a time, covered
by reduced enamel epithelium. Enamel Enamel
In approximately 60% of the
teeth, cementum overlaps the cervical
end of enamel for a short distance
Dentin Dentin
Cementum
Cementum
60% 30% 10%
Fig 2.7: Cementoenamel Junction
Mineralization Sequelae
MINERALIZATION Matrix vesicle formation
SEQUELAE The vesicle is a small

membrane bound structure that buds
Hard tissue formation involves off from the cell to form an
cellular activity whereby an organic independent unit within the first
matrix is produced capable of formed organic matrix of hard tissue.
accepting mineral with the activity of Within the vesicle the first
the enzyme alkaline phosphatase and a morphologic evidence of crystallites
good blood supply. is seen. The matrix vesicle provides a
microenvironment in which all
Organic matrix
proposed mechanisms for initial
Organic matrix of hard
mineralization exist. It contains
connective tissues namely bone,
alkaline phosphatase, pyro
cementum and dentin consists of
phosphatase, calcium ATPase, metal-
fibrous protein (type 1 collagen)
loproteinases, proteoglycans and
associated with varying amounts and
anionic phospholipids which are able
types of other macro molecules
to bind to calcium and inorganic
(proteoglycans, phosphoproteins,
phosphate and form calcium inorganic
phospholipids). On the other hand
phosphate phospholipid complexes.
organic component of enamel consists
These complex are unique to
of distinctive family of enamel
mineralizing situations and when they
proteins.
are selectively removed, the matrix
vesicle is no longer able to initiate
All hard tissues are capable of
mineralization.
accepting mineral in the form of
hydroxyapatite crystals. Heterogenous nucleation
In this mechanism, apatite
Mineralization mechanism crystals are deposited in relation to
Two mechanisms achieve the collagen fibrils although collagen
mineralization of hard connective does not have any role in their
tissue initiation. Some noncollagenous
1. Matrix vesicle formation proteins like phosphoryn (phosphor-
2. Heterogenous nucleation protein) are proposed act as
nucleating agent for mineralization. MINERALIZATION OF ENAMEL

Mineral first appears in the gap zones Takes place in two steps
at the ends of collagen molecules. 1. Primary mineralization
Initially these gaps are filled with In this step immediate
proteoglycans which bind to calcium. mineralization of enamel matrix takes
The proteoglycans are removed by place simultaneously with organic
enzyme proteoglycanses, leaving matrix formation so that no unmine-
behind the calcium. Then phospho- ralized layer of organic matrix is
proteins bind to collagen. found. This results in formation of
partially mineralized (30%) enamel
The enzyme alkaline
matrix.
phosphatase dephosphorylases phos-
phoprotein and provides additional
The way mineral is introduced
phosphate ions. Localized increase in
into the organic matrix of enamel
phosphate ions encourages precipi-
differs from its introduction in other
tation of calcium phosphate
hard tissues. No matrix vesicles are
complexes in the gap zones. These
found in association with the initial
precipitates convert to first
mineralization of enamel protein and
hydroxyapatite crystals. Eventually
there is immediate formation of
hydroxyapatite crystals spread
crystallites in the newly secreted
between collagen fibrils to fully
organic matrix.
mineralize the tissue (Fi g 3.1) .
Proteoglycanases Phosphoprotein
Type 1 Collagen
Alkaline
Phosphatase
Nucleation of Hydroxyapatite
Fig 3.1: Heterogenous Nucleation
Because enamel protein is deposited ELECTRON MICROSCOPY OF

directly onto mineralized dentin, these AMELOGENESIS
first enamel crystallites are thought to
be nucleated by the apatite crystallites The deposition of enamel begins
located within the dentin or the immediately after dentinogenesis has
enamel proteins have also been commenced. Although differentiated
proposed as the nucleator for the first before the odontoblasts, the
enamel crystals. The enamel ameloblasts require the signal of
crystallites, once formed, grow dentin formation to initiate their
rapidly in length within the organic secreted activities.
matrix, which continues to be secreted
by the ameloblasts until the entire Amelogenesis consists of five stages:
thickness of enamel has been laid 1. Morphogenetic stage
down. 2. Differentiation stage
3. Secretory stage
2. Maturation 4. Maturation stage
Once the full thickness of 5. Protective stage
enamel has been laid down the
maturation of enamel takes place by 1. Morphogenetic stage
addition of significant amounts of The cells of the internal dental
mineral to the first formed enamel so epithelium are cuboidal or low
that its crystallites can increase in columner, with large, centrally located
both width and thickness. To permit nuclei and golgi elements in the
such an increase most of the enamel proximal portions of the cells.
proteins are degraded by ameloblast to Mitochondria and other cytoplasmic
low molecular weight proteins that components are scattered throughout
can be easily removed from between the cells.
the crystals. Amelogenins are removed
leaving behind small peptides and 2. Differentiation stage
amino acids and non amelogenins As the cells of internal dental
bound to crystals. epithelium begin to differentiate into
ameloblasts, they elongate, and their
Fig 3.2 Morphogenetic Stage
nuclei shift proximally toward the cell forms a conical projection. These
stratum intermedium. The amount of projections, called Tomes processes,
rough endoplasmic reticulum increase jut into the newly forming enamel,
significantly, and most of the giving the junction between the
mitochondria cluster in the proximal enamel and the ameloblast a picket
region. A reversal of the functional fence or saw toothed appearance.
polarity of these cells takes place by
the migration of the centrioles and At this time the dental organ
golgi regions from the proximal ends collapses. The volume of stellate
of the cells into their distal ends. reticulum is reduced by the loss of its
intercellular material. This reduction
3. Secretory stage - synthesis of in volume, together with the
enamel peripheral migration of ameloblast,
The synthesis of enamel protein brings the blood vessels in the dental
occurs in the rough endoplasmic follicle closer to ameloblasts.
reticulum from where it is passed to
When the Tomes process is
the golgi complex. In the golgi
established, the secretion of enamel
complex it is condensed and packaged
protein becomes confined to two sites.
into membrane bound secretory
Secretion from the first site (i.e.
granules. These granules migrate to
proximal site around the periphery of
the distal extremity of the cell, and
the cell) along with that from
their contents are released against the
adjoining ameloblasts, resulting in the
newly formed mantle dentin.
formation of enamel matrix wall.
Hydroxyapatite crystals are randomly
These walls enclose a pit into which
packed in this first formed enamel and
the Tomes process fits. Secretion from
interdigitate with the crystals of
distal secretory site (surface of Tomes
dentin.
process) later fills this pit with
After this first structure less matrix. Crystals in the pit have a
enamel layer is formed, the different orientation from those in the
ameloblasts migrate away from the wall off the pit. This difference gives
dentin surface and as they do so each structure to the enamel, with the walls
becoming interrod enamel and the inorganic material, the smooth ended
infilling becoming enamel rod. cells with removal of protein and
(Fi g3.2) water (Fi g3.3) . Thus, ruffle ended
Ameloblast ameloblasts possess proximal
junctions that are leaky and distal
junctions that are tight, whereas most
smooth ended ameloblasts have distal
junctions that are leaky and proximal
Proximal Secretory Site ones that are tight. Thus inorganic
material must pass through the ruffle
Distal Secretory ended ameloblasts (because their
site
distal junctions are tight) and,
Fig 3.2: Differentiation stage
conversely, larger molecules
withdrawn from the developing
4. Maturation stage
enamel must pass through the leaky
After the full thickness of
distal junctions between smooth ended
immature enamel has formed there is
cells.
reduction in height of the ameloblasts
and a decrease in their volume and
organelle content. The remaining
organelles congregate at the distal end
of the cell and the plasma membrane
in folds to form a striated border. The
ameloblast is described as ruffle
ended. This morphology alternates
with that of the smooth ended
ameloblast, in which the striated
border is absent. Modulation between
the two forms occurs between five and Inorganic material Organic Matrix
deposited Removed
seven times during maturation. The
ruffle ended ameloblasts are Fig 3.3: Differentiation stage
associated with the introduction of
5. Protective stage This change in the position of

As enamel maturation nears the nucleus reverses the polarity of
completion, the ameloblasts secrete a the cell. Under this influence the
material identical to basal lamina ectomesenchymal cells of dental
between the flattened distal ends of papilla differentiate the form
the cells and the enamel surface. odontoblasts, with their nuclei
Hemidesmosomes also form along the positioned away from the internal
distal cell membrane, providing a firm dental epithelium (Fi g 3.4) .
attachment for the ameloblasts to the
enamel surface. The ameloblasts Internal dental
protect the newly formed enamel epithelium cells
surface from the follicular connective
tissue which can differentiate into Dental papilla cells
cementoblasts and deposit cementum
on the enamel surface 1 7 .
Tall, columnar cells

Dentin mineralization
Dentin is formed by cells, the
odontoblasts, that differentiate from
ectomesenchymal cells of the dental Odontoblasts
papilla following an organizing

influence from cells of the internal Fig 3.4: Induction of Dentinogenesis
dental epithelium. The odontoblasts
produce an organic matrix that Formation of mantle dentin
becomes mineralized to form dentin. Organic matrix formation
Odontoblasts differentiate in the
Before dentinogenesis begins, pre-existing ground substance of the
the cells of the internal dental dental papilla and that into this
epithelium change from short cuboidal ground substance the first dentin
to tall columnar, and their cell nuclei collagen (large diameter) is
migrate toward the pole of the cell synthesized by odontoblasts is
away from the dental papilla. deposited. These collagen fibrils,
together with the ground substance in are deposited, they obscure the
which they aggregate, constitute with collagen fibrils of the matrix. The
organic matrix of the first formed or deposition of mineral lags behind the
mantle dentin. formation of the organic matrix so
there is always a layer of organic
Mineralization matrix, called predentin, found
Coincident with the deposition between the odontoblasts and
of collagen, the plasma membranes of mineralization front.
the odontoblasts adjacent to the
internal dental epithelium push out Formation of primary physiological
short, stubby processes. As the (circumpulpal ) dentin
odontoblast forms these processes, it Matrix vesicles are no longer
also buds off a number of small, generated by the odontoblast, and
membrane bound vesicles known as mineralization involves heterogenous
matrix vesicles, which come to lie nucleation. Phosphoprotein a highly
between the large diameter collagen phosphorylated protein is unique to
fibrils. circumpulpal dentin, absent from
predentin and mantle dentin, and
The odontoblasts then begins to associated with the heterogenous
move toward the center of the pulp; as nucleation. Mineralization occurs by
it does, one of its short, stubby globular (or calcospheric)
processes becomes accentuated and is calcification, which involves the
left behind to form the principal deposition of crystals in several
extension of the cell, the odontoblast discrete areas of matrix. With
process. Hydroxyapatite first appears continued crystal growth, globular
within matrix vesicles as single masses are formed that continue to
crystals. These crystals grow rapidly enlarge and eventually fuse to form a
and rupture from the confines of the single calcified mass. On occasion
vesicle to spread as a cluster of these large globular masses fail to
crystallites that fuse with adjacent fuse fully, leaving small areas of
clusters to form the fully mineralized uncalcified matrix known as inter-
matrix. As the hydroxyapatite crystals globular dentin.
the periodontal ligament of fully

CEMENTOGENESIS developed teeth.
Cementum formation in the

Cementoblasts
developing tooth is preceded by the
Soon after Hertwig’s sheath
deposition of dentin along the inner
breaks up, undifferentiated mesen-
aspect of Hertwig’s epithelial root
chymal cells from adjacent connective
sheath. Once dentin formation is
tissue differentiate into
under way, breaks occur in the
cementoblasts. Cementoblasts synthe-
epithelial root sheath allowing the
size collagen and protein
newly formed dentin to come in direct
polysaccharides (proteoglycans),
contact with connective tissue of the
which make up the organic matrix of
dental follicle. Cells derived from this
cementum. These cells have numerous
connective tissue are responsible for
mitochondria, a well-formed Golgi
cementum formation.
apparatus, and large amounts of
granular endoplasmic reticulum.
At the ultrastructural level,
breakdown of Hertwig’s epithelial
After some cementum matrix
root sheath involves degeneration or
has been laid down, its mineralization
loss of its basal lamina on the
begins. The uncalcified matrix is
cemental side. Loss of continuity of
called cementoid. Calcium and
the basal lamina is soon followed by
phosphate ions present in tissue fluids
the appearance of collagen fibrils and
are deposited into the matrix and are
cementoblasts between epithelial cells
arranged as unit cells of
of the root sheath. Some sheath cells
hydroxyapatite. Mineralization of
migrate away from the dentin toward
cementoid is a highly ordered event
the dental sac, whereas others remain
and not the random precipitation of
near the developing tooth and
ions into an organic matrix.
ultimately are incorporated into the
cementum. Sheath cells that migrate
Cementoid tissue
toward the dental sac become the
Under normal conditions growth
epithelial rests of Malassez found in
of cementum is a rhythmic process,
and as a new layer of cementoid is

formed, the old one calcifies. A thin
layer of cementoid can usually be
observed on the cemental surface.
This cementoid tissue is lined by
cementoblasts. Connective tissue
fibers from the periodontal ligament
pass between the cementoblasts into
the cementum. These fibers are
embedded in the cementum and serve
to attach the tooth to surrounding
bone. Their embedded portions are
known as Sharpey’s fibers. Each
Sharpey’s fiber is composed of
numerous collagen fibrils that pass
well into the cementum.
Interaction between Systemic Conditions and Hard Tissues of Teeth
INTERACTION BETWEEN deficiencies, if present during tooth
SYSTEMIC CONDITIONS AND formation, will adversely affect

formative cells and the matrix that
HARD TISSUES OF TEETH
they produce. Vitamins A, C, and D,
parathyroid hormone, tetracycline and
In bone and dental hard tissues
fluoride affect matrix development
calcium phosphates are present in the
and dentin and enamel mineralization
form of hydroxyapatite crystals
in developing tooth.
[Ca 1 0 (PO 4 ) 6 (OH) 2 ]. This mineral
allows the incorporation of many Effect of systemic fluoride on hard
foreign ions that fit in the crystalline tissues of teeth
structure and affect the solubility. At the beginning of enamel
formation the enamel forming cells
There are three surfaces of an
(ameloblasts) lay down a partially
apatite crystal: the crystal interior, the
mineralized (30% by weight) protein
crystal surface, the hydration shell,
matrix, the thickness of which
all of which are available for the
delineates the external form of the
exchange of ions (Fi g 4.1) . The type
tooth. At this stage, if fluoride is
and concentration of these ions
administered in the diet or drinking
depend on their availability during the
water, the small crystallites take up
formation of the tissues 6 8 .
fluoride from plasma and extracellular
fluids because of increased
Hydration Shell
concentration gradient in extracellular
Crystal Surface
fluids. This is followed by enamel
Crystal Interior maturation in which matrix
degradation and loss takes place
Serum
resulting in tissue porosity and
accumulation of more fluoride ions.
Fig 4.1: Surfaces of Hydroxyapatite
crystal The maturative stage lasts for 1-2
years in primary teeth and from 4-5
years in permanent teeth. Therefore
Certain vitamin and hormone less fluoride is found in primary teeth
than permanent teeth. dental hard tissues

Tetracycline, if available during
Fluoride is incorporated in the
the mineralization phases, may be
hydroxyapatite crystal either by an
incorporated in dentin, enamel,
exchange with the hydroxyl groups
cementum, and bone. The period
(due to similarity in size of ionic radii
marked by mineralization of crowns
of fluoride and hydroxyl ions) or by
extends from approximately five
simple adsorption. The hydroxyl
months in utero to twelve years of age
groups exchange is slower and less
and includes mineralization of both
reversible than adsorption. The
primary and permanent dentitions.
adsorptive process involves weak
During this period tetracycline
electrostatic bonding resulting in
chelates with calcium and causes
dissolution of fluoride ions within 24-
brown to grey discoloration of teeth.
36 hours.
At high concentration, both
Fluoride is most beneficial to ameloblasts and odontoblasts are
the teeth in concentrations of altered resulting in hypoplasia of
approximately 0.5 to 1ppm of water. enamel and dentin matrix.
Concentration of less than 0.5ppm Tetracycline can cross the placental
may not prevent caries. Higher barrier and are available to the human
concentrations, such as 5ppm, cause foetus. Tetracycline antibiotics if
mottling and hypoplasia of enamel administered to the mother doing the
and hypomineralized dentin, with period of tooth mineralization, results
increased interglobular spaces. in staining of decidous teeth at a later
Sodium fluoride can cross the stage 4 2 .
placental barrier and is available to

the human fetus. In pregnancy Vitamin A deficiency
consumption of fluoridated water Deficiency of vitamin A results
during mineralization of the fetal in defective enamel and dentin
teeth, results in incorporation of formation. Defectively differentiated
fluoride in teeth. Such teeth exhibit odontoblasts are associated with this
high resistance to dental caries. condition. There is degeneration of
Interaction between tetracycline and the epithelial derived ameloblasts,
which results in a hypoplastic enamel hypomineralization of enamel. It

matrix. If vitamin A deficiency is leads to wide unmineralized zones of
corrected during subsequent tooth predentin and interglobular areas in
development, normal dentin and the dentin.
enamel are produced, although
defective tissue is not repaired. Parathyroid hormone
The parathyroid glands regulate
Vitamin C deficiency calcium balance in the body. The
Scurvy is a disease resulting imbalance of parathyroid hormone,
from vitamin C deficiency. In severe either deficiency or excess, may affect
cases it causes cessation of bone, bone and tooth formation. Excess
dentin, and cementum deposition due parathormone (hyperpara-thyroidism)
to atrophy of their respective causes mobilization of calcium from
formative cells. Vitamin C is required the skeleton into the blood stream.
for collagen formation. It is necessary Calcium ions may then be excreted in
for the hydroxylation of the amino the urine, feces, sweat and milk.
acids Proline and Lysine. Absence or Calcium excretion results in
deficiency of vitamin C during hypocalcemia or decreased levels of
dentinogenesis results in poorly blood calcium, and the bone, in turn,
formed collagenous matrix. The mobilizes more calcium. When
dentinal tubules become irregular and calcium resorption is greater than
reduced in number. deposition, osteoporosis results.
Osteoporosis weakens the supporting
Vitamin D deficiency alveolar bone of the teeth, results in
Vitamin D is essential for decreased bone density around the
deposition of calcium and tooth, and thinning of the lamina dura.
phosphorous in hard tissues. Its Inactive parathyroid's
presence increases the absorption of (hypoparathyroidism) results in low
dietary calcium and maintains proper blood concentrations of ionized
levels of calcium and phosphorous in calcium. Bone density increases,
the blood. Vitamin D deficiency which results in increased thickness
causes hypoplasia and of the lamina dura and an increased
density of bone trabeculae

(osteopetrosis). Calcium is not
released from mature teeth as it is
from bone, so the structure of teeth is
not affected by hyperparathyroidism
and hypoparathyroidism, except
during the development. Hyper-
parathyroidism during development of
teeth results in hypomineralized
dentin while hypoparathyroidism
results in hypermineralized dentin.
Causes of Demineralization
CAUSES OF and acetic acid. The organic acids
DEMINERALIZATION produced by plaque bacteria are

capable of lowering the pH at the
plaque enamel interface to levels at
Dental hard tissues are
which demineralization can take
constantly undergoing cycles of
place 2 .
demineralization during periods when
pH is low, followed by repair when
The plaque layer covering the
conditions favour remineralization
tooth surface prevents the buffering
leading to variations in mineral status
action of saliva. The effectiveness of
of teeth throughout the day.
salivary buffering of acid is inversely
Ultimately the net loss of mineral
proportional to plaque thickness 7 7 .
determines progressive nature of
Thick plaque is held in deep fissures
caries formation. Various causes of
and grooves, between interproximal
demineralization are as follows:
surfaces, and around rough or
overcontoured restorations. Mecha-
1. Acid dissolution of tooth mineral
nical oral hygiene procedures are not
by plaque bacteria
very effective in removing plaque
A high level of acid concentration
from these sites, which are therefore
with increased contact with tooth
most common areas for
surface leads to demineralization of
demineralization and for caries
the surface. Many acidogenic (acid
initiation.
producing) and aciduric bacteria (that
can grow and multiply in acidic 2. Other acid sources
environment) like Streptococcus Strong acids are available from
mutans, S.mitis, S.salivarius, a variety of extrinsic sources such as
S.sanguis, Lactobacillus, Actinomyces carbonated soft drinks, citrus fruit
are present in the oral cavity and can juices and gastric reflux or
colonise the tooth surface, forming regurgitation. Frequent or prolonged
plaque. These bacteria create an exposure to these can lead to rapid
acidic environment by fermenting demineralization and can turn mild
carbohydrates from food and caries into a rampant attack. Most
beverages to organic acids like lactic common example is “Nursing bottle
Causes of Demineralization
caries” seen in infants who are debris and microorganisms. Decreased

allowed to sleep with a bottle of fruit secretion of saliva (xerostomia or dry
juice being suckled. The pH will drop mouth) can occur due to:
rapidly to a very low level and is a) Certain drugs like
sustained for longer periods. antihistaminics, antidepressants,
antihypertensives, antipsychotic
3. Decreased salivary flow
drugs, hypnotics, anticholinergics
Saliva is one of the major
and diuretics. Withdrawal of the
source of natural protection and repair
drug is followed by a return to
of teeth following acid challenge.
normal salivation.
i. The mineral content of saliva,
b) Therapeutic irradiation of
in particular calcium and phosphate
head and neck
ions act to maintain tooth integrity by
c) From prolonged stress
forming a supersaturated shield
d) Certain medical
around tooth and preventing the loss
conditions like diabetes mellitus,
of mineral ions from tooth.
Sjogrens syndrome, liver and
ii. Bicarbonate buffering system
pancreatic disturbances 4 1 .
of saliva provide a high level of
protection against both organic and Reduction of maximum salivary
erosive acids on the tooth surface. flow to less than 0.7ml/min causes
Unstimulated saliva contains little increased susceptibility of tooth to
bicarbonate buffer. Reflex demineralization by acids and
stimulation of salivary flow by increases caries risk.
chewing or through the presence of
acidic foods (such as citric acid)
increases bicarbonate buffer
concentrations up to sixty times.
iii. Lysozymes and salivary
antibodies (IgA) have an anti-
bacterial effect.
Salivary flow and oral clearance

rate influence the removal of food
Mechanism of Demineralization
MECHANISM OF At equilibrium there is no net
DEMINERALIZATION loss/gain of ions in solution or in the

solid phase and ion activity product
is known as a solubility product
The mineral component of
(Ksp).The solution (saliva) is in
enamel, dentin and cementum is
equilibrium with the solid (tooth
impure hydroxyapatite (HA) which
mineral apatite) and is said to be
also contains significant amounts of
saturated with respect to the solid.
carbonate, sodium, magnesium,
chloride and small amounts of
IAP (in saturated solution) = Ksp
fluoride ions. The demineralization is
the net loss of mineral ions from tooth When the ion activity product
due to reaction between acids and exceeds the solubility product e.g.
tooth mineral which is represented as because of high free ion
concentration, the solution is said to
Ca 1 0 (PO 4 ) 6 (OH) 2 + 14H + be supersaturated with respect to
Toot h Min eral (H A ) A ci ds tooth mineral. If the ion activity
↓ product is smaller than the solubility
product the solution is said to be
10Ca 2 + + 6H 2 PO 4 - + H 2 O
S olu t i on
undersaturated with respect to tooth
mineral. A supersaturated solution is
The stability of tooth mineral in able to induce formation of tooth
oral fluid mineral while an undersaturated
The extent to which tooth mineral solution is able to dissolve tooth
can dissolve in a given solution is mineral.
governed by ionic product of calcium,

phosphate and hydroxyl ions. The Under normal conditions i.e. at
product of soluble ions of a salt in a neutral pH, saliva and plaque fluid 2 3
solution is called ion activity product are supersaturated with respect to
(IAP). enamel apatite which not only

prevents enamel from dissolving but
IAP of HA = (Ca 2 + ) 1 0 (PO 4 3 - ) 6 (OH - ) 2 tends to precipitate calcium phosphate

into a readily formed mineral,
brushite (CaHPO 4 . 2H 2 O) and not pH range 2.1-7.2 to H 2 PO 4 - .

hydroxy-apatite. This precipitation is
promoted by nucleating centers within C a 1 0 (P O 4 ) 6 (OH) 2 10C a 2 + +6P O 4 3 - +2OH -
dental plaque and is called calculus. H+

HP O 4 2 -
Despite the supersaturation of saliva,
H+
mineral deposition on sound, plaque
H2PO4-
free enamel does not normally occur
due to the presence of statherin As this transformation of ionic
(tyrosine rich peptide) in saliva which phosphate takes place, the saliva
inhibits precipitation of calcium ceases to be saturated with respect to
phosphate from supersaturated tooth mineral. Thus the solubility of
44
saliva . Moreover the surface of calcium phosphate (tooth mineral)
teeth are coated with an acquired increases as pH decreases.
pellicle of proteinaceous material
derived from saliva which masks the The pH at which saliva is
underlying crystals. exactly saturated with respect to

enamel apatite is defined as critical
pH. Below the critical pH enamel
Supersaturation Nucleation, formation
of new crystals and may dissolve and about the critical
crystal growth value enamel tends to remineralize 6 7 .
Saturation Equilibrium
Critical pH for hydroxyapatite = 5.3-
Undersaturation Tooth dissolution
5.5
Critical pH for fluorapatite = 4.5
The effect of pH on the solubility of

Fluorapatite is less soluble than
enamel apatite
hydroxyapatite.
At pH 13-14, all ionic
phosphate is in the form of PO 4 3 - . As Mechanism
pH is lowered the free active Bacterial fermentation of
concentration of PO 4 3 - decreases carbohydrates lead to the formation of
because it is transformed in the pH organic acids and a fall in pH.
range 7.2-12.3 to HPO 4 2 - and in the Initially H + ions will be taken up by
buffers in plaque (phosphates) and

saliva (bicarbonates). Eventually,
when the pH declines, the fluid
medium will be depleted of OH - and
PO 4 3 - which will react with H + to form
of H 2 O and HPO 4 2 - . Dissolution of
mineral in calculus adds to the
concentration of calcium and
phosphate in the aqueous phase
whereby the critical pH is lowered.
The buffering continues until the
critical pH for dissociation of
hydroxyapatite is reached at 5.5-5.2.
Below the critical pH, the

aqueous phase becomes under-
Fig 6.1: Mechanism of Demineralization
saturated with respect to hydrox-
yapatite but remains supersaturated
with respect to fluorapatite. This leads
to dissolution of hydroxyapatite and
precipitation of fluorapatite in the
demineralized area if fluoride is
available during this time. If the pH
decreases further below 4.5, which is
the critical pH for fluorapatite
dissolution, even fluorapatite
dissolves. If acid ions are neutralized
and calcium and phosphate ions are
retained, the reverse process of
remineralization occurs.
Intentional Demineralization
INTENTIONAL irregular etched surface, it penetrates
DEMINERALIZATION into the roughened enamel surface

forming resin tags 4 9 . Monomers in the
material polymerize and the material
This refers to the intentional
becomes interlocked within the
removal of hydroxyapatite crystals
enamel surface called micro-
from the surface of enamel and dentin
mechanical retention. Acid etching of
by acid to create microporosities for
dentin is necessary to remove smear
micromechanical bonding of adhesive
layer created by cavity preparation
restorative materials called acid
and exposes collagen fibrils. Resin
etching of enamel and dentin.
monomers impregnate the matrix of
Enamel etching was discovered demineralized dentin forming hybrid
by Buonocore in 1955 when he layer. Hybrid layer is a mixture of
conducted experiments on enamel collagen and resin polymers 3 0 .
surfaces employing a 30 second
Intentional demineralization
treatment of 85% phosphoric acid to
paves the way for the formation of
achieve a simple acidic
resin tags and hybrid layer, thereby
demineralization. He showed that
forming the fundamental basis behind
there was a tremendous increase in
which adhesion to dentin is explained.
surface area due to the acid etching
action, exposing the organic Smear layer
framework of enamel. Droplets of self Smear plug
curing resins attached to the etched

area remained intact for an average of
Collagen fibrils
1070 hours compared with 11.2 hours exposed
on untreated enamel surfaces.
ACID ETCHING
Acid etching transforms the

smooth enamel to a very rough, Hybrid layer
irregular surface by removal of Resin tag
prismatic and interprismatic mineral RESIN INFILTERATION
crystals. When a resin is applied to Fig 7.1: Intentional demineralization
Remineralization – A Dynamic Phenomenon
REMINERALIZATION - A saliva-like remineralizing solutions on
DYNAMIC PHENOMENON enamel lesions. They concluded that

mineral is deposited as calcium
hydroxyapatite, that the deposition is
Remineralization is the
crystalline and remineralization was
replacement of mineral in the partially
the result of regrowth of crystallites
demineralized regions of the carious
affected by the carious process. The
lesions of enamel and dentin.
relative orientation of the crystallites
in remineralized tissue was not as
Remineralization is analogous
perfect as in sound enamel. Sound
to wound healing in soft tissues of the
enamel crystallites are arranged in a
body. It is the result of reversal of a
parallel orientation and in
carious lesion through decreased
remineralized lesions they are
cariogenic attack and increased
randomly orientated.
protective factors like presence of
fluoride in saliva. Remineralization is
Mechanism of Remineralization
enhanced by providing low levels of
Remineralization is the exact
calcium and phosphate in conjugation
reversal of demineralization and can
with minimal amounts of fluoride.
be represented as
The first systematic clinical

10Ca 2 + + 6H 2 PO 4 - + H 2 O
study on caries reversal was reported S olu t i on
by Backer-Dirks in 1966. Two cities ↓
of Holland - Tiel and Culemborg were Ca 1 0 (PO 4 ) 6 (OH) 2 + 14H +
selected. Culemborg was supplied Mi n eral
with non-fluoridated drinking water

The requirement for
and Tiel with 1ppm fluoridated water.
remineralization is that the ion
The carious lesion progression figures
activity product should exceed Ksp.
were smaller in Tiel than Culemberg
indicating the importance of fluoride
(Ca 2 + ) 1 0 (PO 3 - ) 6 (OH - ) 2 > Ksp (tooth
in caries prevention.
mineral)
Ten Cate and colleagues in 1989
investigated mineral deposition from
Remineralization occurs under chemical composition of the outer

neutral pH oral conditions. At neutral layers of enamel, which become some
pH saliva and plaque fluid are what less soluble with time. This
supersaturated with respect to process is known as the post-eruptive
hydroxyapatite. Consequently mineral maturation of the enamel 1 2 .
will precipitate if a suitable
precipitation nucleus is available.
After the consumption of fermentable
sugars, acids are formed in the plaque.
With this decrease in pH, the calcium
and/ or phosphate concentration
needed for saturation increases and in
the pH range below 5.6 the tissues Fig 8.1: Remineralization
will dissolve to maintain saturation 2 9 .

Physiochemical changes in
As a result of the dissolution of
remineralization
mineral the phosphate and hydroxyl
Enamel can be considered as a
ions released will neutralize the acids,
porous solid, in which water in the
thus slowing down the decrease in pH.
intercrysalline spaces serves as a
During the recovery phase the plaque
channel for acids to diffuse and attack
gradually becomes supersaturated
the crystallites. The effective pore
with hydroxyapatite and mineral will
size of sound enamel has been
reprecipitate. Ideally, this occurs at
estimated to range from 1.4 to 2.4nm
the sites ‘damaged’ during the
and to represent 0.1% to 0.8% by
demineralization. The composition of
volume. Acid diffusion into enamel
the apatite then formed depends on
can take place at the microstructural
the composition of the solution from
level through the intercrystalline
which it is precipitated, in this case
spaces and interprismatic spaces
the plaque fluid. For instance, if
(prism junctions) and possibly
fluoride is present this will precipitate
through larger developmental defects
to form a fluoridated hydroxyapatite.
such as cracks in enamel.
This periodic cycling of pH results in
a step-by-step modification of the
Organic acids present in plaque build up at sites in intercrystalline

fluid can be in both the dissociated spaces, they eventually raise the
(H + , A - ) and undissociated form (HA). degree of saturation of the
The relative proportion of these two demineralization fluid to the point
forms is determined by the dissolution where it is now supersaturated with
constant (pKa), which is unique for regard to tooth mineral, thus stopping
each acid. For example, the pKa of the demineralization process and
lactic acid is 3.86. At pH 3.86, there favoring the reprecipitation of
is an equilibrium between the mineral. Therefore, the outward
dissociated and undissociated forms diffusion of mineral ions toward the
of lactic acid. At a pH above 3.86, surface is considered the rate
more lactic acid is in the dissociated determining factor for
form, whereas at a pH below 3.96, demineralization 7 4 . The enamel
more lactic acid is in the surface receives the benefit from
undissociated form. The dissociated calcium and phosphate concentrations
form of organic acids, mainly the building up in plaque fluid as well as
hydrogen ions attacks the enamel reaction products diffusing from the
crystals. The undissociated form of subsurface enamel. These phenomena
the acid (HA), however, can diffuse may explain, in part, why the rate of
into the subsurface enamel, where demineralization is greater for the
conditions are favorable for it to subsurface enamel than for the surface
dissociate rapidly into the dissociated enamel. As conditions change from
form (H + and A - ), which can then undersaturation to super-saturation in
attack the apatite crystals. The the surface enamel, the diffusing acids
undissociated form of the acids serves do not react with the crystals in the
as a reservoir of hydrogen ions and surface layer and continue deeper into
helps drive the reaction. the subsurface enamel, where
conditions are undersaturated. Thus,
As the pH of plaque drops, a
deminerali-zation and
point is reached where the mineral
remineralization can be occurring in
phase of enamel begins to dissolve. As
different locations of a lesion at the
reaction products (dissolved mineral)
same time. The presence of low levels
of fluoride greatly enhances the phosphate dissolved from subsurface

reprecipitation process. enamel and leading to the preservation
of the surface enamel. Under in vivo
Various theories have been conditions, minerals originating from
proposed to explain phenomenon of outside the tooth (saliva, diet,
preferential subsurface dissolution. dentifrice, or rinse) can also be
1. The surface layer is protected involved in remineralization of the
by the presence of surface and subsurface enamel. The
demineralization inhibitors (ionic early (surface softened) lesions are
fluoride in oral fluids and responsive to the oral environment
absorbed organic material and can be rapidly remineralized
principally from saliva and the whereas more advanced subsurface
diet). lesions with relatively intact surface
2. Differences in anatomic layers are difficult to remineralize 1 5 .
structure and composition render
surface enamel less acid soluble White Spot Lesion
than subsurface enamel (high The first visual clinical
fluoride and low carbonate presentation of dental varies is
content). referred to as white spot lesion. The
3. Calcium and phosphate that lesion must progress to a depth of
diffuse outward from the 300-500μm to be clinically detectable.
subsurface are precipitated in the
outer surface layer of enamel in The clinical appearance of the
the form of a more stable calcium white spot lesion is caused by the loss
phosphate phase, thus preserving of subsurface enamel, resulting in the
the surface layer. loss of enamel translucency 4 . The
surface enamel over the white lesion
The last hypothesis has gained can appear as being clinically intact
the most favor. and smooth, generally indicating that
the lesion is not active. White spots
Surface layer of enamel can be with rough surfaces because of
reformed by deposition of calcium and increased porosity indicate that the
lesion is active and may be Thus the interfaces are more

progressing. susceptible to the initial exposure to
The classic work of Backer- acids than are the prisms. At later
Dirks established that the white spot stages of caries evolution, these
stage of caries does not necessarily enlarged interfaces are able to
progress to a frank cavitation and in undergo remineralization pheno-
some cases will over time take on the menon.
appearance of sound enamel. At the
white spot stage, the progress of the Body of the lesion consisted of
lesion may be arrested or reversed by enlargement of sheath regions or
modifying any of the causative factors prism junctions very similar to the
or increasing preventive measures. one observed in the surface layer. This
Arrested lesions may retain the is followed by a progressive and
appearance of white spots or acquire diffuse destruction of apatite crystals
the appearance of a brown spot. The located in the prism cores 5 5 .
reversal of a white spot could be due
to consolidation of the lesion possibly The early enamel lesion is
by remineralization or could be due to characterized by four distinct zones.
a wearing away of the defect by Moving from surface inwards they are
abrasive forces in the mouth and oral 1. Surface zone (1-5% pore
hygiene 6 9 . volume) forming the intact surface
overlying the lesion.
Structural Event in 2. The body of the lesion (>5 to
Remineralisation 25% pore volume) representing the
Enamel majority of the lesion and situated
In the surface layers of approximately 15 to 30 μm beneath
incipient carious lesion, initial the overlying intact surface layer
mineral dissolution occurs 3. The dark zone (2-4% pure
preferentially along the prism volume) situated near the
junctions or prism sheaths, with advancing front just superficial to
broadening of prism sheaths. the translucent zone.
4. The translucent zone (1% pore, carbonate, which is double the amount
volume) along this advancing front for enamel and gives rise to a higher
of the lesion 6 2 . solubility. The solubility is also
Silverstone (1973) and influenced by the size of the
Silverstone et al (1988) considered crystallites, which are considerably
that, the surface zone and the dark smaller in the case of dentine than
zone are formed as a result of enamel 6 6 . Smaller crystallites dissolve
remineralization phenomenon whereas faster when placed in an
the body of the lesion and the undersaturated solution. The collagen
translucent zone were produced as a fraction is the matrix on which the
result of demineralization. apatite crystallites were precipitated
during dentinogenesis. During
If the lesion development
demineralization, the apatite fraction
occurs over the relatively long period
is the first to be dissolved, only
of time, a zone of remineralization
exposing the collagen after its
(dark zone) with reprecipitation of
dissolution. The collagen, while still
mineral phases from the translucent
present in the dentin, serves as a
zone will occur.
diffusion barrier slowing down
demineralization but it is also subject
If lesion formation is over a
to denaturation, enzymatic degrad-
short period of time, the dark zone
ation, and solubilization. Once the
will not form and there will be rapid
matrix is removed it no longer can
advancement of the front with the
nucleate new apatitic crystals 3 7 .
large, heavily demineralized body of
the lesion and a surface zone of
According to Tencate the rate of
minimal thickness 2 2 .
mineral loss of dentin at pH = 5 is
Dentin De-Re Mineralization three times the corresponding value
Dentin differs from enamel for enamel.
due to presence of large proportion
(35vol%) of organic matrix, which is When the local pH is high and
composed mainly of collagen. Dentin calcium and phosphate ions are
contains about 5vol% by weight of present, the demineralization of
carious process is reversed by

remineralization of damaged tooth
structure. The slow rate of caries
progression results from periods when
demineralised tooth structure is
almost remineralised. The slow rate of
caries allows time for extrinsic
pigmentation. An arrested dentinal
lesion is brown to black, hard, and
due to fluoride may be more caries
resistant than unaffected dentin. An
arrested dentinal lesion typically is
open (allowing debridement from
toothbrushing) and this dentin is
termed as eburnated dentin.
Factors Influencing Remineralization
FACTORS INFLUENCING remineralizing rinses and dentrifices
REMINERALIZATION in an effort to increase oral calcium

and phosphate concentrations needed
to effect remineralization. Chewing
Remineralization is greatly
gums and candies are effective
enhanced by maintaining low
vehicles for the delivery of calcium
concentration of ionic fluoride in the
and phosphate because they can
oral environment. Fluoride is derived
produce an elevated mineral
from foods and beverages, by
saturation level for a longer period
fluoridation of drinking water,
than can be produced by a rinse or
fluoride containing dental products
dentifrice application. Furthermore, as
such as toothpastes and mouth rinses.
a consequence of increased salivary
Fluoride agents that are available in
flow, gums and candies can induce a
low dosage, delivered over long
desirable increase in plaque and
period of time and with frequent
salivary pH (Jensen and Wefel, 1989;
exposures (fluoridated toothpastes)
Manning and Edgar, 1993) thereby
are most effective. High concentration
reducing the severity of the challenge
fluoride with less frequent exposure
as well as helping to clear bacterial
(professionally applied topical
acids from plaque. Gums and candies
fluorides) are not as beneficial in
can also be utilized several times a
reducing caries experience and
day at selected times when maximum
remineralization of white spot lesions.
anticaries effect may be realized.
Prolonged and slightly elevated low
concentration of fluoride in the saliva
and plaque fluid decrease the rate of
enamel demineralization and enhance
the rate of remineralization.
Remineralization of early
lesions also requires calcium and
phosphate which are primary derived
from saliva and plaque fluid. There
have been many studies on the use of
Factors Influencing Remineralization - Fluorides
FLUORIDES waters, most soils and virtually all

foods. Thus fluoride is a natural
Fluoride, the pivot of preventive occurring constituent of our food and
dentistry continues to be the drinking water. In the body tissues it
cornerstone of caries prevention ranges from high concentration in
programs. The decline of dental caries skeleton and teeth, to a low level in
prevalence in recent decades has been bloodstream 9 .
explained by widespread use of

fluoride. In addition to the major Fluoride in the lithosphere
benefit of systemic fluorides that are Because of its extreme
consumed by children during the ages reactivity, fluoride rarely occurs in
of tooth development, there are nature in its elemental form, but is
numerous other mechanisms by which found most frequently as inorganic
fluoride ion may act to prevent or fluoride. It concentrates in the last
arrest dental caries. These additional stages of crystallizing magmas and in
mechanisms extend from the post the residual solutions and va pours.
eruptive enamel maturation effect Thus, concentrations are increased in
through the arrestment of incipient siliceous rocks, alkaline rocks, in
caries lesions to the maintanence of geothermal waters and hot springs,
an optimal dentition. and in volcanic fumaroles and gases.

About 150 fluoride-containing
OCCURRENCE minerals are known, of which
Fluoride is present almost Fluorspar (CaF 2 , 49%F), Fluorapatite
everywhere, either as bound fluoride (Ca 1 0 F 2 (PO 4 ) 6 , 3.4%F) and Cryolite
or as ionic form in solution. The (Na 3 AlF 6 , 54% F) are the most
earth’s minerals are its natural important. Fluoride replaces the
source, principally volcanic ash, deep hydroxyl group in hydroxysilicates
lying rock strata and certain ores such and in hydroxyapatites to form
as bauxite. Over the ages water that fluorapatite.
has passed through or over fluoride

rich minerals has dissolved fluoride, In acid soils (pH<6) fluoride is
so that some is present in most bound chiefly in complexes with
aluminum and with iron. At pH>6 the returned by way of rain and snowfall,
dominant species is the fluoride iron. and via the rivers when these events
Soil fluoride varies widely but occur over land. Hot waters
generally ranges from 50 to 500ppm. associated with volcanic activity have
been reported to contain elevated
Fluoride in the hydrosphere fluoride concentrations. Acid spring
waters located close to volcanic
Concentrations are affected by
activity may contain 5000-6000ppm
factors such as availa bility and
fluoride 6 3 .
solubility of fluoride-containing
minerals, porosity of the rocks or
Fluoride in the atmosphere
soils through which the water passes,
Fluorides are found in the air of
temperature, pH, and the presence of
rural communities as well as that over
other elements, e.g. calcium,
cities. The sources are varied and
aluminum and iron, which may
include effluvia from volcanoes, dust
complex with fluoride. Most surface
generated by the weathering of
waters contain less than 0.1ppm of
fluoride-containing soils and
fluoride. Most of the fluoride exists
outcroppings of fluoride-containing
as free fluoride ion, but complexed
minerals, ocean spray, smoke from
fluoride increases with increasing
burning coal and releases from a
salinity, reach ing 50-60% in sea
variety of industrial processes.
water. Sea water contains 1.2-1.4ppm
Gaseous components like HF and SiF 4
fluoride. Concentrations may be
account for more than half of airborne
enhanced locally by undersea vol -
fluorides around industrial sites.
canic activity. Fluoride exists in sea
Sources of airborne fluorides include
water in the ionic form and in
the domestic use of coal as a fuel and
fluoride complexes; MgF +
volcanic activity. Coals have been
constituting nearly half of these.
reported to contain up to
Fluoride is lost from the seas by
approximately 500ppm fluoride.
incorporation in life forms into
carbonates and phosphates and by
ejection or surface spray into the
atmosphere. The air borne fluoride is
ORAL ENVIRONMENT may be destroyed. Phosphate and

hydroxyl ions from the tooth mineral
Fluoride in Teeth and Bone will enter the solu tion and fluoride
The retention of fluoride in the will be deposited as CaF 2 .
body is due almost entirely to the
capacity of apatite (the mineral form Fluoride loss from bones and teeth
that comprises over 99% of the Not all of the fluoride acquired
skeleton) to bind and integrate by a mineralized tissue will be
fluoride ion into its crystal lattice. permanently bound by the mineral.
Fluoride concentrations in the Some superficially located flu oride
unmineralized soft tissues and in the may be lost again, by back exchange,
body fluids are relatively low. In all back-diffusion and migration from
mineralized tissues, fluoride levels the mineral to the surrounding tissue
tend to be grea test at the surface since fluid, blood, saliva or plaque fluids.
this region is the closest to tissue Even some of the firmly bound
fluid supplying fluoride. In the fluoride within apatite crystallites
mineralized tissues, some fluoride is might also be lost as crystals are
incorporated within the interior of the destroyed e.g. by osteoclastic
mineral crystallites as an integral part resorption of mesenchymal tissues
of the crystal lattice. However, (bone, cementum and dentin), by
fluoride may also be more wear, or, in the case of the dental
superficially located, perhaps ab - tissues, by severe acid erosion.
sorbed on crystal surfaces, or loosely
entrapped in the hydration shells of Concentrations of fluoride in dental
the crystallites and some will be enamel
temporarily pres ent in blood and Developing enamel
tissue fluids. The formation of CaF 2 At the beginning of enamel
and other fluoride-rich species is also formation, the enamel forming cells
possible. For example, when fluoride (ameloblasts) lay down a par tially
is applied to a tooth surface in a mineralized (30% by weight) protein
highly concentrated form (often at matrix, the thickness of which
low pH), part of the apatite mineral delineates the external form of the
tooth. At this stage, fluoride has tions at the tooth surface. Young
already been taken up by the tissue anterior teeth, surface fluoride
and, if fluoride is administered in the concentrations were found to be
diet or drinking water, the small highest in the first-formed enamel
crystallites in this region take up near the incisal edge and decreased
fluoride readily. Extracellular matrix steeply towards the more recently
processing occurs throughout the formed enamel near the cervical
stage of matrix secretion. This is region (Fi g 9.1) . In older teeth, the
followed by matrix withdrawal, which pattern is reversed. Fluoride
is completed during the maturation concentrations in the cervical region
stage. The result ing pores are of the enamel surface increase, while
occupied by fluid which, when the high surface concen tration near
removed by drying in air, produces an the incisal edge is gradually re duced
area of chalky white appearance. This by wear.
porous enamel readily accumulates
ions and other molecules and it has Acquisition of fluoride by the
been demonstrated that fluoride is enamel surface appears to continue
also preferentially absorbed at this while the tissue remains porous.
stage. A fluoride peak is usually Penetration of fluoride into fully
found at or just before the enamel mineralized enamel is very slow.
begins to mineralize rapidly, i.e. at Fully mineralized enamel has a
the maturation stage 5 9 . density of about 2.98g/mL with a
porosity as low as about 0.1% space
Erupted enamel by volume. Under normal
Fluoride is not homogeneously circumstances fluoride does not
distributed across the thickness of appreciably penetrate such sound
enamel. In incompletely mineralized mature enamel. The creation of
state, fluoride concentrations are porosity by the chemical destruction
highest at the tooth surface and low at of the apatite lattice is necessary
the interior. In all erupted teeth, before the concentration of fluoride in
fluoride concentrations increase from highly mineralized enamel can be
the enamel interior to high concentra - significantly in creased. This happens
when solutions, gels or pastes metabolically active and continues to

containing high concentrations of flu - grow throughout the life of the tooth.
oride are applied to the tooth surface
especially at low pH. In permanent teeth, the average
concentrations of fluoride in dentin
increases up to the age of about 40
and then plateau at a level related to
the concentration of fluoride in the
environment. Fluoride concentration
are highest at or near the surface
Fluoride, ppm < 25 limits (i.e. the pulpal surfaces) of
Fluoride, ppm 24-45
Fluoride, ppm 45-65 the tissue. Here, fluoride continues
Fluoride, ppm > 65
to be absorbed and probably
Fig 9.1: Fluoride in enamel increases in concentration
throughout life, partly because
Concentrations of Fluoride in dentin continues to form and will
Dentin constantly accumulate fluoride by
Dentin, like cementum and accretion during mineralization,
bone, is a mesenchymal tissue. Unlike where exchange also tends to be
enamel, which is ectodermal, maximal. While newly formed
mesenchymal tissues have dentin, primary or secondary, will
collagenous matrices and these are avidly incorporate fluoride, it may
retained during the pro cess of be present for a rela tively short time
mineralization. The apatite and might therefore have a relatively
crystallites are considerably smaller low fluoride concentration. This is
than those of enamel and much less presumably why fluoride
crystallized. The capacity for fluoride concentrations tend to be low in
uptake in dentin is therefore much secondary dentin, which has had
greater because of the increased relatively little time to accumulate
surface area of the crystallites, the the element. Conversely, a totally
tubular structure and higher degree of quiescent dentin surface may
tissue hydration. Dentin is also
passively absorb and accumulate the cortical compacta due to the

very large amounts of fluoride. relatively high proportion of avail able
surface in cancellous bone. Fluoride
accumulation by developing bones and
Concentration of fluoride in
teeth begins during fetal development.
cementum
Significant fluoride concentrations are
Cementum forms a thin layer
seen in human fetal bones and the
(50-100µm) on the surfaces of tooth
concentration reflects levels of
roots. Like bone and dentin, it is a
fluoride in take. At concentrations of
collagenous mesenchymal tissue. The
fluoride in the drinking water between
small crystal size and poor
0.5 and 1ppm, flu oride concentrations
crystallinity characteristic of
appear to rise with fetal age. This
mesenchymal tissues facilitates
effect was not observed in fetuses
fluoride uptake in cementum
from areas where drinking water
compared with dental enamel. This is
fluoride concentrations were low
further increased by the lower mineral
(<0.2ppm). After the period of growth
content and greater tissue porosity
has ended, the bone fluoride
compared with enamel. The highest
concentration continues to rise more
fluoride concentrations of cemen tum
slowly towards a plateau. Loss will
tend to be found near the outer
also occur due to physiologic
surfaces, falling towards the interior
resorption of bone during
of the tissue 5 8 .
development, remodeling and senile
osteoporosis.
Concentration of Fluoride in Bone
While bone is developing, the
Concentration of Fluoride in
tissue is highly vascularized and
Calculus
tissue fluid can transport fluoride
In both supra- and subgingival
relatively easily. This is a period of
calculus, the outer surfaces tended to
active bone formation when crystals
contain more fluoride than the inner
are growing and the overall rate of
portion, although this will be less well
fluoride uptake is high. Cancellous
defined in the subgingival calculus.
bone incorporates more fluoride than
This is related to availability of
fluoride from the external decisive for re- and demineralization

environment, i.e. from saliva on the of enamel. The plaque fluid is the site
outer surface and from ena mel on the at which, fluoride influences the re-
inner. In addition, the rate of forma - and demineralization process.
tion may be slower towards the
surfaces, per mitting more time for The fluoride in the plaque fluid
fluoride accumulation. Concentrations may originate from many sources:
varies from approximately 100ppm in calcium fluoride on the enamel
the interior to 1000ppm towards the beneath the plaque, calcium fluoride
surfaces. in plaque and fluoride in saliva and
gingival fluid. Plaque fluid fluoride
FLUORIDE IN ORAL FLUIDS AND concentrations are much higher than
DENTAL PLAQUE salivary fluoride concentrations. This
may be due to slow elimination of the
Fluoride in plaque ion from the plaque, due to the
The plaque fluid, the aqueous thickness of the salivary film, or
phase within the plaque is in contact release of fluoride from sources of
with the enamel surface, with the fluoride in the plaque such as calcium
plaque bacteria (which produce the fluoride. There seems to be a large
organic acids) and with saliva and variation between the plaque fluid
gingival fluid. Plaque fluid transports fluoride concentration at various sites
organic acids as well as fluoride, in the mouth. Plaque fluid collected in
calcium, phosphate and other ions to the region of the maxillary incisor site
the enamel surface. To be biologically maintains a much higher concentration
active these have to be in solution. of fluoride than the other sites.
The balance between these factors, of
which fluoride and pH are the most The nature of fluoride in plaque
important, determines whether the is uncertain. Three mechanisms have
tooth mineral will dissolve or not. It been proposed.
is thus the fluoride present in plaque 1. It has been suggested that
fluid and not the fluoride fluoride may be stored inside the
incorporated into the ena mel which is plaque bacteria. However, this is
only a very small amount, which in calcium, the acidic groups on

increases during acidic conditions the surfaces of bacteria will
because of the formation of acquire counterions, mainly
hydrogen fluoride (HF), an calcium. Fluoride can thus be
undissociated weak acid with a associated with calcium
pKa of 3.4 formed at low pH. countcrions. This flouride would
Hydrogen fluoride pene trates the also be released (with calcium)
bacterial cell membrane, reducing when the pH approaches the pK of
the fluoride content of plaque the acidic groups; they release F -
fluid. This mechan ism thus cannot and Ca 2 + at low pH (Fi g 9.2) .
explain the observed release of
Plaque bacterial
fluoride from plaque at low pH. surfaces
2. Another possibility is that
calcium fluoride forms in the
plaque during mouthrinsing or
toothbrushing with fluoride.
During and after a mouthrinse (or
toothbrushing), the plaque fluid is
supersaturated with respect to
calcium fluoride because plaque
fluid contains considerable
amounts of calcium. This flouride
will be mobilized when pH falls
below 6.
3. A third possible mechanism is
retention of fluoride associated
with plaque bacteria surfaces.
These surfaces represent a
formidable total surface area, with Fig 9.2: Retention of fluoride on
plaque bacterial surfaces
a net negative charge and abundant
phosphate and carboxyl groups. In Effect of plaque fluid on De-Re
the oral environment, which is rich Mineralization
The buffering capacity of The concentration of salivary

plaque and its degree of super fluoride from the parotid and
saturation with respect to calcium and submandibular/ sublingual glands is
phosphate will determine if the tooth about two-thirds of the plasma
surface will undergo demineralization fluoride concentration 5 3 . In subjects
or not. Dental plaque sequesters living in a low fluoride area, the
buffering agents (bicarbonate, saliva is less than 1µm/L. The
phosphate, urea) and calcium and fluoride concentration in whole saliva
phosphate ions from saliva. In is related to the fluoride excreted
general, the buffering capacity of from the glands, dietary fluid intake
plaque is substantially greater than and dental fluoride preparations. The
that of saliva (10 fold) and it also has resting saliva fluoride level is
a greater concentration of calcium, influenced by the fluoride
phosphate and fluoride than saliva. concentration in the drinking water
Supersaturation of dental plaque and and also by regular daily use of a
saliva implies that the mineral phases fluoride dentifrice/ mouthrinse.
in saliva and plaque will undergo
dissolutio prior to the hydroxyapatite Fluoride in the crevicular fluid
forming the tooth structure. In The crevicular fluid, which
addition, fluoride sequestered by enters the oral cavity via the gingival
plaque increases the ability of crevice, is closely related to serum.
hydroxyapatite to resist organic acid Its fluoride concentration is low and
dissolution, effectively allowing for a closely related to plasma fluoride
lower critical pH in the presence of concentration. It is unlikely to be an
fluoride. Certain plaque bacteria may important source of fluoride for
modulate the effect of mutans plaque or plaque fluid.
streptococci. Veillone lla metabolizes
lactic acid produced by acidogenic Fluoride and dental enamel
organisms and partially ameliorates Large amounts of fluoride may
acid production. be acquired by enamel exposed to
Fluoride in Saliva fluoride toothpaste during
toothbrushing, which is subsequently
covered by plaque. Calcium fluoride

is the fluoride phase which forms first Fluoride Reservoirs in or on the
under such conditions. The pH cycling Oral Soft Tissue
which occurs in the plaque covering Soft tissue can acquire fluoride
this fluoride-rich enamel contributes during topical applications. Some is
to its rapid mobilization and transfer absorbed through the tissue, and this
of fluoride to the plaque fluid. uptake is pH dependent, because
Demineralized enamel takes up fluoride penetrates more easily when
particularly high amounts of fluoride. protonated (HF). Some of the fluoride
in soft tissues is associated with
Fluoride in enamel, in the form calcium; pretreatment with calcium
of calcium fluoride, is abundant and ions increases fluoride retention. This
available for transfer to the plaque is due to the presence of acidic groups
fluid. This fluoride reservoir can on the surface of the tissues, and
release fluoride and calcium during retention of fluoride is based on
caries challenges. interaction with calcium counterions.
Connective tissue has sulfate and
Enamel (and dentin) not carboxyl groups, whereas the cell
covered by plaque may also take up membranes contain phosphate groups
fluoride, which is sub sequently slowly (in phospholipids). The mucous on the
released. This source is less important surface of the epithelium also has
than fluoride deposited be neath the acidic groups. The soft tissue-retained
plaque. The reaction between the fluoride may supply the saliva with
fluoride in toothpaste and dental fluoride after a mouthrinse, but is not
enamel is probably not mediated a major source of fluoride.
through saliva, because the paste is
applied directly to the tooth enamel.
This fluoride is re plenished regularly
and this reservoir is thus scarcely
depleted. This probably makes tooth -
paste a particularly appropriate EFFECTS OF FLUORIDE
fluoride vehicle.
Effect of firmly bound versus Gate, 1979 1984; Ten Gate and
loosely bound fluoride Duijsters, 1983; Nelson et al., 1983;
In the past decades a lot of Silverstone, 1977) 3 9 . In addition,
attention has been given to the research now shows that fluoride
relative importance of firmly versus applications which are applied
loosely bound fluoride in caries frequently, such as daily-used
prevention. Firmly bound fluoride dentifrices and mouth-rinses, can
refers to fluoride incorporated in the provide renewed sources of fluoride in
crystalline lattice of hydroxyapatite, enamel and plaque, changing our
whereas loosely bound or labial perspective from single high-
fluoride pertains to fluoride adsorbed concentration exposures at infrequent
to apatite and to fluoride leaching intervals (White, 1987, 1988;
from relatively soluble fluoride Featherstone et al., 1985; Reintsema
containing deposits. The latter et al., 1985; Stookey et al., 1985;
includes calcium fluoride, whereas Featherstone, 1983)
firmly bound fluoride concerns
fluorohydroxyapatite 2 6 . Ogaard et al in 1988 5 1 placed
shark enamel (consisting fluorapatite)
In recent years, there has been on hawlay retainers and studied the
renewed interest in loosely bound enamel demineralization. The enamel
fluoride as a reaction product of specimens were covered with
fluoridation to act as a potential orthodontic bands to create a space
"reservoir" or "depot" source of for plaque formation. Besides the
solution fluoride enhancing experimental group with shark
remineralization and retarding enamel, a group with human enamel
demineralization processes. Research specimens was investigated. After 4
has demonstrated that fluoride in the weeks in situ caries lesions were
solution, rather than in the bulk solid formed not only in human enamel but
phase has the most dramatic impact also, although less severely, in shark
upon both re- and demineralization enamel. This observation indicated
reactions of enamel minerals (Wonget that structurally bound fluoride was
al, 1987; Arends et al., 1984; Ten not very effective in inhibiting enamel
demineralization Additional Fluoride topical applications, in

information was obtained from a third particular when acidified, result in
group of subjects who rinsed their the formation of globular deposits of
mouth daily with a 0.2% sodium calcium fluoride (like) materials.
fluoride rinse. In their case caries was These globules do not dissolve as
inhibited to a significantly greater quickly as expected due to the
extent than in the shark enamel group. presence of phosphate and protein
In this direct comparison ambient rich surface covering these globules 3 8 .
fluoride showed a greater caries The dissolution of the fluoride from
preventive effect than firmly bound the globules is pH dependent, because
fluoride. Consequently fluoridation of the phosphate ions on the surface are
the enamel, with the aim of producing released when protonated at low pH.
high levels of incorporated fluoride, Reduction in
is not a sufficient method of
inhibiting tooth decay.
Calcium fluoride, as Fig

a 9.3:
fluoride pH Formation
Calcium Fluoride from 7 to 5 or 4 gave an increased
reservoir on the tooth surface, only rate of solubility of phosphate/
forms during treatments with high protein coated calcium fluoride. By
concentration fluoride solutions. this mechanism fluoride is dissolved
from the globules at the time fluoride activity is 4000 times higher (about
is most needed (i.e., at low pH) 5 2 (Fi g 4x10 - 5 mol/L) in the same plaque fluid
9.3) . (Birkland and Charlton, 1976). As a
result, IAP (FAP) is about several
Effect of Fluoride on
orders of magnitude larger than IAP
Demineralization
(OHAP) in cariogenic plaque.
When fluoride is incorporated
into tooth mineral it replaces the
This, together with the lower
hydroxyl ions in the hydroxyapatite
Ksp for FAP, make the cariogenic
lattice resulting in the conversion of
plaque about six order of maginitude
hydroxyapatite to fluorapatite(FAP)
with the formula of Ca 1 0 (PO 4 ) 6 F 2 and
fluorapatite, while it is slightly
the corresponding solubility
expression.
hydroxyapatite. Therefore, tooth
mineral rich in fluoride would be less
IAP (FAP) = (Ca 2 +) 1 0 (PO 3 - 4 ) 6 (F - ) 2
soluble in cariogenic plaque than
Substitution of hydroxyl ion by mineral that has a low fluoride
fluoride leads to a reduction in content. Several studies have shown
solubility because the Ksp for (LeGeros and others, 1983, Ogaard,
fluorapatite is 101 - 1 2 1 (Moreno, Rolla and Helgeland, 1983; Tanaka,
Kresak and Zahradrnik, 1977), is Moreno and Margolis, 1993; Takagi,
about four orders of magnitude lower Liao and Chow 2000) that enamel
than the Ksp for hydroxyapatite. Even containing higher amounts of tooth
when partially fluoridated, in which bound fluoride was much more
only some hydroxyl ions are replaced resistant to demineralization.
by fluoride ions, the mineral appear to
have lower Ksp than that of Interaction between solution
hydroxyapatite (HAP) (Driessens, fluoride and tooth bound fluoride
1982). According to Arends and other,
Also the hydroxyl ion activity 1983; Borsboom, Vander Mei and
is 10 - 9 mol/L in cariogenic plaque Arends, 1985; Margolis, Moreno and
fluid with a pH of 5, while F ion Murphy, 1986, a small amount of
fluoride present in the demineralizing advancing front region where it is

solution (ambient fluoride) is highly most needed.
effective in reducing demineralization
whether or not the mineral contained a Thus both ambient fluoride and
high level of tooth bound fluoride. tooth bound fluoride play important
roles in reducing tooth
Ambient fluoride (in the form demineralization and formation of
of salivary and plaque fluid fluoride) both types of fluoride should be
can be elevated by fluoride considered as important goals in
dentrifices, rinses and other topical designing effective fluoride
treatments that deposit labile fluoride treatment 7 6 .
in the oral cavity. This labile fluoride
then dissolves in the mouth, thus Effect of Fluoride on
serving as a source for ambient Reminerlization
fluoride. For ambient fluoride to exert When incorporated into mineral
its effects, it must penetrate the crystal structure as tooth – bound
advancing front of lesion where fluoride, it is in a highly stable form
mineral destruction is occurring. and is not released into the solution
However, tooth mineral is an efficient except under extremely acidic
scavenger of solution fluoride and as conditions.
fluoride diffuses into enamel it is
partially consumed by reaction with Thus tooth bound fluoride does
mineral (Duckworth and Braden 1967; not play a significant role in
Tarbet and Fosdick 1971). remineralization. In contrast, ambient
Fluorapatite formation in enamel, by fluoride is a very important parameter
systemic incorporation during tooth in remineralization. A small amount
formation, topical fluoride treatment of fluoride in solution will cause the
or by previous cariogenic attack, ion activity product of fluorapatite to
would make mineral less reactive to be significantly greater than ion
solution fluoride, thereby facilitating activity product of hydroxyapatite.
penetration of fluoride ion to the This solution fluoride results in
significantly greater oral
supersaturation levels with respect to content of a conceptual entity known

fluorapatite compared to hydroxy- as unit cell, which is the least member
apatite which provides a greater of calcium, phosphate and hydroxyl
thermodynamic driving force for the ions able to establish ionic
rapid precipitation of fluoride relationships. The unit cell of
containing tooth mineral. hydroxyapatite was the shape of a
stubby rhombic prism, when stacked
together, these prisms form the lattice
Physiochemical Effects of Fluoride
of a hexagonal crystal.
– Tooth Interaction
Incorporation of fluoride into
Biological hydroxyapatite is a
enamel renders enamel more resistant
hexagonal crystal with two equal axis
to acid dissolution due to stabilization
of apatite lattice. Such a stabilization (a and b) 120 apart and a third axis
is a result of hydroxyapatite having (c-axis) perpendicular to the first two.
inherent voids due to missing groups. a=b=9.432 A
Fluoride ion fills these voids and add c= 6.881 A

their hydrogen bonding tendency to
the forces which hold the crystal The hydroxyl groups in
together. In order to understanding the hydroxyapatite are arranged in
exact chemistry of its action, it is columns parallel to c axis that are
essential to visualize the structure of surrounded by channels formed by
hydroxyapatite. triangles of calcium ions. In one unit
cell there are two calcium triangles
Hydroxyapatite–structural overview that lie perpendicular to the
Hydroxyapatite is the most crystallographic c-axis. One triangle
important biological apatite found in is located ¼ the way up the c-axis and
mammalian bones and teeth enamel. It the second one is situated ¾ of the
is essentially a calcium phosphate salt way along c-axis. These triangles are
approximating in composition to twisted 180 relative to each other.
calcium hydroxyapatite which is The calcium triangles are repeated
represented as Ca 1 0 (PO 4 )(OH) 2 . This along c-axis from unit cell to unit cell
formula indicates only the atomic resulting in cylindrical arrays of
calcium ions that run throughout the the enamel crystal and the crystals are
length in the c-axis direction. The aligned so that their long axis are
calcium ions that form the c-axis toughly parallel to the rod axis. Since
channels are coordinated to oxygen the rods extends from dentinoenamel
atoms from hydroxyl groups and junction towards the enamel surface,
phosphate groups. Phosphate groups the channels containing hydroxyl
occupy the bulk of the space between groups are pointed perpendicular to
the calcium channels in the structure. the outer surface of enamel.
The hydroxyl groups are lined

Effects of Ionic substitutions
up along the central axis of the
Ionic exchanges between
channels of calcium ions, thereby
crystals and their fluid environment
forming columns running in the c
can be isotonic when one ion is
direction. The individual hydroxyl
replaced by the same type ion (as Ca
groups are slightly displaced from the
with Ca) or heteroionic when the
planes of the calcium triangles.
replacing ion is of different type (as F
However, a single hydroxyl group is
for OH). These ionic exchanges are
closely associated with each triangle,
governed by the size and charge of the
and is oriented with its hydrogen atom
ions. Ions of similar size and change
directed away from the triangle along
are more apt to exchange for each
the channel axis. The orientation of
other.
the hydroxyl group either above or
below the plane of the calcium
Hydroxyapatite crystal can
triangle varies in a random fashion
accommodate a variety of
from columns to columns, with half
substitutions without drastic alteration
the columns having hydroxyl groups
of its structural configuration. Three
pointed in the +c direction and half
surfaces in hydroxyapatite crystal are
having hydroxyl groups pointed in the
available for exchange of ions: the
–c direction.
crystal interior, the crystal surface
and the hydration shell i.e. a layer of
The c-axis of the apatite unit
water existing around each crystal.
cell corresponds to the long axis of
Magnesium and sodium can within the channels formed by the

substitute in the calcium position, calcium triangles.
fluoride and chloride in the hydroxyl
position and carbonate in both Fluoride ions, in contrast to the
hydroxyl and phosphate positions. hydroxyl groups, are situated in the
Ions may also be adsorbed to the planes of the cal cium triangles
crystal surface by electrostatic equidistant from the three cal cium
attraction or bound in the hydration ions (Fi g 9.4) .
layer.
One of these substitutions i.e.

replacement of some of the hydroxyl
groups of hydroxyapatite by fluoride
ions, has been extensively studied and
is of special importance to dentistry.
Fluoride ion is compatible with the
requirements of the apatite lattice, so
that it can be found in any of the three
surfaces of hydroxyapatite.
Incorporation of fluoride in the
crystals reduces their solubility while
the presence of fluoride in the
hydration shell or the surrounding
fluid enhances remineralization. Fig 9.4: Incorporation of fluoride
ions in hydroxyapatite
Incorporation of fluoride ions
Incorporation of fluoride ion into the columns of hydroxyl groups
Fluoride ions become can exert several sub stantial effects
incorporated into hydroxyapatite by on the chemical and physical
substituting for hydroxyl groups; properties of hydroxyapatite. By
these ions then occupy positions along occupying a position at the center of
the columns of hydroxyl groups the calcium triangle, the relatively
small fluoride ion is able to form within hydroxyl columns that contain
stronger coulomb interactions with the fluoride (Fi g 9.5) .
calcium ions than the hydroxyl group
can form. Materi al Ca- -- Ca Ca- -- An i on
Fl u orap ati te 3.975A 0 2.295A 0
H yd roxyap ati te 4.084A 0 2.389A 0
Calcium-fluoride contact
distances are also appreciably shorter
than those of calcium-hydroxyl
contacts. This results in the shrinkage
of the calcium triangle, with the
calcium ions actually pulled in
closer to the fluoride ion despite
the increase in re pulsive forces
between cations. The calcium-calcium
and calcium-anion distances at the
calcium triangle in fluorapatite are
also decreased. Substituted fluoride
ions may also affect the chemical and
physical properties of apatites by
Fig 9.5: Formation of highly
establishing hydrogen-bonding inter-
stabilized fluorapatite
actions with neighboring hydroxyl
groups. Within the columns, adjacent
Such hydrogen-bonding inter-
hydroxyl groups are separated by a
actions, together with the enhanced
spacing of 3.44A. This distance is too
ionic effects, are responsible for
great to permit hydrogen bonding.
most of the increased stability of
However, the distance between fluo -
fluoride-substituted apatite relative
ride ions (which are in the center of
to pure hydroxyapatite. Even trace
the calcium triangles) and neighboring
amounts of fluoride have dramatic
hydroxyl groups (which can be
effects on the stability of enamel, as
displaced toward the fluoride
reflected by lower acid solubility,
substituents) is short enough to per mit
decreased rates of demineralization
strong O—H---F hydrogen bonds
and enhanced rates of and F - . This lowers the intracellular

remineralization. concentration of HF, which results in
a continued diffusion of HF into the
EFFECT OF FLUORIDE ON ORAL cell, which again dissociates. This
MICROFLORA continued diffusion and dissociation
As early as 1940 it was leads to the accumulation of fluoride
demonstrated that the carbohydrate in the cell and to the acidification
metabolism in pure cultures of oral (accumulation of H + ) of the cell
streptococci and lactobacilli was cytoplasm. At a low external pH
inhibited by fluoride. fluoride effectively is taken up as a
result of the high proportion of HF.
Uptake of fluoride by oral bacteria

Once fluoride has entered the
In order to be able to exert
cell the greater part is bound to cell
antimicrobial effect fluoride has to
constituents. Most of these bindings
enter the cell. The uptake of fluoride
do not affect active sites of enzymes.
by cells may occur in the absence of
But, the binding to two enzymes,
an energy source, in the presence of
enolase and proton-extruding
metabolic inhibitors, and at a wide
adenosine triphosphatase (ATPase),
range of temperatures. Fluoride
inhibits effectively the carbo hydrate
uptake is increased at low external
metabolism of acidogenic oral
pH and fluoride can be accumulated
bacteria, including the uptake of
in the cell against a fluoride
sugars 7 3 .
gradient. Fluoride diffuses into the
cell as hydrofluoric acid which has a
pKa of 3.15. The lower the external Inhibition of enolase, proton-
pH, the more HF is formed and the extruding ATPase and sugar
more HF diffuses into the cell. transport
Because cells, such as the oral Enolase is an enzyme for one of
streptococci, normally maintain a the reaction steps in the glycolytic
higher internal pH than the out side pathway. This reaction yields
+
pH, HF dissociates in the cell into H phosphoenolpyruvate, which is
important for the transport of sugars. external ratio of the products and an
Enolase is sensitive to fluoride and to active transport of protons by
acidification of the cytoplasm. membran associated proton-extruding
ATPase, which is energized by ATP
In intact metaboliz ing cells, the
hydrolysis. The proton-extruding
addition of fluoride at pH 7.2 and 5.8
ATPase of a variety of oral bacteria
resulted in the rapid increase of the
can be inhibited by fluoride.
intracellular level of the substrate of
enolase and a reduction in the level of Sugars like glucose are
the reaction product, phosphoenol- actively transported across the cell
pyruvate 6 . membrane and are chemically
modified in this process. This
As an alternative explanation
transport mecha nism is called the
for the inhibition of the glycolytic
phosphotransferase transport system.
pathway in the presence of fluoride,
The energy for this system is derived
Marquis proposed the cytoplasmatic
from the high energy phosphate bond
acidification, occurs when HF enters
of phosphoenolpyruvate, which was
the cell. Enolase, other enzymes of
the product of the enolase-mediated
the glycolytic pathway, and the sugar
reaction. By a cascade of reactions
transport system are sensitive to
the phosphate is transferred to a
cytoplasmatic acidification.
membrane protein enzyme II, which
is then activated to transport the
The end products of the
sugar. A final step in this transport
glycolytic breakdown are actually
process involves the transfer of the
formed inside the cells. Without
phosphate to the sugar with
regulation this leads to a rapid
regeneration of the original enzyme
intracellular acidification to pH
II. The phosphorylated sugar, once
values at which all cellular processes
released into the cell, cannot reattach
for maintenance and growth stop. Oral
to the enzyme II, which ensures that
streptococci maintain a high internal
the active transport is unidirectional.
pH above the external pH by two
When the enzyme enolase is inhibited
processes: the efflux of the acid end
by fluoride, or by acidification of the
products depending on the internal-
cytoplasm, intracellular levels of the cell. Because the glycolytic

phosphoenolpyruvate (PEP) drop. breakdown that yields energy as ATP
These low levels of PEP reduce the has priority above glycogen stor age,
capacity of the sugar phosphotrans - reduced uptake of sugar by fluoride
ferase transport system and results in less intracellular
subsequently the uptake of the sugar. polysaccharide formation (Fi g 9.6) .
At around environmental pH
5.5 sugars may also be transported in
symport with protons. Once the sugar
has entered the cell, it is
phosphorylated. The influx of protons
is mediated by the proton motive
force. The proton motive force
depends on the ApH and the
electrochemical gradient across the
cell membrane. The ApH dissipates as
a result of the acidification of the
cytoplasm when HF is taken up in the
cell. Fluoride may also dissipate the
electrochemical gradient by extruding
K + from the cells. Both fluoride-
mediated dissi pations reduce the Fig 9.6: Effect of fluoride on oral microflora
activity of proton motive force-driven
sugar transport mechanisms.
When there is an excess of FLUORIDE APPLICATIONS
sugar available oral bacteria may

store phosphorylated sugar as a The mainstay of caries
glycogen, known as intracellular prevention and remineralization
polysaccharide . When the uptake of revolves around the delivery of
sugar is blocked by fluoride there is fluoride, either in a systemic or
less phosphorylated sugar available in topical form. Systemic fluoride is
considered to be important, but has posteruptive period of enamel

less of an effect on demineralization maturation (topical effect).
and remineralization than topical
forms of fluoride. McKay stated, in a review on
water fluoridation as late as 1952, that
SYSTEMIC FLUORIDES “it is not necessary to continue the
Mechanism of action use of fluoridated water after the
Systemic fluoride provides a enamel has been calcified”. However,
low concentration of fluoride to the some authors (Klein, 1946; Russell,
teeth over a long period. It circulates 1949 a, 1949b) had previously
through the blood stream and is demonstrated an effect of the post-
incorporated into developing teeth. eruptive consumption of fluoride.
After teeth erupt fluoride contacts Later, Backer Dirks et al. (1961) and
teeth directly through salivary Marthalar (1967) confirmed this
secretions. At the time of teeth observation and drew attention to the
eruption, the enamel is not yet fact that the pre-eruptive effect would
completely calcified and undergoes a be lost unless fluoride was also
posteruptive period, approx. 2 years consumed post-eruptively. Lemke et al
in length during which enamel (1970) found that after
calcification continues. Throughout discontinuation of water fluoridation,
this period called the period of enamel the caries incidence of children
maturation there is a continued increased to the level of those in the
accumulation of fluoride as well as non-fluoridated area in a period of 4
some other elements in the more to 6 years. This provided strong
superficial portions of enamel. This support for post eruptive effect.
fluoride is derived from the saliva as In vitro studies revealed that
well as from the exposure of teeth to the reduction in enamel solubility by
fluoride-containing water and food. pre-eruptive incorporation of fluoride
Thus most of the fluoride incorporated is small. (Newesely 1972). It is
into enamel occurs during the pre- therefore unlikely that the ability of
eruptive period of enamel formation fluoride to produce a decrease in the
(i.e. systemic effect) and the rate of enamel dissolution when
incorporated into the apatite lattice, fluoridation i.e. the addition of

mainly as fluoridated hydroxyapatite, fluoride to public water supplies.
plays an important role in the
observed caries reduction (Harsen, Unfortunately fluoridation is
1973; Fejerskov et al, 1981). It is not available to all individuals; not
now believed that the effectiveness of every community for example has a
fluoride is due to its presence in the public water supply. Systemic fluoride
aqueous phase during enamel can be obtained through dietary
dissolution and that it acts in three fluoride supplements in these
different ways situations.
a) Inhibition of demineralization
b) Enhancement of Optimal fluoride concentrations and
remineralization climatic conditions
c) By effects on bacteria In order to determine the
(Tencate and Duijisters, 1983; amount of fluoride that should be
Theuns, 1986) added to water, Galagan and
Vermillion (1957) developed an
The best effect is achieved if empiric formula for estimating the
fluoride is available from birth but amount of daily fluid intake based on
about 85% of the greatest reduction is body weight and climatic conditions,
obtained when fluoride consumption using the mean annual maximum daily
starts between ages 3 and 4. air temperature as follows:
The effect of systemic fluorides ppm F = 0.34/E where,

is primarily systemic (preeruptive) but E = -0.038 + 0.0062 x Temperature of
they have little topical effect the area in o F.
(posteruptive) also. In the above formula, 'E' is the
estimated daily water intake of
WATER FLUORIDATION children in oz/lb of body weight.
The most common form of
systemic fluoride administration is Richards et al (1967) made a
comprehensive study of temperature
and water fluoridation and the developing countries, where caries is

appearance of dental fluorosis. In this increasing sharply, centralized water
study, the cut-off point in determining distribution system, which is the
acceptable fluoride levels in water crucial requirement for community
supplies was the absence of moderate water fluoridation, is often lacking
fluorosis. Since no moderate fluorosis even in densely populated urban areas
were detected in areas with a water and they are rarely found in rural
supply containing 1.1-1.3ppm of areas.
fluoride and with a mean temp. of
18 o C, it was suggested that Milk and Salt –Alternative Methods
communities with mean annual of Systemic Fluoridation
temperature of 18.3 o C or lower should Since in India about 70% of the
consider this concentration of fluoride population lives in areas devoid of
as optimal. central piped water supply, it becomes
imperative to look for other dietary
Temp. in o C Recommended ppm agents which can be possibly utilized
< 18.3 1.1 – 1.3 for systemic fluoridation.
18.9 – 26.6 0.8 – 1.0
> 26.7 0.5 – 0.7 Different dietary components
have been tried as alternatives to
Limitation of community water water fluoridation in order to provide
fluoridation continued systemic ingestion of
The crucial requirement for fluoride viz. fluoridated salt, milk
community water fluoridation is a flour, vitamin tablets etc.
well established, centralized piped
water distribution system. To
appreciate the global importance of SALT FLUORIDATION
caries prevention and the potential of The impetus for introducing
water fluoridation it should be fluoridated salt was in Switzerland for
remembered that approximately 50% the first time in 1955. Concentration
of the world's population reside in the of fluoride in salt ranged from 90mg
rural areas. Unfortunately, in most fluoride/salt initially in Switzerland
to 200-350 mg/kg salt in Columbia, children and its consumption can be

Spain and Hungary. confined to groups who need it most,
but practically this method does not
Feasibility in India seem to be viable and feasible because
Salt fluoridation appears to be a of the following facts:
viable and feasible method of fluoride a. In India, majority of the
ingestion systemically because its children population living in rural
distribution can be easily monitored and urban areas could not afford
as the supply can be effectively milk daily and moreover there does
controlled especially for those areas not exist a central milk supply
which do not need supplemental system in these areas.
fluoride i.e. endemic fluoride belts. b. Variation of intake and
Moreover individual monitoring is not quantity of milk is another factor
required as the levels are so adjusted which cannot be controlled since it
so as to provide optimum levels of depends upon the socio-economic,
fluoride keeping in view the fact that religious and ethnic factors.
on an average an individual consumes
5-8gms of salt per day. Dietary Fluoride Supplements
Fluoride supplements were first
Moreover the cariostatic introduced in the late 1940's and were
effectiveness equals that provided by intended as a substitute for
fluoride in water when fluoride fluoridated water for children in non-
content of the salt is adjusted (259mg fluoridated areas.
per salt) so as to provide urinary
fluoride excretion levels similar to The most common method of
those associated with optimal fluoride systemic, or dietary, supplements are,
content of water. 1. Fluoride drops
with/without vitamins.
MILK FLUORIDATION 2. Fluoride tablets
Though theoretically milk with/without vitamins.
fluoridation is advantageous, in
addition to being the staple food for
3. Lozenges intended to be most widely used dental products in

sucked slowly or permitted to home and in dental offices.
dissolve slowly in the month.
4. Oral rinse supplements Topical fluorides may be
(swished and swallowed) applied by dental health personnel in
dental offices or clinics or may be
Dosage for fluoride supplements self-applied. In general, high-fluoride
Fluoride tablets are comer- concentration agents are applied
cially available as NaF tablets of professionally and low-fluoride
2.2mg, 1.1mg and 0.55mg yielding concentration agents or products are
1mg, 0.5mg and 0.25mg fluoride resp- applied by the individuals themselves.
ectively. Neuromuscular coordination Topically applied fluorides do not
necessary for swallowing solids is not increase the fluoride concentration of
fully developed until about 16 to 18 enamel greatly; rather, they tend to
weeks of age. Therefore for children provide local protection at or near the
under this age and upto 2 years, drops tooth surface by incorporating and
are preferable mode of fluoride concentrating fluoride in plaque and
administration. For best topical the oral mucosa. This fluoride serves
effects, fluoride tablets should be first as a reservoir of available fluoride
chewed and then swallowed. ions. During a cariogenic challenge,
fluoride from these sources is
The daily recommended dose of mobilized to as sist remineralization.
fluoride, for a child below 2 years is
upto 0.5 mg, between 2-3 years is 0.5- Mechanism of action
0.7mg and above 3 years is 1.0mg to
Moreno and Margolis, 1988;
1.5mg.
Carey et al., 1986) showed under
TOPICAL FLUORIDES
resting or fasting conditions, dental
Introduction plaque fluid is supersaturated with
Topical fluorides for the respect to calcium phosphate. When
prevention of dental decay are the dental plaque is exposed to topical
fluoride agents, such as mouthrinses
and dentifrices, which contain to enamel mineral. In the presence of

relatively low concentrations (from increasing concentrations of fluoride,
200 to 1000ppm) of fluoride, fluoride the solution becomes more highly
can diffuse into the plaque fluid and saturated with respect to fluoridated
(temporarily) increase its ion activity hydroxyapatite, thus accelerating the
with respect to fluoridated hydroxy- redeposition of mineral in the form of
apatite. Concentrations of 0.1 to 2ppm fluoridated hydroxyapatite phases
of fluoride have been shown within the partially dissolved enamel
(Varughese and Moreno, 1981) to surface. Consequently, under appro-
accelerate the rate of seeded crystal priate conditions, the net rate of
growth of fluoridated hydroxy- mineral loss is reduced, giving rise to
apatites. Thus, the enhanced fluoride formation of subsurface lesions when
ion activity within resting plaque enamel is exposed to solutions which,
fluid will increase the driving force in the near absence of fluoride,
for mineral deposition; this can occur resulted in formation of cavitations.
either within, a partially demin- When the rate of deposition of
eralized enamel surface, resulting in fluorapatite exceeds the rate of
remineralization of the tooth transport of ions out of the enamel
structure, or within plaque itself, surface, enamel demineralization is
creating fluoridated mineral de posits. effectively inhibited 2 7 .
Thus, free fluoride pro vided by
topical application can, foster the Other possible mechanisms
remineralization of incipient lesions. include
1. Antimicrobial effect via
inhibition of bacterial metabolic
In solutions undersaturated with
pathways following diffusion of
respect to enamel, the transport of
hydrogen fluoride into bacteria.
ions (Ca, P) out of the enamel
2. Desorption of bacteria from
surface, resulting in an incipient
hydroxyapatite and reduction in
dissolution, will occur at a given rate.
bacterial adherence to
This rate is function of the degree of
hydroxyapatite.
saturation of the solution with respect
3. Elevation of plaque pH Ca 1 0 (PO 4 ) 6 (OH) 2 + 20F -

indirectly and limiting the action ↓
of streptococci mutans and 10CaF 2 + 6HPO 4 3 - + 2OH -

lactobacilli.
The reaction involves the
4. Reduction in caries
breakdown of the apatite crystal into
susceptibility of recently erupted
its fluoride and calcium ions to form
teeth and root surfaces, via post-
calcium fluoride and a net loss of
eruption maturation.
phosphate ions from treated enamel.
5. Fluoride - releasing preventive
Newer fluoride systems incorporate a
and restora tive materials.
means to prevent such phosphate loss.
The term topical fluoride
therapy encompasses the use of The nature of the reaction
fluoride rinses, dentifrices, pastes, products is markedly influenced by a
gels and solutions that are applied in number of products, including
various manners. fluoride concentration, the pH of the
solution, and the length of exposure.
FLUORIDE SOLUTIONS For example, the use of acidic
In 1941 began the era of topical fluoride solutions with fluoride
fluorides when the first clinical study concentrations of 100ppm or less
of NaF was carried out by Bibbly resulted primarily in the formation of
using a 0.1% NaF solution. fluorapatite, while higher fluoride
concentrations resulted in the
While it was initially postulated formation of calcium fluoride. Since
that the effectiveness of topically topical applications of sodium
applied sodium fluoride was due to fluoride involve the use of 2.0%
the formation of a solutions ( slightly over 9000ppm), it
fluorohydroxyapatite, subsequent follows that the use of these solutions
investigations indicated that the involves essentially the formation of
primary reaction product involved the calcium fluoride.
transformation of surface
hydroxyapatite to calcium fluoride. The second fluoride compound
developed for topical use during the
1950s was stannous fluoride, SnF 2 . 1. If the pH of the fluoride system

Compared to that of sodium fluoride, were made acidic to enhance the
the reaction of stannous fluoride with rate of reaction of fluoride with
enamel is unique in that both the hydroxyapatite and
cation (stannous) and the anion 2. If phosphoric acid were used to
(fluoride) react chemically with increase the concentration of
enamel components. phosphate present at the reaction
site, it should be possible to obtain
Ca 1 0 (PO 4 ) 6 (OH) 2 + 19SnF 2 greater amounts of fluoride
H ydroxyapat i t e S t an n ous deposited in surface enamel as
F lu ori de
fluorhydroxyapatite with minimal
↓ formation of calcium fluoride and
minimal loss of enamel phosphate.
10CaF 2 + 6Sn 3 F 3 PO 4 + SnO.H 2 O
C al ciu m S t an n ou s F lu oro H ydrat ed
F lu ori de ph osph at e Ti n oxi de
On the basis of this chemical
reasoning, APF systems were
The formation of stannous developed and shown to be effective
fluorophosphates prevent, at least for caries prevention.
temporarily, the phosphate loss typical

of sodium fluoride applications. Ca 1 0 (PO 4 ) 6 (OH) 2 + F -
↓
A third topical fluoride system
was developed during the 1960s CaF 2 + Ca 1 0 (PO 4 ) 6 (OH.F) 2
known as APF, acidulated phosphate Fl u oroh ydroxyapat i t e
fluoride. This system was developed

The primary chemical reaction
by Brudevold and coworkers in an
product with all three types of topical
effort to achieve greater amounts of
fluoride systems (i.e. NaF, SnF 2 and
fluorhydroxyapatite and lesser
APF) is the formation of calcium
amounts of calcium fluoride
fluoride on the enamel surface.
formation.
They concluded that
The amount of CaF 2 formed is a topic applications of fluoride will

direct function of the fluoride have to be done 5 .
concentration in the method. That is,
more CaF 2 is formed immediately
Cax(PO4)Y
following a 0.2% NaF mouth washing
Cax(PO4)Y
than with a 0.05%.
CaF2 pH
CaF2 + YPO4 + xCa
Upon application of fluoride to pH
Cax(PO4)Y
the tooth, a CaF 2 layer is formed on it. FLUORIDE VARNISHES
Immediately after that, saliva Ca and The topical fluoride solutions
P ions deposit on the CaF 2 forming a (NaF,SnF 2 ,APF in aqueous form)
protective coat of calcium phosphate currently in use have a major
[Ca x (PO 4 ) y ] which revests the calcium disadvantage that they remain in
fluoride and diminishes its contact with teeth under in vivo
solubilization in the oral medium. conditions for a very short time i.e. 5-
When the patient ingests sugar, the pH 10 minutes before getting diluted by
in the plaque is reduced (pH↓) saliva and consequently can exert
dissolving the Ca x (PO 4 ) y layer and relatively a superficial effect on the
exposing the CaF 2 which, partly dental enamel. Baud and Bang (1970)
solubilized, liberates F into action, in their in vitro investigation showed
whereby demineralization is reduced fluoride penetration at an average
and remineralization is activated in depth of 50µm after 4 minutes
the enamel. As soon as a normal pH is application of APF (1.23%), however
regained (pH↑), whatever CaF 2 was prolonging the application time to 72
left is again coated with Ca and P, hours, increased the penetration to
being now ready to participate in the about 170m. Prolonging the
new de- and remineralization cycle. In application time does not only
this way, the CaF 2 works as a increase the penetration of fluoride in
continuous fluoride reservoir to enamel but results in a more bound
control the caries process. That means form of fluoride as well. A second
the greater the risk of caries an drawback with topical fluoride
individual has, the more frequent solutions is that soon after application
much of the acquired fluoride possibly ability to inhibit caries is far less than
representing the unreacted F- and duraphat.
CaF 2 leaches away (Melberg 1966,
Brudevold 1967, Brnet al 1973). Arends and Schutof (1975)
According to Brudevold most of the showed that silane fluoride of
loss may occur within first 24 hours. Fluorprotector reacts with water to
produce considerable amount of
Consequently, for prolonging hydrofluoric acid (HF) which
contact time with teeth, the use of penetrates into enamel more readily
-
fluoride containing varnishes in caries than F . The probable reaction being
prevention has become the treatment R-SiF 2 OH + H 2 O = R-Si(OH 3 ) + 2 HF
of choice. The two most commonly suggesting a possible mechanism of
used varnishes are Duraphat (NaF greater F - deposition. Koritzer and
varnish containing 2.26%F) in organic Levy (1979) suggested that
lacquer and Fluorprotector (Silane fluorosilanes enhance retention and
Fluoride with 0.7%F). They have a penetration of fluoride in enamel by
high fluoride concentration and also utilizing enamel network as a conduit.
have the ability to adhere to the The fact that Ca dissolution is reduced
enamel thereby extending the fluoride more with Duraphat than
exposure time to several hours Fluorprotector suggests that part of
forming a depot from which fluoride fluoride deposited after treatment with
is slowly released 1 9 . Fluorprotector may be in some form
other than the bound form i.e.
Fluorapatite (Seppa – 1983).
According to Arends, in 1980
Fluorprotector Vs Duraphat fluoroprotector, a highly viscous
A perusal of literature shows varnish penetrates the porosities of
that inspite of lower F content in enamel forming tags 0.5-1.0µm long
Fluorprotector as compared to which it act as a fluoride reservoir
duraphat, the F deposited in enamel is accounting for more fluoride
twice as more and on the contrary its deposition in enamel. On the other
hand these tags further block the
pathways for fluoride and do not let 6Ca 5 (PO 4 ) 3 F + 2CaF 2 + 6Ca 3 (PO 4 ) 2 +10H -
remineralization of initial lesions A part of CaF 2 so formed in low
occur explaining the less caries concentrations further reacts with
inhibition. An additional factor may hydroxyapatite crystals.
be a chemical alteration of enamel by
the presence of silane agent. 2Ca 5 (PO 4 ) 3 OH + CaF 2
↓
Duke and Forward (1978) 2Ca 5 (PO 4 ) 3 F + Ca(OH) 2
suggested that the strongly acidic
conditions produced by reaction However a major part of CaF 2
between silane fluoride and oral fluids gets dissolved in oral fluids and is
enhances the formation of CaF 2 and lost in less than a week time after
this forms an adherent precipitate on application.
and within the enamel which leads to FLUORIDE TOOTHPASTES
slow release of fluoride to the deeper Toothbrushing with a fluoride
layers. toothpaste is by far the most common
form of caries control in use today.
Mechanism of Action of Duraphat
This method of using fluoride is the
Duraphat is NaF varnish with
simplest and most rational way of
neutral pH. When applied topically
combatting caries in individuals of all
under clinically controlled conditions,
ages. It com bines the mechanical
a reservoir of F - ions gets build up
effect of toothbrushing on cariogenic
around the enamel of teeth. From
plaque with delivery of fluoride to the
this, fluoride keeps on slowly
plaque-tooth interface.
releasing and continuously reacting
In clinical trials of fluoride
with the hydroxyapatite crystals of
toothpastes during 1945-1985 nearly
enamel over a long period of time
all tested products contained about
leading to deeper penetration of F - and
1000 ppm fluoride (0.1% F = 1 mg F/g
formation of fluorapatite. The
paste). This concentration of fluoride
reactions involved are
has been achieved by adding one of
10Ca 5 (PO 4 ) 3 OH + 10F -
the following four fluoride salts:
↓ sodium fluoride (0.2% NaF), sodium
monofluorophosphate (0.76% Studies with SnF 2 did not

Na 2 PO 3 F), stannous fluoride (0.4% show good results. The explanation
SnF 2 ) or amine fluoride. for this may lie in the instability of
the stannous fluoride salt which is
Sodium fluoride toothpastes
subject to hydrolysis with time,
Toothpastes containing sodium
resulting in formation of a variety of
fluoride have been compared with
complex ions. Stannous fluoride
placebo pastes during 1945-1985. The
toothpastes have now been abandoned
first four studies (1945-1961) used
because these toothpastes caused
toothpastes in which the abrasive
brown staining of the teeth and
component of the toothpaste was
metallic astringent taste.
calcium carbonate or calcium
orthophosphate and none of these
Amine Fluorides
studies showed a caries reducing
Experiments showed organic
effect of the products tested. In 1961,
fluorides to have antibacterial and
Ericsson produced evidence which
antisolubility properties which were
showed that in products containing
superior to inorganic fluorides
calcium salts, the fluoride from the
(Muhlemawn et el, 1957; Marthaler,
highly soluble so dium fluoride reacts
1961).
to produce insoluble cal cium fluoride.
Torrild and Ericsson (1965) sub -
Only a few trials have been
sequently tested a new toothpaste
reported. The results were
formulation where the conventional
encouraging but the last trial which
calcium-based abrasive was replaced
was conducted in the USA gave
by sodium bicarbonate. This study
negative results and the possible
demonstrated, for the first time, a
toxicity of the compound has been
statistically significant reduction in
questioned.
caries increment over a 2-year period
as a result of using a sodium fluoride
Monofluorophosphate toothpastes
toothpaste.
The basic incompatibility of the
NaF and SnF 2 compounds with
Stannous fluoride toothpastes
calcium abrasives leading to
decreased available fluoride has been is released at the solution crystal

overcome with the introduction of interface by means of hydro!ysis and
MFP. this fluoride reacts with hydroxy-
apatite to form fluorapatite.
Monofluorophosphate denti-
frices are considered to be more PO 3 F 2 + H 2 O → H 2 PO 4 + 2F -
advantageous than SnF 2 and NaF Ca 1 0 (PO 4 ) 6 (OH) 2 + 2F -
because MFP has a neutral pH (6.5) H ydroxyapat i t e
compared to SnF 2 (4.8). It has greater
↓
stability to oxidation and hydrolysis
Ca 1 0 (PO 4 ) 6 (OH.F) 2
than SnF 2 providing it a greater shelf
Fl u oroapat i t e
life and no staining of teeth.
The second mode of action

When calcium containing
(Ingram et al., 1972) attributes the
abrasives are used sodium
anticariogenic activity due to MFP as
monofluorophosphate is the fluoride
such and it may exchange with
of choice. Sodium monofluoro-
phosphate groups in the apatite
phosphate holds the fluoride ions in
crystals and this reaction is not
complex form, which prevents their
competitive of fluoride. According to
reacting with the abrasive. The mono-
Hodge et al, 1980, MFP contains 1%
fluorophosphate ion releases free
NaF as impurity, so anticaries activity
fluoride when it hydrolyzes on
may be due to NaF.
exposure to phosphatase enzymes
naturally present in the mouth. Increased dentifrice fluoride
Mechanism of action concentrations
According to Ericsson, 1963, In an effort to achieve increased
MFP is deposited in the crystalline cariostatic activity with fluoride
lattice and in subsequent intra- dentifrices, a number of studies have
crystalline transposition, fluoride is been conducted using fluoride
released and replaces the hydroxyl concentrations greater than the
group to form fluorapatite. Gron et original 1000ppm.
al., (1971) postulated that fluoride ion
In 1984 Buhe et al. reported a and 1500ppm fluoride. Conti et al

comparison of the cariostatic benefits (1988) reported significantly (22%)
of dentifrices containing about 1000 greater cariostatic activity associated
and 1500ppm fluoride as Na 2 P0 3 F and with use of a dentifrice containing
observed significantly greater 1500ppm fluoride. Simi larly, Fogels
benefits with the elevated-fluoride et al. (1988) observed a significant
dentifrice. Stephen al. (1988) (14%) anticaries superiority with a
compared the cariostatic activity of a formulation containing 1500ppm
series of hydrated alumina dentifrices fluoride. On the basis of these
containing Na 2 P0 3 F at fluoride studies, the American Dental
concentra tions of 1000, 1500, and Association accepted the superiority
2500ppm. Results indicated that of a dentifrice containing 1500ppm
increasing fluoride levels resulted in fluoride as Na 2 P0 3 F over a similar
significantly greater car iostatic formulation containing this
activity; as compared with the compound at 1000ppm fluoride.
conventional amount of 1000ppm
fluoride. Increased fluoride It is apparent that increasing
concentrations of 1500 and 2500ppm the concentration of fluoride in
resulted in benefits of about 8% and dentifrices above the conven tional
19%. Similarly, Triol et al. (1987) 1000ppm level results in a modest,
compared the effects of dentifrice but statistically significant, increase
containing dicalcium phosphate as in cariostatic benefit. This effect
the abrasive system and Na 2 P0 3 F at occurs with both Na 2 PO 3 F and NaF
fluoride concentrations of 1000, containing dentrifices. However
1450, and 2000ppm. In creased caution should be exercised in the use
fluoride concentrations of 1450 and of elevated fluoride dentrifices,
2000ppm produced significantly particularly in preschool-age
greater cariostatic benefits of 8% and children 6 4 .
13%, respectively. Two additional
studies compared the effects of Decreased dentifrice fluoride
hydrated silica dentifrices containing concentrations
Na 2 P0 3 F at concentrations of 1000
Because of widespread toothpastes is to reduce total fluoride

unsupervised fluoride dentifrice exposure in pre-school children in
usage and the potential for these order to reduce the risk of
preparations to increase the preva - development of dental fluorosis.
lence of fluorosis through inadvertent Although fluoride toothpaste are
ingestion, several inves tigators have intended for topical application, it is
evaluated the cariostatic activity of estimated that almost 50% of the
dentifrices containing reduced fluoride from a denti frice is ingested
fluoride concentrations. These studies by 2-3 year olds. Fortunately, the
have evaluated formulations amount decreases with age, reaching
containing either Na 2 P0 3 F or NaF. 25% in 6-7-year-olds.Assuming that
the average amount of dentifrice used
With regard to sodium fluoride, per brushing is 0.5g and that children
Reed (1973) studied the cariostatic brush on average twice daily with a
activity of dentifrices containing 250, dentifrice containing 1000ppm
500, and 1000ppm fluoride and fluoride, fluoride ingestion through
observed that the benefits were toothpaste can be substantial.
directly related to dentifrice fluoride Ingestion of fluoride from toothpaste
content. Koch et al. (1988) reported alone can exceed rec ommended daily
significantly less (26%) cariostatic dosage for young children and
activity with a dentifrice containing represents a major contribution to
250ppm fluoride (as NaF) compared their total fluoride intake 4 3 .
with the use of a 1000ppm fluoride Reducing the amount of
formulation. dentifrice may also be an efficient

way to maintain efficacy while
Overall, the results of low decreasing the risk of fluorosis.
fluoride studies support the

hypothesis that there is an inverse Dentifrice placed in a
relationship between fluoride transverse relation to the bristles of
concentration in a toothpaste and the toothbrush and not in a
caries increments. The main argument longitudinal direction is commonly
for lowering the fluoride content of recommended. Villena in 2000
evaluated a method of placing tooth and is taken up by the enamel as

dentrifice in a transverse relation to fluoroapatite, calcium fluoride or
the bristles (TT) and compared it to even free fluoride. Rinsing the mouth
the standard (longitudinal) tech nique after brushing rapidly drops the
used (ST) and to the "pea size" (PS) salivary fluoride concentra tion to 1
and concluded that TT could be ppm or less within 15 minutes 8 .
recommended for young children to However, the treat ed tooth enamel,
decrease the amount of fluoride and perhaps the oral mucosa, acts as a
dentifrice dispensed, minimizing sink for fluoride and, subsequently,
inadvertent dentifrice ingestion and releases it to the oral cavity.
the risk of developing dental
fluorosis. In the same study, it was Analyses of saliva show that
also reported that the PS varies with fluoride concentrations during the
individual whereas TT was easy to be long periods between brush ing range
standardized 5 4 . between 0.02 and 0.08ppm. During
these intervals, this residual fluoride
Recently dentrifrice tubes with promotes the transfer of calci um and
different orifices (moon shaped) are phosphate ions from saliva into the
produced in order to reduce the enamel and helps in remineralization.
amount of the dentrifrice dispensed.
Fluoride Toothpaste and root caries
In these ways, use of fluoride The etiology and pathogenesis
dentifrice will continue to be an of root and coro nal caries are similar.
important caries preventive tool, Thus fluoride should be considered
while minimizing its role in the fundamental to the control of root
etiology of dental fluorosis. caries as well as enamel caries.
Amount of fluoride after Studies done by Nyvad and

toothbrushing Fejerskov in 1986 have shown that
Most toothpastes avail able toothbrushing with a fluoride
contain about 1100ppm fluo ride. dentifrice can convert active lesions
During a typical one-minute brushing to inactive lesions.
period, fluoride rapidly permeates the
Use of fluoridated dentrifrice is

effective for the prevention of root Compounds used for
surface caries. Fluoride applications mouthrinsing are Sodium fluoride,
should be restricted to maintenance, Stannous fluoride and Acidulated
recall visits rather than at extensive phosphate fluoride. Sodium fluoride
scaling, root planning and surgical (NaF) mouthrinses are usually
visits that involve significant soft formulated at concentration of either
tissue manipulations. This is because 0.2% sodium fluoride (900ppm F) for
fluoride solutions may impede healing weekly use or 0.05% sodium fluoride
of the periodontal tissues. In (225ppm F) for daily use. These rinses
particular, application of fluoride are intended to be used by forcefully
should be avoided during root swishing 10ml of the liquid around
preparation in open flap surgery, as the mouth for 60 seconds before
this may damage the healing ability of expectorating it.
the periodontal tissues 4 8 .
FLOURIDE MOUTHRINSES
The frequent use of low
The Rational Use of Topical
concentration of fluoride is more
Fluoride
cariostatic than less frequent use of
For that patient with low caries
higher concentration fluoride for
activity, or in whom it is kept under
topical applications. The topical effect
control, high fluoride frequency and
of fluoridated water in addition to its
low concentration methods would
systemic effect is the best way of
suffice, such as fluoridated water,
providing frequent applications to
fluoride supplements or fluoridated
teeth. In those areas, where water
tooth paste.
fluoridation is not possible or has not
been implemented, the fluoride mouth
In cases where greater caries
rinses have been found to be an
activity or risk exist, low fluoride
effective tool in prevention of dental
concentration and high frequency
caries. The use of a fluoride
methods (toothpastes) are combined to
mouthrinse was first described by
high fluoride concentration and high
Bibby et al in 1946.
frequency methods (mouthrinses). associated with silicate cement

Consequently the association of restorations. Silicate cement is the
fluoridated toothpastes and daily oldest material to be identified as
0.05% NaF mouthrinses become caries preventive, a property
effective for the control of caries in conferred by the material's fluoride
those who wear orthodontic brackets, content.
representing high risk patients. As the
patient stops presenting active caries Amalgam
lesions, the use of fluoride is cut By the mid-1970’s some
down. Mouth rinsing should than be fluoride-releasing amalgams were
discontinued, and the fluoridated commercially available in Europe
tooth paste (or fluoridated water) (Forsten, 1976). While the initial
maintained. release of fluoride of amalgam was
found to be significant, the material
More rigorous caries control was found to be release only minor
measures will have to be adopted in amounts after 1 week.
the case of high caries activity or risk,
applied to those patients who, on Tveit and Gjerdet in1981 found
account of diseases, radiotherapy, or that the total amount of fluoride
the use of certain drugs, have a low released into solution was highest for
salivary secretion. They would need a silicate cement samples followed by
more frequent professional plaque the glass ionomer and was lowest for
control, besides greater frequency of the amalgam. This difference was due
topical fluoride applications. to the very large starting content of
fluoride available from both silicate
FLUORIDE RELEASING DENTAL cement and glass-ionomer samples
RESTORATIVE MATERIALS when compared to the amalgam.
For many years , there has been Forsten (1990) also found the total
a need for restorative materials to fluoride release from glass ionomers
contain caries-preventive elements . to be greater than from fluoride-
In 1940s, dentists observed that containing amalgams. These results
secondary caries were rarely were supported by studies on
restorations in extracted teeth where Protection is conferred on the enamel

glass ionomer gave the better of the crown for some distance from
protection against demineralization the restoration.The influence of
than fluoridated or unfluoridated fluoride is found in a zone of
amalgam (Valenzuela and others, resistance to demineralization which
1994). is at least 3mm thick around a glass-
ionomer restoration (Kidd, 1978:
Glass-Ionomer Cement
Hicks et al., 1986: Hotz, 1979:
The concept of combining the
Wesenberg and Hals, 1980).This
strength, rigidity, and fluoride-release
favourable result has been attributed
properties of silicate cements with the
to the release of fluoride from the
biocompatibility and adhesive
cement and its movement into
qualities of polyacrylic cements led to
adjacent enamel.
the introduction of glass-ionomer
cements to the dental profession in the
early 1970’s (Wilson and Kent, 1972; Source and mechanism for fluoride
Wilson and McLean 1988). release
Glass-ionomer cements are the The source of fluoride ions
best known fluoride-releasing from glass-ionomer cements are
materials and like silicates, have been calcium fluoride (CaF 2 ), strontium
shown to have anticariogenic
fluoride (SrF 2 ), sodium hexaflouro-
properties due to their significant
release of fluoride (Muzynski and aluminate (Na 3 AlF 6 ), and aluminium
others, 1988; Benelli and others fluoride (AlF 3 ) inclusions of the low-
1993); the uptake of fluoride in cavity
temperature glasses used to formulate
walls (Wesenberg and Hals, 1980),
the powder components .The primary
enamel and plague (Benelli and
role of these fluorides is to lower the
others, 1993); and the enhanced
glass fusion temperature during the
reprecipitation of calcium and
manufacturing process, although they
phosphate promoted by the fluoride
also improve handling properties and
release (Wesenberg and Hals 1980).
increase cement strength and
The spread of caries is arrested at the
translucency. In fully set cements,
restoration/ cavity wall margin.
fluoride is located in the partially inverse of the square root of time

degraded glasses that form the glass (Wilson et al., 1985; Kuhn and
core and in the polysalt matrix, Wilson, 1985). Substantial amount of
primarily in the form of aluminium fluoride are taken up by enamel,
complexes. When a fully set glass- dentine and cementum in cavity walls
ionomer is exposed to neutral aqueous adjacent to the cement and become
solutions, it absorbs water and resistant to acid attack (Maldonado et
releases ions such as sodium, calcium, al., 1978: Wesenberg and Hals,1980
Retief et al., 1984; Shimokobe et al.,
silica and fluoride. Of the total
1987).
amount of fluoride in the set cement,
only a small fraction is available for
The chemical composition and
release .This is not related to the total
type of mixing are the main factors
fluoride content, but depends on the
affecting the kinetics of fluoride
amount of the sodium that maintains
release. Studies have shown that
cement electron neutrality after
cements with lower powder-to-liquid
fluoride release. Only the fluoride
ratios demonstrated greater fluoride
present in the matrix is available for
release. McKnight - Hanes and
elution at neutral conditions. The fact Whitford (1992) also found that the
that the fluoride released from release rate of fluoride in a glass
conventional product is mostly sodium ionomer cement was inversely
fluoride, along with the observation proportional to powder-to-liquid ratio
that this is not a critical salt for the used to prepare experimental disks.
formation of polysalt matrix, explains Hand mixed glass ionomers have been
the lack of anticipated weakening of shown to release significantly less
the material following fluoride fluoride than mechanically triturated
release 1 . glass ionomers (Miller and others
1995). All of these studies
The mechanism of fluoride demonstrate the importance of
release is complex, but it is dominated establishing well-defined material
by a diffusion mechanism where the preparation and handling procedures
rate of release is proportional to the
to produce optimal and consistent early release but stabilized after two
fluoride release. weeks to comparable low release
levels of 0.16 µg/mm 2 to 0.42µg/mm 2
The varnishing of disks made of material. Creanor in 1994 found the
from glass ionomer materials has been same effect. After 60 days, the
found to sharply reduce fluoride concentration of fluoride released had
release, while finishing varnished slowed from 15.3 -155.2µg/ml at day
disks produced a significant increase 1 to 0.9-3.99µg/ml.
in the fluoride release. (McKnight–
Hanes and Whitford 1992). Likewise, A significant increase in
Kupietzky (1994) found a significant fluoride release is observed at low pH
reduction in fluoride release from values, suggesting that an erosive
glass ionomer restorations covered mechanism is activated at these
with a sealant. This finding is conditions from the preferential
important when considering that the dissolution of the glass particles in
objective of coating an ionomer to the matrix. A study done by P
provide protection during maturation Karantakis, M Helvatjoglou, S
may be counterproductive to the Theodoridou, Papadogiannis in 2000
subsequent fluoride release 1 0 . showed significantly greater amount
fluoride release in lactic acid as
Amount of fluoride release compared to water or artificial
All glass ionomers have been saliva 3 4 . In several vitro studies,
shown to have a burst effect, releasing demineralization and reminerali-
considerably more fluoride in vitro zation cycles were performed to better
soon after restoration placement than simulate intraoral pH fluctuations.
later (Forsten 1994). DeSchepper in Carvalho and Cury in1999 compared
1991 found that glass ionomer fluoride release in pH cycling media
cements released the greatest with deionised water and artificial
proportion of their cumulative total saliva. The specimens were immersed
fluoride in the first 24 hours after 6 hours in demineralizing solution
mixing. The fluoride levels varied for (pH4.3) and 18 hours in
different types of ionomers during this remineralizing solution (pH 7.0). The
greatest amount of fluoride was 1994), and with fluoride rinses and
released in pH cycling solution and fluoridated dentifrices in the
lowest in saliva. When nonstimulated remineralization of incipient enamel
human saliva was used as an caries (Donly 1994: Hatibovic-
immersion medium, a significant Kofman and Koch 1991). The
reduction in the fluoride release mechanism of this synergy is thought
occurred which was mainly attributed to be recharging effect, where
extrinsic fluoride is deposited back
to the adsorption of HPO 4 2 - and
into the ionomer, resupplying the
saliva protiens onto material surfaces
release from the ionomer into the
in the form of pellicle inhibiting
surrounding environment.
11
fluoride release .
Remineralization of Adjacent Hard

Another factor governing Tissues
fluoride release is its concentration in The fluoride uptake of hard
the immersion solution. In the dental tissues adjacent to glass-
presence of an inverse fluoride ionomer materials has been considered
concentration gradient, glass- a fundamental factor for inhibition of
ionomers may absorb fluoride from secondary caries attack.
the environment and release it again
under specific conditions. Thus, the To evaluate the perfomance of
concept of fluoride recharging old the fluoride released from glass-
glass-ionomer fillings was introduced, ionomer restorations under simulated
in vitro evidence for which supports conditions of secondary caries attack,
the theory that such interactions are a series of artificial caries
feasible through an ion exchange experiments was conducted and
process. Glass ionomers may have showed that the frequency and extent
synergistic effects when used with of lesions was reduced around glass-
extrinsic fluorides (Creanor and ionomer restorations in the vitro
others 1995), including topical APF (Dionysopoulos, Kotsanos, Papa-
(acidulated phosphate fluoride) dogiannis, Konstantinidis in 1998) 1 4 .
treatments (Kupietzky and others The reduction in the extent of the
outer lesion, which is considered to Fluoride release from four

resemble primary caries, was bands of resin-modified glass-ionomer
attributed to the diffusion of fluoride cement over 11-month test period was
ions through the artificial caries found to be comparable to that from a
medium, whereas the reduction in the chemically cured glass-ionomer
depth of the wall lesion was attributed (Forsten 1995). These resin-modified
to the low solubility of the cavity materials were also found to posses
walls to the hydrogen ion diffusion the fluoride recharging capability
gradient set at the interface, due to previously demonstrated in
fluoride release and uptake unmodified ionomers. Caries
procedures 3 6 . inhibition for resin modified glass
ionomer was also demonstrated on
Resin - Modified Glass Ionomer extracted teeth and found to be
Cement comparable to a conventional ionomer
Resin-modified glass ionomers cement (Dunne and others 1996) 2 5 .
have been in use for several years, Metal Reinforced Glass Ionomer
and have found popularity both as Cements
restorative materials and as cement Glass ionomer cements can
for crowns and fixed prostheses. They be reinforced by physically incorpo-
contain about 80% glass ionomer and rating silver alloy powder with glass
about 20% resin. The fluoride release powder referred as silver alloy
from hybrid ionomer comes from the admixed or by fusing glass powder to
aluminosilicate glass constituent that silver particles through sintering
is dissolved by the acid present in the called cermet. Amalgam alloy
mixture. They do not require a admixed cements were found to
bonding agent for proper retention. release higher or equal amounts of
They have a natural bond to dentin by fluoride to those of conventional
means of a calcium carboxylate ion
glass-ionomers due to increased
bond. The direct contact between the
microporosity, which increases the
hybrid ionomer and the tooth structure
effective surface area for release. For
causes high amount of fluoride to be
silver cermet cements, in which silver
released into tooth structure.
particles are sintered to glass
particles, the effective contact area between the acidic functional groups
between the glass particles and within the matrix and silicate glass
polyalkenoic acid is reduced, leading particles. It is the acid-base reaction
to a reduction in fluoride release, induced by water absorption that
especially during the initial elution eventually sustains fluoride release.
period . Study done by Erik Asmussen and
Anne Peutzfeldt in 2002 showed that
Compomer fluoride release from compomer was
The search for a material that relatively small initially but the rate
has the fluoride-releasing capability of release increased significantly after
of conventional glass ionomer and the a number of months when sufficient
durability of composites has led to the water had been absorbed into the
introduction of polyacid-modified material to make acid-base reaction
composite, or compomer. This take place to appreciable extent 1 8 .
material has a structure and physical
properties to those of composites. It Because of the absence of water
also has the ability to release fluoride in the formulation, the cement mixture
and it undergoes an acid-base reaction is not self-adhesive like conventional
in the presence of saliva. GIC and resin modified GIC. Thus a
separate dentin-bonding agent is
It consists of silicate glass needed for compomers used as
particles, sodium fluoride and restoratives. The bonding agent
polyacid - modified monomer without reduces the amount of fluoride that
any water. It is sensitive to moisture, can penetrate into the dentin.
so it is often packaged in a moisture However, compomers release
proof pouch. Setting is initiated by significant amount of fluoride from
photo-polymerization of the acidic their external surfaces into the oral
monomer that yields a rigid material. environment.
During the service life of the
restoration, the set material begins to The recharging ability in the
absorb water in the saliva that glass-ionomer cement and compomer
contributes the acid-base reaction is dependent on the glass component
of the material and in particular upon The pre-reaction can involve only
the structure of hydrogel layer around the surface of the glass particles
glass filler particles following (called surface pre-reacted glass
reactions between the glass and ionomer or S-PRG) or almost the
polyacid component. The acid-base entire particle (termed fully pre-
reaction is more extensive in glass- reacted glass ionomer or F-PRG).
ionomer cements and this results in a Giomers are similar to compomers and
more well-defined matrix layer in resin composites in being light
these materials than in the compomers activated and requiring the use of a
in which the acid-base reaction plays bonding agent to adhere to tooth
only a small part in the overall setting structure.
process. Hence, the greater recharging

Toshiyuki Itota, Thomas
ability of the glass-ionomer cement
Carrick, Masahiro Yoshiyama, John
may be due to an ability of fluoride to
McCabe in 2004 showed that giomer
temporarily reside in the hydrogel
released more fluoride than compomer
layer which is more prevalent in this
or composites. Giomer contains a
material than in the compomers 7 2 .
flouridated glass filler with a glass-
Giomer
ionomer matrix layer, but this glass
Giomers are combination of
filler has a significantly thicker
glass ionomers and composites. They
hydrogel layer which has been made
have properties of both glass ionomer
by almost complete reaction with acid
(fluoride release and recharging) and
to form a substructural glass-ionomer
resin composites (excellent esthetics,
matrix layer before incorporation in
easy polishbility, biocompatibility)
the resin matrix. This glass-ionomer
Giomers are distinguished by the fact
matrix contains much complexed
that, while they are resin-based, they
fluoride and is easily penetrated by
contain pre-reacted glass-ionomer
water resulting in a significant
(PRG) particles. The particles are
fluoride release from this material.
made of flourosilicate glass that has
Hence, it is likely that the extent of
been reacted with polyacrylic acid
the hydrogel matrix of the glass filler
prior to being incorporated into resin.
incorporated into the materials affects release from this material is

the amount of fluoride released. predominantly related to dissolution
of the glass filler to release fluoride
Composites salts. On the other hand, compomer,
The release of fluoride from contains a strontium-flouro-silicate
composite resins has been postulated glass filler in which a thin layer of
to protect against secondary caries in glass-ionomer matrix has been formed
enamel and dentin. Fluoride releasing on the surfaces of the glass particles
composite has been shown in vitro to by reaction of glass with acid which is
inhibit enamel demineralization present in the resin matrix.
(Arends and Vander 1990; Arends,
Ruben and dijkman, 1990; Dijkman Adhesive Primers
and Arends 1992). Donly and Gomez Kerber and Donly (1993)
(1994) have also demonstrated the studied the effect on demineralization
remineralizing effects of a fluoride- of adding ammonium fluoride to two
releasing composite. Their results different dentin primers. Results
showed a statistically significant area showed that primers containing
reduction in the body of artificial fluoride demonstrated significantly
caries like lesions exposed to the less demineralization 0.25mm from
fluoridated composite at 2-week and the dentin margins of experimental
3-month intervals, as compared with restorations than control primars
restorations composed of a resin without the fluoride.
containing no fluoride. Toshiyuki
Itota, Thomas Carrick, Masahiro Orthodontic Bonding Materials
Yoshiyama, John McCabe in 2004 Decalcification has always been
showed that composite released less a problem during orthodontic
fluoride than either giomer or treatment with fixed appliances. Early
compomer. Composites contains in the history of fluoride-releasing
flouro-alumino-silicate glass, but this restorative materials it was suggested
glass has not been reacted with acid that bracket bonding agents that
and therefore it has no glass-ionomer release fluoride could supply the
matrix layer. It is likely that fluoride
component to the tooth area most 24 hours and 1 week, the study
prone to decalcification. showed that more than 2 µg/ml of
fluoride was still being released from
Underwood, Rawls and the fluoride adhesive after 6 months.
Zimmerman (1989) demonstrated the Wiltshire and Janse van Rensburg
durability and caries inhibition (1995) also reported a burst effect
potential of a fluoride exchanging from two light-cured orthodontic
resin for orthodontic adhesion. The adhesives, with one adhesive releasing
first fluoride containing commercial measurable fluoride for 22 days and
orthodontic bonding composite was the second adhesive continuing to
introduced in the late 1980’s. It was release fluoride at a level of 0.5µg/ml
found to release only very small for upto 85 weeks. They concluded
amounts of fluoride. that fluoropatite formation resulting
from fluoride release from the tested
Glass ionomer based materials adhesives could be more advantageous
have generally been found to release in reducing decalcification during
more fluoride than resin based fixed appliance treatment than other
materials (Chadwick and Gordan preventive measures.
1995a). Oggard and others (1992),
while investigating the cariostatic Glass-ionomer cement was also
potential in vivo of a visible light- investigated in the late 1980’s for its
cured composite adhesive for bonding potential as a fluoride releasing
orthodontic brackets, determined that orthodontic bonding material.
the regular use fluoride toothpastes Hallgren, Oliveby and Twetman,
was insufficient to inhibit lesion (1990) found a significant increase in
development around orthodontic salivary fluoride concentration the
brackets. The study showed that the day after cementation of brackets with
fluoride adhesive reduced lesion glass-ionomer cement. However, after
depths by about 48% over the non 7, 14, and 28 days, salivary fluoride
fluoride adhesive control. Although a levels were not satistically different
burst effect peaking at a fluoride from baseline values.
content of 8µg/mL occurred between
Fischer-Brandies and others evaluation period, beginning at a level

(1991) measured the fluoride content of 3.5µg/ml on the first day and
of enamel in vitro after bonding declining at a level of 0.41µg/ml on
orthodontic fixtures with glass- the last two days. This same product
ionomer cement. A rise of more than was clinically compared to a
120% in enamel fluoride was observed conventional glass-ionomer sealant,
after the first 10 days, and a where it was found that retention of
saturation value was reached after 40 the fluoride-releasing resin was much
days. The fluoride penetrated more higher and caries incidence much
than 20µm in to the surface of the lower than the glass ionomer (Rock
enamel and more than 3mm laterally and others 1996).
from the edge of the cement.
Hicks and Flaitz (1992) studied
The efficacy of using glass- surface lesion depth and progression
ionomer cement as a bracket bonding around in situ class V preparations
matrial has been confirmed in other restored with glass ionomer, fluoride-
studies (Hallgren, Oliveby and releasing composite sealant and
Twetman 1993). While most studies conventional sealant materials. They
have shown that glass ionomers found that the glass ionomer provided
inhibit demineralization, one has the greatest degree of caries
shown remineralization in protection: 7.5% of the specimens had
demineralized enamel adjacent to enamel lesions, while the
glass ionomer bonded orthodontic conventional sealant group had 17.5%
bands 1 6 . of the specimens with caries like wall
lesions. In another in vitro study
Pit and Fissure Sealants (Jensen, Garcia – Godoy and Wefel,
A fluoride containing composite 1990), a fluoride-releasing pit and
sealant (fluoroshield, LD Caulk/ fissure sealant was found to
Dentsply) was introduced in the late substantially reduce the amount of
1980’s. Cooley and McCourt in 1990 enamel demineralization adjacent to
evaluated it in vitro and found it to the material, compared with a
release fluoride over a 7 day conventional sealant. Seppa and Forss
(1991) found that fissure sealed with a rate of release (DeSchepper and
glass-ionomer sealant were more others, 1990; McCourt, Cooley and
resistant to demineralization than Huddleston, 1990; Cooley and
were unsealed controls, even after McCourt, 1990; Horsted-Bindslev and
macroscopic sealant loss. They Larsen, 1991;Garcis-Godoy and
suggested that the result may be the others, 1990). Most of these studies
combined effect of fluoride release found that some brand released more
and residual material in the bottom of fluoride than others and that the long-
the fissure. term release varied over a range of
0µg/ml to 7µg/ml.
Liners/ Bases and Cavity Varnishes
Cavity liners/ bases, Glass-ionomer cements have
particularly calcium hydroxide also been used as a liner material
materials, are routinely used to under amalgam restorations. They
provide pulpal protection under deep have been shown to contiue releasing
restorations. Varnishes may also be mesurable amounts of fluoride in the
used in shallow cavities or to range of 0.3µg/ml to 1.1µg/ml after
supplement liners in deep cavity one year (Garcia-Godoy and chan,
preparations. 1991), and to reduce artificial
recurrent caries in vitro when placed
Fluoride-releasing liners have under amalgam restorations (Garcia-
been found to significantly reduce Godoy and Jensen, 1990). A light
lesion areas under amalgam -cured and a chemically cured glass-
restorations, as compared to amalgam ionomer cement liner were found to
alone or two layers of copal varnish have a similar effect in inhibiting
and amalgam (Jensen and others, demineralization, and both demon-
1990). Most have been found to have strated significantly less demin-
a burst effect in the release of eralization than a non fluoride
fluoride, with the largest proportion releasing control liner (Souto and
of total fluoride release occuring in Donly,1994).
the first days or weeks of a study,
followed by dramatic reduction in the
Factors Influencing Remineralization - Saliva
of exposed tooth surfaces to

SALIVA
cariogenic attack, therefore
decreasing the likelihood of demin-
Saliva has a critical role in the eralization and favoring repreci-
prevention or reversal of the caries pitation of organized mineral
process. It provides calcium and components (remineralization) into
phosphate that maintain super- the previously demineralized enamel
saturation of calcium in the plaque and root surfaces 7 0 .
fluid; proteins and lipids that form a
protective pellicle on the surface of Several salivary proteins like
the tooth; antibacterial substances and statherin, histatins, cystatins bind
buffers. The saliva components hydroxyapatite and aid in the
neutralize the acids produced by maintenance of the supersaturated
bacterial metabolism in the plaque, state of saliva. This allows calcium
raise the pH and reverse the diffusion and phosphate containing mineral
gradient for calcium and phosphate. components to remain in solution at
Thereby, they return calcium and the resting pH of saliva (approxi-
phosphate to the surface lesion where mately 7.0) and avoid removal by
these ions can regrow new surfaces on precipitation out of solution. These
the crystal remnants that were salivary proteins release calcium and
produced by demineralization. These phosphate ions when levels drop in
remineralized crystals form a veneer the saliva. Not only do these salivary
of much less soluble mineral. Saliva components maintain calcium and
also clears carbohydrates and acids phosphate suspended within the
from the plaque 2 0 . saliva, but they also increase the
Saliva and Remineralization stability of the mineral phases within
Calcium and phosphate in saliva exposed tooth surfaces. The
Saliva is supersaturated with concentration of various components
calcium and phosphate with respect to secreted by the glands is closely
hydroxyapatite. The presence of related to its flow rate. Increasing the
calcium, phosphate and fluoride rate of salivary flow by stimulation
within saliva enhances the resistance increases the concentration of
calcium, bicarbonates and proteins cavity (about 1ml) indicate that

like statherin but phosphate ions do fluoride from the ductal saliva is not
not increase in proportion to flow normally an important source of
rate 5 0 . fluoride in plaque or plaque fluid.
However following topical application
Fluoride in Saliva of fluoride in the form of
The fluoride content of saliva is mouthrinses, tooth paste, or any other
low (0.03ppm) 6 0 but can be increased fluoride vehicles, there is a 100- or
by fluoride intake (systemic fluorides) even 1000-fold increase in salivary
and topical application of fluorides. fluoride concentration depending on
the fluoride concentration of the
The concentration of salivary fluoride agent. This high concen-
fluoride from the parotid and tration of fluoride in saliva falls
submandibular/ sublingual glands is rapidly. Depending on the concen-
about two-thirds of the plasma tration and type of fluoride agent, the
fluoride concentration. In subjects saliva fluoride concentration is
living in a low fluoride area, the reduced to a few ppm within an hour,
saliva fluoride concentration is less and within the next 3-6 hours returns
than 1µm/l. The fluoride concen- to the baseline level.
tration in whole saliva is related to
the fluoride excreted from the glands, Saliva is in direct contact with
dietary fluid intake and topical the plaque fluid and plaque, a transfer
fluoride applications. The resting of fluoride from saliva to plaque or
saliva fluoride level is influenced by plaque fluid may occur during or
the fluoride concentration in the immediately after mouth rinsing.
drinking water and also by regular When the mouth rinse is spat out, the
daily use of a fluoride dentifrice/ concentration of fluoride decreases
mouthrinse. and saliva again becomes less
important as a source of plaque
The low concentration of fluoride.
fluoride and the small volume of
resting saliva present in the oral
Saliva and its Antibacterial salivary buffering capacity.

Properties Individuals with a resting salivary pH
Antibacterial properties of of approx. 7.0 tend to have low caries
saliva do not have any direct effect on activity or no caries; while those with
demineralization and remin- a resting pH of 5.5 have very high
eralization of tooth structures but caries experience. Those with pH
reducing the number of bacteria helps values between 5.5 and 7.0 have less
in reducing the decrease in pH caused severe caries activity 3 2 .
by acids produced by bacteria.
Salivary substances like lysozyme, Bicarbonate is the major
lactoferrin, salivary peroxidase and buffer in saliva and its concentration
secretory immunoglobin A have direct increases as salivary flow increases.
bacteriostatic or bactericidal effects. The greater the acidity, the more
Glycoproteins like mucins promote likely demineralization of the tooth
clearance of bacteria from the oral surface is to occur. A reduction in
cavity by masking the bacterial salivary flow leads to a corresponding
surface adhesion molecules and reduction in buffer capacity with
inhibiting bacterial colonization of important implications on dental
the mucosa and exposed tooth plaque pH and caries susceptibility.
surfaces. Other buffers present in saliva include
urea, which is metabolized by plaque
Saliva as Buffering Fluid urease, resulting in the release of
The importance of saliva as ammonia and an increase in plaque
buffer depends largely on its ability to pH. Some urea originates from the
control the reductions in pH resulting gingival crevices, however human
from bacterial action on metabolic parotid saliva contains up to 9mg/dl
substrates found in dental plaque. under stimulated conditions. Other
Saliva has significant buffering buffer sources include proteins that
activity and it varies from patient to can generate alkaline substances. One
patient. The resting pH of saliva tends such class of proteins is the arginine-
to predict the caries experience of the rich protein group, which on
individual and also is an indicator of metabolism generates arginine and
ammonia. Phosphate is likely to be

important as a buffer only at
unstimulated flow rates. A protein
called pH rise factor/ sialin and other
basic proteins allow a more rapid
return to neutral pH following an
acidic challenge 2 1 .
Other Salivary Factors

Pellicle, which arises from
saliva, provides a high level of
protection against an acid challenge.
It acts as a physical barrier to
diffusion of acid ions into the tooth,
as well as to the movement of
dissolution products from apatite out
of the tooth. It may also inhibit
mineralization of apatite to form
calculus from the supersaturated
levels of calcium and phosphate ions
in saliva. On the other hand, pellicle
indirectly promotes demineralization
by forming a base for adhesion of acid
producing microorganisms and
development of dental plaque.
Salivary flow and oral clearance

rate influence removal of food debris
and microorganisms.
Factors Influencing Remineralization – Miscellaneous Factors
MISCELLANEOUS FACTORS agents. Sugarless gums chewed after

eating have been recommended as a
Remineralization is the means of boosting salivary flow
replacement of lost mineral mainly (Leach, Lea and Edger in 1989) 4 0 .
calcium and phosphate in the partially Stimulated saliva contains a higher
demineralized regions of the carious concentration of alkaline buffers than
lesions of enamel and dentin. Passive unstimulated saliva, thereby
transport of calcium and phosphate neutralizing plaque acid more rapidly.
ions down the concentration gradient Stimulated saliva also provides high
from saliva and plaque into the body concentration of calcium ions 3 1 . A low
of the lesion are the main driving pH leads to mineral loss from the
forces for remineralization. Thus it is enamel surface. It follows that the
the increase in oral fluid calcium and more rapidly the pH rises following a
phosphate that drives the remin- meal, the sooner mineral loss will
eralization process. The major short- stop and remineralized would be
coming of currently available fluoride initiated 3 5 . This higher pH can
toothpastes, mouthrinses and topical increase tooth mineral saturation
applications is the fact that their during a challenge and thus decrease
ability to remineralize enamel is demineralization.
limited by the low concentration of

calcium and phosphate ions available Increase calcium and phosphate
in the saliva 3 . concentration in the oral environment

can also increase tooth mineral
Therefore, remineralization can saturation in oral fluids (Ashley and
be enhanced by providing low levels Wilson in 1977; Vogel et al in 1990;
of calcium and phosphate, in Margolis and Morena in 1992).
conjugation with minimal amounts of Therefore, an increased anticaries
fluoride. Mouthrinses, dentrifices, effect might be anticipated from the
chewing gums and candies are release of these ions during chewing
potential delivery vehicles for calcium of gum fortified with appropriate
and phosphate. Chewing gums are calcium phosphate minerals. Chewing
considered to be potential anticaries gums can produce a significant
increase in salivary and plaque gum) and tricalcium phosphate

calcium and phosphate levels over a fortified gum was used immediately
15 minute period (Chow and others in after the sucrose intake, an increase in
1995). These results suggest that plaque fluid pH was observed by both
chewing gums and possibly candies gums. However, the fortified gum also
can be effective vehicles for the produced a large increase in plaque
delivery if calcium and phosphate fluid calcium phosphate levels, which
because they can produce an elevated together with the pH increase,
mineral saturation level for a longer completely eliminated the acidic
period than that can be produced by a change. The ion activity product was
rinse or dentifrice application. maintained at the same level as in the
resting plaque. It may be concluded
Studies of candies and gums that while chewing an ordinary gum
fortified with the calcium phosphate immediately after a sucrose intake
dihydrate have not demonstrated raised plaque pH, the use of calcium
clinical efficiency (Richardson et al in and phosphate releasing gum
1972; Ashley and Wilson in 1977; completely neutralized the acid
Rankin et al in 1989). This failure has challenge 7 5 .
been described to the low solubility of
Casein phosphopeptide-Amorphous
this mineral at neutral pH and the
calcium phosphate (CPP-ACP)
correlated difficulty of inducing a
An interesting development in
calcium phosphate plaque reservoir
the delivery of calcium and phosphate
from an insoluble source. (Vogel et al
ions to the oral cavity has occured
in 1988). Recently, it was demon-
over past few years. In 1981,
strated (Vogel et al in 1988) that when
Professor Eric Reynolds at the School
an acidic gum is used to increase the
of Dental Sciences at the University
solubility of a calcium phosphate
of Melbourne in Australia showed
additive (α-tricalcium phosphate) a
milk, milk concentrates, powders and
substantial increase in plaque fluid
cheese have antiocariogenic activity
and saliva calcium and phosphate
in animals and in situ caries models.
concentration could be attained. In
Further research showed that the
this study, when the control (sugarless
anticariogenic properties of milk were
due to the casein phosphopeptides. the CPP stabilize and localize ACP at
They showed that these peptides can the tooth surface, thereby buffering
actually bind calcium and phosphate plaque pH, depressing enamel
and keep them in a soluble, demineralization and enhancing
amorphous state. Normally, adding remineralization. Recent in vitro
calcium and phosphate together will experiments (Reynolds, 1997) have
result in the formation of insoluble shown that CCP-ACP solutions
calcium phosphate crystals. But in the promote remineralization of enamel
presence of CPP, this doesn't happen subsurfaces lesions. In these
and the calcium and phosphate stay in experiments, a 1.0% w/v CCP-ACP
a form that can actually penetrate into solution produced 63.9% remin-
the tooth enamel and repair areas that eralization of enamel sub-surfaces
have been damaged by demin- lesions over a 10-day period 6 1 .
eralization.
Recently, Slien et al (2001)
have shown that 18.8mg and 56.4mg
Incorporation of CPP-ACP in mouth
of CPP-ACP in a sugar-free chewing
rinses and chewing gums
gum enhanced remineralization of
In a human in situ enamel
enamel subsurface lesions in situ by
demineralization study, a 1.0% w/v
101% and 151%, respectively, when
CPP-ACP solution used twice daily
compared with the control sugar-free
produced a 51% reduction in enamel
gum not containing CPP-ACP.
mineral loss caused by frequent sugar-
solution exposure (Reynolds, 1998).
The twice daily use of the 1.0% CCP- Incorporation of CPP-ACP into
ACP solution resulted in a 144% Glass-ionomer Cement
increase in calcium level and 160% The CPP-ACP have been shown
increase in the inorganic phosphate to interact with fluoride ions to
level in the plaque recovered the produce an additive anticariogenic
removable intra-oral appliance effect through the formation of a
(Reynolds, 1998). These results stabilized amorphous calcium fluoride
suggested an anticariogenic phosphate phase (Reynolds et al.,
mechanism for the CPP-ACP where 1995; Reynolds, 1998). The CPP-ACP
in the GIC also increases microtensile reservoir of soluble calcium

bond strength of GIC by the phosphate ions capable of diffusing
incorporation of the CPP-ACP into subsurface enamel and promoting
nanoparticles into the cross-linked remineralization.
matrix of the GIC. In this study,
fluoride release was significantly CPP are responsible for not
higher from the CPP-ACP containing only the stabilization and water
GIC than from the control GIC. It is solubility of ACP but also the
possible that the CPP-ACP promoted incorporation of ACP into plaque by
the release of fluoride ions from the binding to bacteria cell surfaces and
GIC by forming casein phospho- onto adsorbed macromolecules on the
peptide-amorphous calcium fluoride tooth surface. The immuno-
phosphate (CPP-ACP) nanocomplexes localization study revealed that CCP
(Reynolds, 1998) which were released were bound to the surfaces of
from the cement matrix 4 7 . bacterial cells as well as to the
intercellular matrix. However, some
Mechanism of Action bacterial species were intensely
The casein phosphopeptides are stained at the cell surface, suggesting
multiphosporylated peptides derived a high affinity of the CPP for
from enzymatic digestion of casein molecules on the surfaces of some
from cow's milk. Through the multiple bacterial species. The bacterial cell
phosphoseryl residues, the CPP binds contains both hydrophilic and
to form nanoclusters of ACP, hydrophobic molecules on its surface
preventing their growth to the critical (Rose et al., 1997). The CPP
size required for nucleation and phase molecules also contain hydrophilic
transformation. (Reynold, 1998) Thus, and hydrophobic regions, and it is
CPP inhibit the transformation of possible that binding to the bacterial
amorphous calcium phosphate into cell surface is mediated by Ca 2 + cross-
crystalline phases (Holt and Van linking of the negative charges on the
Kemenade, 1989) such that they peptide and the cell surface molecules
should not directly promote calculus (e.g., phosphoryl and carboxylate
formation but instead provide a plaque groups) as well as by hydrophobic and
hydrogen-bond-mediated interactions. other oral care products and the use of

the CPP-ACP technology in other
This efficient incorporation of
applications are expected to follow in
the CPP-ACP nanocomplexes into
coming years.
plaque, where the CPP carrying the
stabilized nanoclusters of hydrated
Xylitol
ACP bind onto bacterial cell and
Xylitol is naturally occurring,
intracellular matrix macromolecules
low–calorie sugar substitute not
localizes the bioavailable calcium and
fermented by oral microorganisms.
phosphate ions at the tooth surface 5 7 .
Chewing xylitol containing chewing
Products Available gums helps indirectly in preventing
A complex of casein demineralization by its effects on
phosphopeptides and amorphous streptoccus mutans in the oral
calcium phosphate (CPP-ACP) is environment. Bacteria become tolerant
called Recaldent. to xylitol and are able to grow in the

presence of increase concentration of
Recaldent has been introduced xylitol yet do not ferment xylitol into
as an ingredient in Trident White, tooth damaging acids. Xylitol tolerant
Trident for kids, Recaldent by Trident bacteria adhere less well to tooth
and Recaldent for kids chewing gums surfaces and produce less acid than do
in USA, Europe, and Japan. Chewing xylitol sensitive bacteria 4 5 . Also, the
sugarless gums containing Recaldent effect of xylitol may be non specific
for 15 minutes or longer allows and may be the result of increased
optimal dispersion of the Recaldent salivary flow by chewing xylitol
complex through the oral cavity. gum 2 4 . Thus decreased lactic acid
Recaldent is also the main ingredient production by streptococcus mutans
of "GC Tooth Mousse". and increased salivary flow results in
GC Tooth Mousse is water based, increased buffering of plaque acids
sugar free crème that can be applied and enhanced clearance of sugars
to patients teeth. from mouth. To maximize the caries

preventive effects, habitual xylitol
The addition of Recaldent to gum chewing should be started at
least one year before permanent teeth

erupt 1 3 . Study done by Sintes and
Augusto et al in 2002 showed that a
dentrifice containing 0.836% sodium
monofluorophosphate in a dicalcium
dehydrate base plus 10% xylitol was
effective in caries prevention better
than a similar dentrifice without
xylitol 3 3 .
De Re Mineralization – The Balance
Conclusion
CONCLUSION
There is a delicate balance

between health and disease, involving
acid arising from bacterial laden
plaque competing with protective
factors that are provided through
normal salivary flow and good
hygiene. In most individuals, there are
numerous acid challenges daily as
fermentable carbohydrates are
ingested and the struggle between the
pathological factors and the protective
factors takes place. The balance
between demineralization and
remineralization is the key to
progression or reversal of caries at
any time. The balance can be used to
assess the risk of an individual
developing caries in the future, to
determine why the individual has
caries now, or to drive a preventive or
interventive program for the
individual. At any time, the direction
of the caries balance can be tipped
towards caries progression and
demineralization of tooth mineral or
towards repair of tooth mineral by
remineralization as a result of one or
more protective factors.
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giomer, component and resin

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Introduction and History

INTRODUCTION AND by oral bacteria. This theory

HISTORY highlights the interaction between

The phenomenon of reminerali-

prevalence of dental caries and rate of

This library dissertation

COMPOSITION OF DENTAL potassium, sodium and fluoride are

HARD TISSUES also present as described below.

Mineral composition in weight (%) 2 8

Water Water lins are rich in Glycine and Aspartic

amelogenin proteins persist in fully 

encountered are the rods or 100 – 400A0

Fig 2.3: Fish scale appearance of

enamel called TOMES Ameloblast

Crystal structure of Hydroxyapatite atoms both from the hydroxyl groups

right angles to long axis of DENTIN

between cross striations is By weight

to the dentinoenamel junction, and the HISTOLOGY OF PRIMARY

Peritubular dentin mass within mature dentin. These

has been completed. This dentin

Interglobular in greater amounts on the roof and

Peritubular protecting the pulp from exposure in

DEFENSIVE MECHANISMS OF PULP

Intertubular DENTIN ORGAN

first defensive mechanisms Eventually, the odontoblasts will pave

deposited at a daily rate of 4 µm. medium for the attachment of collagen

60% 30% 10%

Fig 2.7: Cementoenamel Junction

MINERALIZATION Matrix vesicle formation

SEQUELAE The vesicle is a small

nucleating agent for mineralization. MINERALIZATION OF ENAMEL

Fig 3.1: Heterogenous Nucleation

Because enamel protein is deposited ELECTRON MICROSCOPY OF

5. Protective stage This change in the position of

Tall, columnar cells

papilla following an organizing

the periodontal ligament of fully

Cementum formation in the

and as a new layer of cementoid is

INTERACTION BETWEEN deficiencies, if present during tooth

SYSTEMIC CONDITIONS AND formation, will adversely affect

than permanent teeth. dental hard tissues

Fluoride is most beneficial to ameloblasts and odontoblasts are

the teeth in concentrations of altered resulting in hypoplasia of

approximately 0.5 to 1ppm of water. enamel and dentin matrix.

Concentration of less than 0.5ppm Tetracycline can cross the placental

concentrations, such as 5ppm, cause foetus. Tetracycline antibiotics if

mottling and hypoplasia of enamel administered to the mother doing the

and hypomineralized dentin, with period of tooth mineralization, results

increased interglobular spaces. in staining of decidous teeth at a later

Sodium fluoride can cross the stage 4 2 .

placental barrier and is available to

consumption of fluoridated water Deficiency of vitamin A results

during mineralization of the fetal in defective enamel and dentin

teeth, results in incorporation of formation. Defectively differentiated

high resistance to dental caries. condition. There is degeneration of

Interaction between tetracycline and the epithelial derived ameloblasts,

which results in a hypoplastic enamel hypomineralization of enamel. It

density of bone trabeculae

CAUSES OF and acetic acid. The organic acids

DEMINERALIZATION produced by plaque bacteria are

caries” seen in infants who are debris and microorganisms. Decreased