dental Cariology /certified fixed orthodontic courses by Indian dental academy

CARIOLOGY

INDIAN DENTAL ACADEMY
Leader in Continuing Dental Education
www.indiandentalacademy.com

CONTENTS
• INTRODUCTION
• DEFINITION
• CLASSIFICATION
• ETIOLOGY OF DENTAL CARIES—EARLY THEORIES
CURRENT CONCEPTS
• CLINICAL FEATURES OF CARIES
• CARIES AS A SPECIFIC MICROBIAL INFECTION
• CONCEPT OF CRITICAL pH
• NUTRITION,DIET AND DENTAL CARIES
• EFFECT OF DEMOGRAPHIC FACTORS ON DENTAL
CARIES
• ROLE OF SALIVA ON DENTAL CARIES


• CARIES PROCESS—MORPHOLOGICAL AND
CHEMICAL EVENTS
• HISTOPATHOLOGY OF ENAMEL CARIES
• DENTINAL CARIES—HISTOPATHOLOGY
• ELECTRON MICROSCOPIC STUDIES OF
CARIOUS ENAMEL
• ENAMEL CARIES MECHANISM AT A
CHEMICAL LEVEL
• CONCLUSION
• REFERANCES


INTRODUCTION
• TEETH ARE TOOLS that have evolved to ensure survival
of species. Caries is a biosocial disease rooted in the
technology and economy of our society. Dental caries is
unique not only in terms of pathological mechanism ; other
aspects, social and economic , are also worthy of note. The
uniqueness of dental caries makes it a fascinating study from
a scientific standpoint. As living standards improve the
severity of disease usually increases. Dental caries
constitutes a very real personal problem to virtually every
man, woman and child. While it is true that diseases of the
teeth and their supporting tissues do not normally kill
humans they certainly affect the persons efficiency and they
can , if neglected, provoke serious conditions elsewhere in
the body. Their contribution to the general fund of human
misery is legendary

• DEFINITION
• Dental caries is defined as a
progressive, irreversible, microbial disease
affecting the hard parts of the tooth exposed to
the oral cavity ,resulting in decalcification of
inorganic constituents and dissolution of organic
components, there by leading to a cavity
formation.


• CLASSIFICATION DENTAL CARIES
A : On the basis of clinical features and patterns dental
caries may be classified according to three basic factors
1) Morphology i.e according to anatomical site of
lesions
a) Occlusal caries (pit fissure caries)
b) Smooth surface caries
Interproximal
Cervical or gingival
c) Root caries
d) Linear enamel caries ( Odontoclasia)


• 2) Dynamics i.e according to severity and rate
of progression of lesions
Based on the severity
Class 1: Very mild caries
Class 2: Mild caries
Class 3: Moderate caries
Class 4: Severe caries
Class 5: Very severe caries


• 3) Chronology i.e according to age patterns
at which lesions predominate
a) infancy caries
b) Adolescent caries

4)Based on the graphical representation of
pathway of dental caries it is classified into
1) Forward decay
2) Backward decay


• 5. Based on treatment and restoration design
( Therapeutic classification) – G.V. Black classified into
a) class 1 Pit and fissure cavities of posterior teeth, the
occlusal two- thirds of buccal and lingual surface of
molars, lingual surface of maxillary incisors.
b)class 2 cavities seen on proximal surface of posterior
teeth
c)class 3 cavities seen on proximal surfaces of anterior
teeth which do not involve the incisal angle
d) class 4 cavities seen on proximal surfaces of anterior
teeth that involve the incisal angle
e) class 5 cavities seen on gingival third of facial and
lingual surfaces of all teeth
f) class 6 cavities seen on incisal edges of ant teeth and
occlusal cusp heights of posterior teeth

e) based on carious surfaces involved, it is classified into
1 simple[1surface]
2 compound [ 2 surface]
3 complex [3 or more surfaces]
f) based on whether the lesion is a new one attacking a
previously intact surface or whether it is occurring
around the margins of a restoration it is classified into
primary [virgin] caries
secondary [recurrent] caries
g) based on degree and rate of caries progression
1 incipient
2 arrested caries
3 xerostomia induced caries[radiation]

Early Theories of caries formation;
THE LEGEND OF THE WORM
• The earliest reference to tooth decay and toothache came from the
ancient Sumerian text known as The legend of the worm.
• It was discovered on a clay tablet, excavated from an ancient city
within the Euphrates valley of the lower mesopotamian areas which
dates from about 5000 BC.
• In Japanese the word for dental caries is Mush-ha, meaning hollow
teeth. In china the term for hollow tooth is Chung-choo.
• The early history of India, Egypt, and the writing of homer also
makes reference to the worm as the cause of toothache.
• Fumigation devices consisting of burning of leeks and hyocyamus
where used by the Chinese and Egyptians.
• An interesting therapeutic method applied by the Chinese about
2700BC for the treatment of various diseases including dental tissues
was acupuncture.
• Atleast at the subconscious level this theory survives to our day
when we refer toothache as a gnawing pain .

ENDOGENOUS THEORIES
HUMORAL THEORY
The ancient Greeks consider that a persons physical and mental
constitution was determined by the relative proportions of the
four elemental fluids of the body.-blood, phlegm, black bile,
yellow bile- which correspond to the four humors – sanguine
,phlegmatic melancholic, and choleric.
All diseases including caries could be explained by an imbalance of
these humors.
Hippocrates, the father of medicine, while favoring the concept of
humoral pathology , also referred to the accumulated debris
around teeth and to their corroding action.
He also stated that stagnation of juices in the teeth was cause of
toothache


VITAL THEORY
This theory regarded dental caries as originating
within the tooth itself, analogous to bone
gangrene.
This theory ,proposed at the end of 18th century
remain dominant until the middle of 19th
century.
A clinically well- known type of caries is
characterized by extensive penetration into the
dentin, and even into the pulp , but with barely
detectable catch in the fissure


EXOGENOUS THEORIES

CHEMICAL THEORY

Parmly[1819] rebelled against the vital theory and
proposed that an unidentified chemical agent was
responsible for caries.
He stated that caries began on the enamel surface in
locations where food putrefied and acquired sufficient
dissolving power to produce the disease chemically.
Support for chemical theory came from Robertson[1835]
and Regnart[1938] , who actually carried out
experiments with different dilutions of inorganic
acids[such as sulfuric and nitric] and found that they
corroded enamel and dentin.

PARASITIC[SEPTIC] THEORY
In 1843 , Erdl described filamentous parasites in
the surface membrane[ plaque ] of teeth.
Shortly thereafter Ficinus[1847] , a Dresden
physician, observed filamentous microorganisms,
which he called denticolae, in material taken
from carious cavities.
He implied that these bacteria caused
decomposition of the enamel and then the
dentin. Neither Erdl or Ficinus explained how
these organisms destroyed tooth structure

CHEMICO-PARASITIC [ACIDOGENIC] THEORY

This theory was proposed by W.D MILLER[1890]

Essential features of this theory
That the microorganisms of the mouth, by secretion of enzymes or
by their own metabolism , degrade the fermentable carbohydrate
food material so as to form acids.
The chief acids formed are namely lactic, butyric, acetic, formic,
succinic and other acids.
Carbohydrate food material lodged between and on surfaces of
teeth is the source of the acid which demineralises the lime salts
of the tooth.
He believed that starchy foods were more effective than soluble
sugars . Thus the enamel is destroyed by the acid of fermentation
and the disintegrated enamel is subsequently mechanically
removed by forces of mastication.


After penetration of enamel, the dissolution of dentin is
brought about in the same manner with the organisms
penetrating along the dentinal tubules.
The final breakdown of dentin results from the secretion
of proteolytic enzymes that digest the organic part of
dentin and form a cavity.
Significance of Millers observations
• He assigned an essential role to 3 factors in carious
process.
• The oral microorganisms in acid production and in
proteolysis.
• The carbohydrate substrate which microorganisms
fermented
• The acid which causes dissolution of tooth minerals


Limitations of acidogenic theory
• This theory was unable to explain the predilection of
specific sites on a tooth to dental caries . The initiation
of caries on smooth surfaces was not accounted for by
this theory . Miller, while a disciple of koch who was an
avid advocate of specific bacterial etiology of infectious
disease nevertheless worked with mixed cultures from
saliva and with techniques that did not attempt to
ascertain types of organisms present.
• Miller believed that dental caries was caused by a
multiple species of bacteria this is understandable since
many bacterial species posess glycolytic abilities. While
current evidence for a specific bacterial infection in
dental caries is tantalizing, the concept is not disputable

• This theory does not explain why some
populations are caries –free
• The phenomenon of arrested caries is not
explained by this theory.
• Miller believed that in some systemic conditions
the inorganic salts within a tooth could be
withdrawn and that the organic-inorganic bonds
would be weakened.
• He did not produce any experimental evidence
that the adult tooth is subject to such systemic
influences.
• The concept of tooth resistance while logical did
not have any experimental support

• Proteolytic theory (Gottlieb)

The surface coverings found on the tooth in
grooves and pits are organic in nature , also
enamel contains small but significant amounts of
organic materials.
These observations and the fact that carious lesions
are characterized histologically by pigmentation,
the phenomenon that was interpreted, without
evidence as being indicative of proteolysis, led to
the development of the proteolytic theory
proposed primarily by Gottlieb(1947) Frisbee and
nuckolls(1947) and Pincus(1950).

They described carious like lesions that were initiated by
proteolytic activity at a slightly alkaline ph and
conceded that the process involved depolymerisation
and liquefaction of the organic matrix of the enamel.
Gottlieb 1947 proposed that microorganisms invade
organic pathways(lamellae) of enamel and initiate caries
by proteolytic action.
Subsequently the inorganic salts are dissolved by
acidogenic bacteria.
Pincus (1950) also maintained that the initial process was
the proteolytic breakdown of the dental cuticle, the
organic membrane found on all teeth.


Limitations:
• The above conclusions were made on the basis of the
early histological observations.
• An interpretation of a molecular mechanism based on
morphological evidence is highly suspect.
• To date no one has under physiological conditions
successfully demonstrated significant loss of enamel
tissue through proteolytic activity.
• Enamel is highly structured tissue and the accessibility
of organic material to enzymatic action before
decalcification is restricted.
• Enamel can be dissolved under physiological conditions
only by demineralization with acids , chelating or
complexing agents

• PROTEOLYSIS CHELATION THEORY:

This theory proposed by Schatez et al (1955) implies a simultaneous
microbial degradation of the organic components (proteolysis)
and the dissolution of the minerals of the tooth by the process of
chelation.
The word chelate is derived from the Greek word chele’ meaning
claw, and refers to compounds that are able to bind metallic ions
as calcium, Iron, copper, zinc and other metals by the secondary
valence bonds.The resulting chelates are non ionic and usually
soluble.
According to the proteolytic chelation theory dental caries results
from initial bacterial and enzymatic proteolytic action on the
organic matter of enamel without preliminary demineralization.
Such action, the theory suggests produces an initial carious and a
release of variety of complexing agents such as amino acids,
polyphosphates and organic acids. The complexing agents then
dissolve the crystalline apatite.

Limitations:

• Less than one percent of mature enamel is organic in
nature and the suggestion that this material upon
degradation can give rise to a significant concentration
of chelator sufficient to dissolve upto 96% mineral
matter has no experimental support.
• Also there is no substantial experimental evidence that
the initial carious lesion stems from a break down of
organic matter that is due to proteolytic action.
• While proteolysis chelation is an important biological
phenomenon, its primary role in the etiology of the
dental caries has not been corroborated


Other Theories of caries etiology
SULFATASE THEORY
Pincus[1950] advanced the sulfatase theory, , whereby
bacterial sulfatase hydrolyses the mucoitin sulphate of
enamel and the chondroitin sulphate of dentin
producing sulfuric acid that in causes decalcification of
the dental tissues.
Limitations
The concentration of sulfated polysaccharides in enamel is
very small and not readily accessible as a substrate for
enzymatic degradation.
This is a highly unlikely hypothesis for the degradation of
tooth enamel.

COMPLEXING AND PHOSPHORYLATING
THEORY [LURA-1967]

It can be readily demonstrated that uptake of phosphate
by plaque bacteria occurs during aerobic and anaerobic
glycolysis and the synthesis of polyphosphates.
According to this theory , the high bacterial utilization of
phosphate in plaque causes a local disturbance in the
phosphate equilibrium in the plaque and the tooth
enamel resulting in loss of inorganic phosphate from
enamel. soluble calcium- complexing compounds
produced by bacteria cause further tooth disintegration .


LIMITATIONS:

Saliva is an abundant source of inorganic phosphate for
bacterial utilization.

Hence it is highly improbable that depletion of phosphate
in plaque by oral microbial metabolism results in
phosphate withdrawal from enamel


CURRENT CONCEPT.
Primary factors in the etiology of dental caries
(essential factors).
In the epidemiological model dental caries is due to
an inter play of three primary factors- the host,
the agent, or recruiting factor and environmental
influences.
Obviously many secondary factors influence the
rate of progression of disease.


HOST factors
Composition
Studies of the chemical composition of enamel indicate
that surface enamel is more resistant to caries than
subsurface enamel
. Surface enamel is more highly mineralized and tends to
accumulate greater quantities of fluoride, zinc, lead and
iron than the underlying enamel.
The surface is lower in carbon-dioxide, dissolves at a
slower rate in acids, contains less water and has more
organic material than subsurface enamel .
These factors apparently contribute to caries resistance
and are partly responsible for the slower disintegration
of surface enamel than of the underlying enamel in initial
carious lesions.

MORPHOLOGIC CHARACTERISTICS OF THE TOOTH
It has been suggested that morphology of tooth may influence the
initiation of caries.
The feature that predispose to the development of caries is the
presence of deep, narrow, occlusal fissures or buccal and lingual
pits.
Such fissures tend to trap food, bacteria and debris and caries may
develop rapidly in these areas.
Conversely as caries advances, the inclined planes become flattened,
providing less opportunity for entrapment of food in the fissures
and caries predisposition diminishes.
TOOTH POSITION
Teeth which are malaligned, out of position, rotated or otherwise
not normally situated may be difficult to clean and tends to favor
the accumulation of food and debris.
This in susceptible persons would be sufficient to cause dental caries

ESSENTIALITY OF ORAL BACTERIA

Microorganisms are a pre requisite for caries initiation.
A single type of organism for example enterococcus strain
is capable of inducing caries.
The ability to produce acid is a pre requisite for caries
induction but not all acid producing organisms are
cariogenic.
Streptococcus strain that are capable of inducing caries are
also able to synthesis extra cellular dextrans or levans.
Not all strains that produce extra cellular polysaccharides
are capable of caries induction.
Organisms vary greatly in their capacity (virulence) to
induce caries.

Cariogenic suitable
Bacterial + local --- organic acids
plaque substrate

organic tooth
acids + mineral ---- loss of enamel
(in plaque)

demineralized + bacterial
tooth(dentin) proteolytic ------ cavitation
enzymes


CLINICAL FEATURES OF CARIES

PIT AND FISSURE CARIES
pits or fissures with high steep walls and narrow bases are more
prone to develop caries .
Deep narrow pits or fissures favor the retention of food debris and
microorganisms, and caries may result from fermentation of this
food and formation of acid.
Early caries may appear brown or black and will feel slightly soft and
catch a fine explorer point.
The enamel directly bordering the pit or fissure may appear opaque
bluish- white as it becomes undermined. This under-mining
occurs through lateral spread of caries at the dentino- enamel
junction.


And penetrates into the dentin
along the dentinal tubules
without fracturing away the
over-hanging enamel.Thus
there may be a large carious
lesion with only a tiny point
of opening in advanced
lesions it forms a cone
shaped cavity with apex at
outer surface and base
towards DEJ


SMOOTH SURFACE CARIES
caries that develops on the proximal surfaces of
teeth or on the gingival third of the buccal and
lingual surfaces


PROXIMAL CARIES
It usually begins just below the
contact point and appears in
the early stage as a faint
opacity of enamel without
apparent loss of continuity of
enamel surface. The early
white chalky spot becomes
slightly roughened due to
superficial decalcification of
the enamel . As the lesion
advances it forms a cone-
shaped lesion with apex
toward DEJ and base towards
the enamel surface

CERVICAL CARIES
• It occurs on buccal, lingual or labial surfaces and
usually extends from opposite the gingival crest
occlusally to the convexity of the tooth surface
making the self cleansing portion of this surface.
• The typical cervical carious lesion is a crescent –
shaped cavity beginning as a slightly roughened
chalky area that gradually becomes excavated.


ROOT [CEMENTUM] CARIES

HAZEN defined root caries as- A soft, progressive
lesion that is found anywhere on the root surface
that has lost connective tissue attachment and is
exposed to the oral environment.

Enamel may become secondarily involved if it is
undermined during the progression of the lesion .

Dental plaque and microbial invasion are an
essential part of the cause and progression of this
lesion.

• This type of caries is
predominately found in
dentitions of older age
groups with significant
gingival recession and
exposed root surfaces.
• In the 50-59-year age
group almost 60% of
patients examined had
root surface lesions
[Banting and ellen-1976]


LINEAR ENAMEL CARIES[ODONTOCLASIA]

An atypical form of dental caries, called linear enamel
caries, has been observed in the primary dentition of
children, in Latin America and Asian countries.
The lesions predominate on the labial surfaces of the
maxillary teeth, in the region of neonatal zone .
This zone represents the demarcation between pre- and
post- natal enamel and is a histological feature of all
primary teeth. It is thought to result from the metabolic
disturbances associated with the trauma of birth .
More recent evidence indicates that the specific metabolic
disturbance causing the neonatal line is transient
hypocalcemia associated with transient
hypoparathyroidism- a normal feature of neonatal period.


A variant of linear enamel caries in the primary
teeth of children in the far east has been named
odontoclasia.
The morphological aspects of this type of caries is
atypical and results in gross destruction of the
labial surfaces of incisor teeth,.
This may be an inherent structural defect in teeth
resulting in a rapid carious process


RAMPANT CARIES

One of the most distressful clinical conditions for both patient and
practitioner is rampant caries in which there occurs a sudden, rapid
and almost uncontrollable destruction of teeth.
Rampant caries also involves surfaces of teeth that are ordinarily
relatively caries-free.
A caries increment of 10 or more new caries lesions over a period of
about a year is characteristic of a rampant caries attack.
Proximal and cervical surfaces of anterior teeth, including the
mandibular incisors which are relatively caries free, may be affected.
It is mostly seen in primary dentition of young children and
permanent dentition of teenagers 11-19 years.
Dietary factors affecting oral substrate and oral flora and physiological
factors affecting saliva are often significant in the development of
rampant caries.


RECURRENT CARIES
A carious lesion that develops at the inter-face of a restoration and
the cavo-surface of enamel is called recurrent caries.
It may indicate an unusual susceptibility to caries attack , a poor cavity
preparation, a defective restoration or a combination of these
factors.
ARRESTED CARIES
It has been described as caries which becomes static or stationary and
does not show any tendency for further progression.
It occurs almost exclusively in caries of occlusal surfaces and is
characterized by a large open cavity in which there is lack of food
retention and in which , the superficially softened and decalcified
dentin is gradually burnished until it takes on a brown stained,
polished appearance and is hard, this has been referred to as
Eburnation of dentin.
Another form of arrested caries is that seen on the proximal surfaces
of teeth in which the adjacent approximating tooth has been
extracted..

• XEROSTOMIA- INDUCED
CARIES[RADIATION CARIES]
• A common complication of radiotherapy of oral cancer lesions is
xerostomia.
• Such patients develop rampant dental caries and confirm the
important role of salivary secretions in the maintenance of the
integrity of teeth.
• Xerostomia is accompanied by major changes in the salivary
flow, salivary composition, salivary and serum proteins and a
shift towards a more caries-producing micro flora.
• Carious lesions appear as early as 3 months after the onset of
xerostomia and all patients may be affected irrespective of their
past caries history.
• Xerostomia may be caused by other factors than radiation like
tumors of salivary glands , auto immune diseases, anti- sialogogue
drugs , prolonged illnesses etc


INFANCY[SOOTHER OR NURSING BOTTLE] CARIES

Numerous reports by pediatricians and pedodontists
describe a rapidly progressing type of dental caries that
affects the primary teeth of children, usually during the
first 2 years of life and as early as the first year. In
children with infancy caries there is a unique distribution
of dental decay.
The 4 maxillary incisors are affected first, these teeth are
anatomically so positioned in the mouth as to be most
frequently bathed by a feeding formula.
If unchecked, the decay may extend to the maxillary and
mandibular molars. Initially the lower ant teeth may not
be involved because of the protective environment of
the mandibular salivary secretions and the cleansing
action of tongue muscles.

Infancy caries is most often seen in children with
an unusual dietary history such as an addition of
syrup, honey or sucrose to the formula or the
use of pacifier dipped in honey or other
sweeteners.
In addition to improper formula in bottle-feeding,
it has been reported that prolonged and
unrestricted night-time breast- feeding can result
in increased caries rates.
The stagnation of milk about the neck of ant teeth
and the fermentation of disaccharide lactose
contribute to the carious process.


ADOLESCENT CARIES
The acute caries attack seen at 11-18 years of age is
characterized as adolescent caries .
ITS CHARACTERISTIC FEATURES ARE:
• lesions in teeth and surfaces that are relatively immune
to caries
• Relatively small opening in enamel with extensive
undermining of enamel
• Rapid penetration of enamel and extensive involvement
of dentin
• The rapid progression of lesion which does not permit
an effective pulpal response with little or no secondary
dentin


CARIES AS A SPECIFIC MICROBIAL
INFECTION
• Definition of dental plaque:
Plaque is a specific but highly variable
structural entity resulting from colonisation of
microorganisms on tooth surfaces, restorations ,
other parts of oral cavity of salivary components
like mucin, desquamated epithelial cells, debris
and microorganisms all embedded in gelatinous
extra cellular matrix


EVIDENCE OF BACTERIAL ROLE IN
CARIES ETIOLOGY
1.germ free animal do not develop caries.
2. antibiotics fed to animals are effective in
reducing the incidence and severity of caries.
3. Totally unerupted and unexposed teeth do not
develop caries.
4. oral bacteria can demineralise enamel and dentin
in vitro and produce caries like lesions.
5. micro organism have been histologically
demonstrated invading carious enamel and
dentin. They can be isolated and cultivated from
carious lesions

PROPERTIES OF CARIOGENIC PLAQUE

The rate of sucrose consumption was noticeably higher in
cariogenic plaques.
The rate of lactic acid formation was considerably higher in
cariogenic plaques.
Bacteria in cariogenic plaques synthesized more intracellular
glycogen-amylopectin-type polysaccharides.
Upto 20% of sucrose consumed within 15 minutes was
converted into intracellular polysaccharides by cariogenic
plaque.
Cariogenic plaques formed more lactic acids from stored
intracellular polysaccharides.
Cariogenic plaques formed approximately twice as much
extra cellular polysaccharides from sucrose as did
noncariogenic plaques.
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Cariogenic plaques contained higher levels of
streptococcus mutans than noncariogenic plaques.-
Noncariogenic plaques harboured higher levels of
S.sanguis and Actinomyces than cariogenic plaques.

Noncariogenic plaques had significantly higher proportion
of dextranase producing organisms.

Noncariogenic plaques had higher levels of veilonella and
contained slightly lower concentration of lactic acids
and slightly higher con of acetic and propionic acids.


NON SPECIFIC PLAQUE HYPOTHESIS:
There is no question, dental caries is an infection.
In the past, and has an extension of miller’s chemico parasitic
theory, the total plaque was viewed as a pathogenic structure
which had to be eliminated or reduced if caries was to be
prevented.
If all plaques were similar in their potential to induce caries, the main
difference between health and disease states might be expected in
the quantitative aspects of plaque accumulation.
This possibility carries with it the implication that mechanical
debridement should be the dominant method of disease
control(loesche-1982).
Further specific anti microbial agents should be limited in their
efficacy since the accumulation or activity of the old plaque
requires suppression.

SPECIFIC PLAQUE HYPOTHESIS:

On experimental evidences it is impressive that qualitative
nature of the flora in plaque determines the metabolism
and the potential for caries production.this view is
termed the specific plaque hypothesis.
Inherit in this concept is that certain plaques are more
cariogenic than others because they contain higher
numbers of specific bacterial species that cause caries.
The species implicated in enamel caries are S. mutans and
lactobacilli and in root caries A.viscosus.


According to this hypothesis , most but not all
carious lesions are due to specific bacterial
species.
Further the hypothesis implies that plaque in some
sites is not disease- producing.
The concept of specific plaque hypothesis suggests
the development and implementation of
preventive procedures that treat dental caries as
a specific bacterial infection.


CONCEPT OF CRITICAL pH

The loss of tooth mineral during caries formation is
caused by the formation of bacterial acids which lower
the pH to the point where the hydroxyappatite mineral
of enamel dissolves.
The concept of critical pH was initially applied to indicate
the pH at which saliva was no longer saturated with
respect to calcium and phosphate ions , thereby
permitting hydroxyappatite to dissolve.
However it is now realized that the immediate fluid
environment involved in demineralization of a tooth is
not saliva but the fluid phase of plaque , now known as
‘plaque fluid.;

It has been shown experimentally that both saliva
and plaque fluid caese to be satured at Ph values
in the range of 5-6 with an average of 5.5.
The critical Ph varies in different plaques
depending mainly on the concentrations of
calcium and phosphate ions but is also
influenced by the buffering power and ionic
strength of the environment.
However it is unlikely that demineralization would
occur above 5.7 and this value has often been
accepted as being safe for the teeth


. These considerations are specially important in the
very early stages of caries when the outer enamel
is being dissolved.
As a carious lesion develops , the demineralization
occurs within the body of the lesion rather than
on the outer surface which retains a higher degree
of mineralization .
This implies that acids must diffuse into the enamel
and dissolve the apatite within the lesion .
There is good evidence that unionized lactic acid
molecules diffuse more readily into enamel.


Being uncharged , the unionized molecules
are less likely to react with apatite than
their constuient hydrogen and lactate ions.
The critical pH may therefore be the Ph at
which the environment of the enamel
becomes unsaturated and in addition that
Ph at which sufficiently high
concentrations of unionized acid are
present to ensure the inward diffusion of
enough acid to extend the inner lesion


STEPHAN CURVE
Stephan [1940], using antimony microelectrodes ,
recorded the pH values of dental plaques in situ
before , during and after a glucose rinse.
These curves are often referred to as stephan
curves and they have 3 main charecteristics.
Under resting conditions , the pH of plaque is
reasonably constant, though differences can be
noted in the individuals .
Following exposure to sugars , the pH drops very
rapidly[ in a few minutes] to its lowest level and
then slowly returns to its original value over a
period of approximately 30-60min.

Stephan[1944] observed that plaques of
caries-free or caries-inactive individuals
usually had a resting pH of between 6.5
and 7 and they usually remained above
pH 5 following exposure to glucose.
In contrast , plaques of highly caries –
prone persons had a lower resting pH
and attained acidities well below pH 5
after exposure to glucose


• Stephan postulated that there must be microbial
differences between plaques in caries – free and
caries prone individuals. In addition to this ,
other factors which may affect the extent and
rate of pH changes in plaque are the type and
concentration of carbohydrates and other
substrates ingested , the frequency of ingestion,
salivary composition and flow, and the thickness
and age of the plaque


• NUTRITION,DIET AND DENTAL CARIES
• Diet----carbohydrates
• Others[calcium,phosphorus,vit.D,K,B6,
proteins,lipids,trace elements]
• Product related variables
type of carbohydrate
concentration of carbohydrate
stickiness, retention time
• individual related variables
frequency of eating
oral clearance time

ROLE OF SUCROSE IN DENTAL CARIES

• Many oral bacteria utilize sucrose,glucose,fructose and other
simple sugars to produce organic acids(lactic,acetic and propionic
acid) in sufficient concentration to lower the pH of plaque to
levels that may result in some demineralization of enamel.
• It is only from sucrose, however, that most bacteria are able to
synthesize both soluble and insoluble extra cellular polymers
which increase the bulk of plaque and facilitate the attachment of
bacteria, especially S.mutans to it.
• Unlike other disaccharides such as maltose or lactose, sucrose can
serve directly as a glycosyl donor in the synthesis of extra cellular
polymers.
• The high free energy of hydrolysis of sucrose permits this reaction
to proceed without other sources of energy.
• This property along with the high specificity of enzymes involved
in the synthesis of extra cellular polymers has led some workers to
regard sucrose as having a unique role in caries


EFFECT OF TRACE ELEMENTS ON DENTAL CARIES
____________________________________________________________
__________________
EFFECT TRACE ELEMENT

cariostatic F,P
Mildly cariostatic M,V,Cu,Sr,B,Li,Au
Equivocal effect Be,Co,Mn,Sn,Zn,Br,I.
No effect Ba,Al,Ni,Fe,Pd,Ti
Caries potentiating Se,Mg,Cd,Pt,Pb,Si.
_______________________________________________________


MECHANISM OF ACTION OF
FLUORIDES IN CARIES REDUCTION

1 increased enamel resistance/reduction in
enamel solubility
2 increased rate of post-eruptive maturation
3 remineralisation of incipient lesions
4 fluoride as an inhibitor of demineralization
5 interferance with microorganisms


EFFECT OF DEMOGRAPHIC FACTORS ON
THE PREVALENCE OF CARIES
• sex
• age
• race
• familial factors
• time factors for caries development after eruption
• latitude


ROLE OF SALIVA IN DENTAL CARIES
composition
1. Inorganic constituents:
Positive ions- Ca ,H+,Mg,K
Negative ions- carbondioxide,carbonate,Cl, F,phosphate,thiocyanate.

2.Organic constituents:
Carbohydrate-Glucose
Lipids-cholesterol,lecithin
Nitrogen –nonprotein- NH3,nitrites, urea and aminoacids.
Nitrogen protein-globulin,mucin,total proteins
Enzymes-
carbohydrases(amylase,maltase),proteases(trypsin),oxidases(catalase,
oxidase)


• pH of saliva:
It is determined mainly by the bicarbonate concentration.(85%)
.Phosphates and proteins in saliva constitute the other buffer systems, but the
constitution of these in saliva are too low to be of significance. So the pH will
vary according to the bicarbonate content. The saliva pH increases with flow
rate. It may be slightly acidic as it is secreted at an unstimulated flow rate but
it may reach a pH of 7.8 .Other salivary components contributing to the
ability of saliva to neutralize the acidity are ammonia, urea and statherin.
Sialin is an arginine peptide which is the recently described pH rise factor
present in saliva which rapidly clears glucose from plaque, increases base
formation and elevates pH in the plaque.

QUANTITY OF SALIVA: The normal secretion is 700 to 800 ml per day.It
may influence caries incidence.This is especially evident in cases of salivary
gland aplasia and xerostomia in which salivary flow may be entirely lacking
with rampant dental caries the typical result.

VISCOSITY OF SALIVA:It depends on the mucin content.A high caries
incidence is associated with thick mucinous saliva.


• ANTIBACTERIAL AGENTS OF SALIVA:
1.Lactoperoxidase
2.Lysozyme
3.Lactoferrin
4.Ig A

LACTOPEROXIDASE
These enzymes participate in killing microorganisms by catalyzing
the hydrogen peroxide mediated oxidation of a variety of
substances in the microbes.
Utilizing thiocyanate ions in saliva, it generate highly reactive
chemical compounds that bind and inactivate several intracellular
microbial enzyme systems, as well as microbial surface
components.
It has high affinity for enamel surface and it forms an important
defence mechanism, limiting early microbial colonization of tooth
surfaces.


LYSOZYME
It is a small ,highly positive, enzyme that
catalyzes the degradation of negatively
charged peptide-glycan matrix of microbial
cell walls.
There is strong evidence that lysozyme,
which is highly positively charged, binds to
hydroxyappatite and maintains its activity
after binding.


LACTOFERRIN
It is an iron binding basic protein which tends to bind and
limit the amount of free iron.
Since iron is essential for microbial growth, this salivary
protein is an active host defence mechanism
Ig A
Secretory Ig A is an effective agglutinin because each
molecule posesses 4 antigen binding sites.
It inhibits adherence and thereby prevents colonization of
teeth by organisms, facilitating their disposal by
swallowing.


• HISTOPATHOLOGY OF DENTAL
CARIES
ENAMEL CARIES
Light microscopic studies of carious
lesions of enamel without cavitation, have
revealed four distinct zones, which
represent varying degrees of hard tissue
transformation, beginning on the dentinal
side of the lesion


ZONE 1:TRANSLUCENT ZONE
It is the deepest zone and represents
the advancing front of enamel lesion. It is not
always present.
The name refers to its structureless appearance
when perfused with quinoline solution and
examined with polarized light.
In this zone , pores or voids form along the
enamel prism [rod] boundaries, presumably,
because of the ease of hydrogen ion penetration
during the carious process.
The pore volume of this zone is 1%[10 times
greater than normal enamel]

ZONE2:DARK ZONE
It lies adjacent and superficial to the translucent zone . It
is called dark zone because it does not transmit
polarized light .
This light blockage is caused by the presence of many tiny
pores too small to absorb quinoline.
The total pore volume is 2% to 4%.It has been referred to
as positive zone because it is usually present
Experimental remineralization has demonstrated increases
in the size of dark zone at the expense of body of lesion
There is also a loss of crystalline structure in this zone ,
suggesting of process of demineralization and
remineralization.
The size of dark zone is probably an indication of the
amount of remineralization that has recently occurred.

ZONE 3:BODY OF THE LESION
It lies between the relatively unaffected surface layer and the
dark zone. It is the area of greatest demineralization.
It has the largest pore volume, varying from 5% at the periphery to
25%at the centre.
The striae of retzius is well marked in this zone, indicating mineral
dissolution along these areas of relatively higher porosity.
The first penetration of caries enters the enamel surface via the striae
of retzius.
The inter prismatic areas and these cross striations provide access to
rod cores, which are then preferentially attacked .
Bacteria may be present in this zone if the pore size is large enough
to permit their entry.
Studies using TEM and SEM demonstrated the presence of bacteria
invading between the enamel rods [prisms] in the body zone


ZONE 4: SURFACE ZONE
This zone is relatively unaffected by the carious
attack. It has a lower pore volume than the body
of lesion [less than 5%]and a radio opacity
compared to the unaffected adjacent enamel.
It has been hypothesized that hypermineralisation
and increased fluoride content of superficial
enamel are responsible for the relative immunity
of enamel surface


ZONES OF DENTINAL CARIES
Caries advancement in dentin proceeds through 3 stages.
1 weak organic acids demineralise dentin
2 organic material of dentin particularly collagen
degenerates and dissolves and
3 the loss of structural integrity is followed by invasion
of bacteria .
• Five Different zones have been described in carious
dentin.
• The zones are more clearly distinguished in slowly
advancing lesions. In rapidly progressing caries, the
difference between the zones becomes less distinct


ZONE 1:NORMAL DENTIN
The deepest area is normal dentin which has
tubules with odontoblastic process that are
smooth and no crystals are in the lumen .
The intertubular dentin has normal cross banded
collagen and normal dense apatite crystals .
No bacteria are in the lumens .
Stimulation of dentin [eg. by osmotic gradient , a
bur, dessication from heat or air] produces a
sharp pain


ZONE 2 SUBTRANSPARENT DENTIN
• This is a zone of demineralization of inter tubular
dentin and initial formation of very fine crystals in
the lumen at the advancing front .
• Damage to the odontoblastic process is evident
• However no bacteria are found in this zone
• Stimulation of dentin produces pain, and the
dentin is capable of remineralization


ZONE3: TRANSPARENT DENTIN
It is softer than normal dentin . and shows further loss of
mineral from the inter tubular dentin and many large
crystals in the lumen of dentinal tubules .
Stimulation of this region produces pain . No bacteria are
present.
Although organic acids attack both the mineral and
organic content of dentin , the collagen cross linking
remains intact in this zone .
The intact collagen can serve as a template for
remineralisation of the intertubular dentin, and thus this
region is capable of self- repair provided the pulp
remains vital.


ZONE 4: TURBID DENTIN

It is the zone of bacterial invasion and is marked
by widening and distortion of dentinal tubules,
filled with bacteria .
There is very little mineral present, and the collagen
in this zone is irreversibly denatured.
The dentin in this zone will not self- repair this
zone cannot be remineralized and must be
removed before restoration.


ZONE 5 :INFECTED DENTIN

It is the outermost zone consists of decomposed
dentin that is teeming with bacteria
There is no recognizable structure to dentin and
collagen and mineral seem to be absent.
Great number of bacteria are dispersed in this
granular material.
Removal of infected dentin is essential to
sound . ,successful restorative procedures as well
as prevention of spreading of infection


ELECTRON MICROSCOPIC STUDIES OF
CARIOUS ENAMEL

Ultra structural studies of enamel caries have shown that
the intercrystalline space increases.
This can only happen if some mineral substance from the
surface of enamel crystallites is removed or if there is
selective dissolution of a separate amorphous calcium
phosphate phase between crystals.
The surface of a crystals in a carious lesion show slight
etching as evidenced by the irregularity of the margins.
Evidence for the existence and removal of an amorphous
intercrystalline phase is lacking.
The most common crystal damage detected in electron
microscopic studies is central or core defects due to
preferential loss of minerals.

This causes the enamel crystals to assume a hairpin
appearance in a longitudinal view .
The finding is most easily explained on the basis of
existence of lattice defects and or different
solubilities between the central core and the
exterior of crystals.
It is known that dislocations in the form of lattice
defects increase in the core of crystals.
Chemical reactivity increases at dislocation points,
thus causing preferential loss of the crystal
centres. It has also been suggested , but not
proven , that there is a higher concentration of
carbonate in the crystal centre, carbonate is
preferentially dissolved in an acidic environment.


• At the electron microscope level some enamel crystals at
the periphery of the prism in the body of the lesion are
often seem to be thicker and more electron-dense than
in normal tissue.
• The larger crystals are thought to be formed in the
process of recrystallisation or remineralisation.
However, the remaining crystals within the body of
lesion zone being smaller than those in sound enamel
as a result of acid dissolution
• Recently a new microdissection technique coupled with
high resolution scanning electron microscopy has
revealed [Silverstone,1983] that the crystals in both the
dark zone and the surface zone of the lesion are larger
in diameter than those of sound enamel.


• With this new technique, it has been shown that the
crystals in sound enamel have a diameter of 35-40nm ,
in the translucent zone there was a small decrease in
size to 25-30nm, and in the body of lesion crystal
diameter varies from 10-30nm however in the dark
zone crystal diameters were found to be in the range of
45-100nm.
• The crystals in the surface zone were also seen to be
larger than those of sound enamel being 40-75nm in
diameter
• These observations showed remineralisaton occurring
in the dark zone and the surface zone of enamel lesion.


ENAMEL CARIES AT CHEMICAL LEVEL
•A protective organic film of strongly adsorbed
protein, the acquired salivary pellicle forms on
the surface of enamel mineral.Acquisition of
fluoride in surface enamel and loss of carbonate
from the enamel surface may contribute to the
solubility of the outer enamel surface.
• In the presence of a suitable carbohydrate
sustrate’such as sucrose ,cariogenic plaque
bacteria produce organic
acids(lactic,acetic,propionic) localized within the
plaque in juxtaposition to enamel

• Production of these organic acids produces a
concentration gradient that causes the hydrogen
ions (H+) and the undissociated acid(HA or
HL,etc) to diffuse into the enamel.
• As diffusion proceeds the undissociated acid
molecules continually dissociate providing H+
ions .These hydrogen ions are rapidly used up in
the reaction with enamel, producing calcium and
phosphate and promoting further acid
dissociation.


• The undissociated HA and HL form a reservoir
of H+ ions.Dissociation is dependent on the pH
and the concentration of undissociated
molecules.As the HA and HL diffuse,dissociation
into H+,L- and A- occurs in an attempt to
establish an equilibrium.
• -The H+, and to a lesser extent L- and A- ,attack
the apatite crystals particularly at vulnerable
lattice points such as where carbonate is present.
• This causes Ca2+,OH-, PO4- ,F- ,CO3-, Na+
and Mg2+ to be removed from the lattice and to
diffuse to the solution phase between the crystals.

• Fluoride in solution markedly inhibits this
dissolution stage of the process.
• This ions and their appropriate
complexes(CaHPO4 ,CaL+,CaH2PO4+ ,etc)
will diffuse according to their concentration
gradient through the newly enlarged pores of the
carious enamel so that Ca and PO4 are lost to
the external environment.Mineral loss,or
demineralization proceeds as long as sufficient
acid is available


• As more enamel disolves and the concentration of
the Ca and PO4 ions increases remineralisation
may occur on the surface of existing crystals.
• New crystals may also form as CaHPO4 or other
PO4 phases.As more HA and HL diffuses and
reaches a critical concentration it will cause some
of the new crystal forms to dissolve as well as
more enamel apatite crystals.
• This reactions mostly occur in the demineralised
subsurface layers particularly the body of the
carious lesion which may be as much as 70%
demineralised.

• -As Ca and PO4 diffuse outward remineralisation
becomes more and more likely as diffusion slows.
• This leads to the formation of an apparently intact
enamel surface layer,about 20 to 40 micrometer
thick,where the mineral content is higher than the
body of the lesion.
• This isa remineralisation phenomenon where
damaged crystals have been repaired and an
equilibrium eventually exists which maintain this
surface layer but with some loss of minerals.
• The loss of ions to the plaque is balanced by the
deposition of ions diffusing outwards from the
subsurface

If subsurface dissolution continues and repair
cannot keep pace with mineral loss this leads
eventually to more extensive damage to crystal
structure and cavitation.
Dissolution of mineral salts eventually exposes the
organic matrix of enamel and dentine to
proteolytic enzymes of the oral flora.
Proteolysis is important in the breakdown of dentin
and cementum,less so in enamel as much of the
protein is acid soluble and lost.


• CONCLUSION
Caries, because of its uniqueness as a disease,its ubiquitous
nature, and its stubborn resistance to resolution remains
as one of man’s most common oldest and singly
costliest ailment. The total health handicap due to dental
caries is staggering. In western countries there has been
a dramatic decline in caries over the past decade.But in
the economically developing countries caries prevalence
is increasing as dietary habits of industrialized nations
are adapted. For this reason, it is important that the
subject of dental caries is given as broad a readership as
possible. Recognition of the enormity of the problem
should spur effects to reduce the ravages, the pain and
the cost of this disease.


• REFERANCES
• TEXTBOOK OF CARIOLOGY—GORDON
NIKIFORUK
• TEXTBOOK OF CARIOLOGY—MUNKSGAARD
• TEXTBOOK OF CARIOLOGY---SILVERMAN-
• CARIOLOGY—[THIRD EDITION]—ERNEST
NEWBRUN
• A TEXTBOOK OF ORAL PATHOLOGY[FOURTH
EDITION]—SHAFER
• PRINCIPLES OF PREVENTIVE AND COMMUNITY
DENTISTRY-SOBEN PETER
• OPERATIVE DENTISTRY[FOURTH EDITION]—
STURDEVANT

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