Microbiology of dental caries/ orthodontic course by indian dental academy

DEPARTMENT OF CONSERVATIVE AND
ENDODONTICS
COLLEGE OF DENTAL SCIENCES, DAVANGERE.
SEMINAR ON
DENTAL CARIES
Presented By

ree Ganeshaya Namaha
MULTIFACTORIAL CAUSE OF DENTAL CARIES
Dental caries has been traditionally described as a multifactorial disease
in which there is an interlay of three principal factors namely ;
1) Host factors
a) Tooth factor
i) Morphology and position in arch
ii) Chemical nature
b) Saliva
i) Composition, pH and antibacterial activity
ii) Quantity and viscosity of flow
c) Immunization
2) Microflora
3) The substrate / diet
a) Physical nature
b) Chemical nature
Fourth factor :
4) Time
Most important is the understanding that the caries process does not
occur in absence of “Dental Plaque” or dietary fermentable carbohydrate and
thus dental caries must be considered a “Dietobacterial disease”.
A modern concept of caries includes the importance of social,
behavioural, psychological and biologic factor which interact with the genetic
background in a highly complex and interactive manner.
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Disease
Genetic Environmental
Biologic Factors
Social factors
Behavioural factors
Psychological factors
Dental Caries Conceptualised as an interaction between genetic and
environmental factors
HOST FACTORS :
a) Tooth Morphology and Arch Form :
Tooth morphology has been long been recognized as an important
determinant. There are four factors which determine the tooth for caries
susceptibility.
1. It is known that P and F areas of posterior teeth are highly susceptible to
caries, because food debris and microorganism readily impart in the
fissures. Investigation have shown the relationship between caries
susceptibility and depth of fissures.
2. Certain surfaces of tooth are more prone to decay, when compared to
others. Eg. Mandibular first molar  likelihood of decay in descending
order is occlusal, buccal, mesial, distal and lingual.
Maxillary first molar : Occlusal, mesial, lingual / palatal, buccal and distal.
Mx. lateral incisor : Lingual surface more susceptible.
The difference in decay rates of various surfaces on some tooth are in
part due to morphology. i.e. Eg. Buccal pit of mandibular molars, lingual
groove of maxillary molars, cingulam of maxillary incisors.
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The distal surface of first permanent molars is freely accessible to saliva
for about 4-5 years until 2nd
molar erupt at 10-11 years. Whereas approximal
plaque may form on mesial surface from 6-7 years.
3. Intraoral variation exists in susceptibility to caries between different tooth
types.
Most susceptible one : Mandibular first molar – maxillary first molar –
mandibular and maxillary, 2nd
molar – 2nd
premolar, maxillary incisors – first
premolars. Mandibular incisors and canines least susceptible.
4. Irregularities in arch form, crowding and overlapping of teeth also favour the
development of carious lesions.
TOOTH COMPOSITION / CHEMICAL NATURE :
Presence of inorganic constituents, such as Dicalcium phosphatase
dehydrate and fluoroapatite etc make the enamel resistant to some extent.
Surface enamel is harder than the underlying enamel. These differences
are likely to be related to the many difference between composition of the
surface and that of the rest of the enamel. The surface enamel has more
minerals and more in organic matter but relatively less water. In addition
certain elements, including fluoride, chloride, zinc, lead and iron accumulate in
the enamel surface while other constituents, such as carbonate and magnesium
are sparse in surface as compared with sub surface enamel.
Changes of the enamel, such as decrease in density and permeability and
an increase in nitrogen and fluoride content with age. These alterations are part
of the “Post-operative maturation” process whereby teeth become more
resistant to caries with time. The concentration of fluoride of the surface layer
of enamel increases as the fluoride concentration of drinking water increases
and such enamel is less soluble in acids. Furthermore higher the fluoride
concentration of water supply the lower the prevalence of caries.
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HOST FACTORS – SALIVA :
In this context saliva refers to the mixtures of secretions in oral cavity.
This mixture consists of fluids derived from major salivary glands (Parotid,
submandibular, sublingual), from minor salivary glands of oral mucosa and
traces from the gingival exudates. This fluid is given a term as oral fluid.
The environment of oral cavity particularly the saliva in which teeth are
in constant contact and are bathed in it profoundly influences D.C. process.
The complex nature of saliva and the variation in its composition with various
factors like flow rate, nature of stimulation, duration of stimulation, plasma
composition and time of day which it is collected directly influences the dental
health.
Most of the saliva is produced during the meal items and as a response
to stimulation due to tasting and chewing. In healthy individuals teeth are
constantly bathed by upto 0.5 ml of “resting saliva” which helps to protect or
pharynx. Salivation virtually stops during sleep because of the salivary glands
do not secrete spontaneously in humans.
Normal stimulated secretion rate in adults is 1-2 ml / minute. However,
it may be less than 0.1 ml/minute in patients with salivary gland
malfunctioning.
Hundred years ago W.D.Miller described the basic mechanism of caries
etiology which is the foundation of our understanding today. While Miller’s
experiments showed that saliva is an essential factor in the pathogenesis of
caries, little more than 20 years head recognized the role of saliva in protecting
enamel and repairing the effect of carious attack. The role of saliva in caries
has since then been extensively researched.
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Major sources of saliva are the major and minor salivary glands. The
mechanisms of secretion have been extensively studied and the importance of
neurotransmitter and hormonal influences on various major and minor salivary
glands are well known.
The secretory products of these glands can be divided into 2 major
categories.
1. Water and electrolytes.
2. Macro molecules particularly proteins and
glycoproteins.
The “acetyl choline” released from the postganglionic parasympathetic
nerve endings stimulates muscarinic cholinergic receptors on secretory cells.
Nor epinephrine released from the adrenergic nerve endings of the
sympathetic nervous system stimulates adrenergic receptors also locate don
secretory cells.
The α-adrenergic receptor locate din salivary gland cells, similar
to the β-adrenergic receptor, and also responsive to epinephrine. Other neuro
transmitters, such as substance –P, vaso active intestinal peptide (VIP) and
Adenosine Triphosphate (ATP), also seem to play role sin stimulation of
secretion.
The stimulation of one receptor often complements and amplifies the
response to another. Moreover, not all the salivary glands respond in the same
manner to neurotransmitters. The sublingual lingual, which contains mostly
mucus containing acinar cells, is regulated primarily by the parasympathetic
nervous system and stimulation of muscarine receptors.
Individual neurotransmitters and hormones have some what selective
effects on H2O and electrolyte secretion on the one hand and secretion
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macromolecules on the other, depending on the gland. Therefore if one alters
the external signals that influence the salivary glands, one can effect both, the
amount and the composition of saliva, which can inturn, effect the integrity of
the tooth structure.
SALIVA – BUFFERING FLUID :
Importance of saliva as buffer depends largely on its ability to control
the reductions in pH resulting from bacterial action on metabolic substrates that
are found in dental plaque. Saliva has a significant buffering activity and this
buffering activity varies from patient to patient (Stephen 1944).
The work of Stephan indicated a difference in resting pH values for
different patients and lower pH values correlating with a higher level of caries
activity. Recent studies, show that patients with low or no caries activity had
resting salivary pH of around 7.0. Those with extreme caries activity had a
resting pH of around 5 – 4.5 and pH values between those 2 extremes were
reported for those with less severe caries activity. This varies from person to
person and different age groups.
A major determinant of salivary pH is its buffering capacity.
Bicarbonate is the major buffer in saliva and its concentration in its saliva
increases as salivary flow rate increases. The greater the acidity, the more
likely is the demineralization of tooth surface. A reduction in salivary flow
leads to a corresponding reduction in buffer capacity with important
implications on dental plaque pH and caries susceptibility.
FUNCTIONAL ROLES OF INDIVIDUAL COMPONENTS OF SALIVA,
ANTIBACTERIAL PROPERTIES AND MINERALIZATION EFFECTS :
In addition to the ability of saliva to act as lavage vehicle and to provide
buffering of acid on the tooth surface, individual components of saliva have
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been shown to have effects either on – bacterial activity, demineralization and
remineralization of tooth structure.
Some salivary substances have direct – Bactericidal or, bacterio static
effect.
While some other substances can cause aggregation of oral bacteria
resulting in an increased clearance of oral bacteria.
LACTOFERRIN :
It is an iron binding protein with certain similarities to transferring the
iron binding protein found in blood.
 It is shown to have antimicrobial activity and it displays this activity in the
oral cavity.
 Organisms most susceptible are aerobic and facultative anaerobic bacteria.
 It appears to have an antimicrobial activity, that is independent of its ability
to bind to iron.
 Growth of streptococcus mutans is sensitive to this and the inhibition
appears to be iron dependent.
LYSOZYME :
It is a hydrolytic enzyme that has direct antimicrobial effects.
 It cleaves the β 1-4 linkage between N-acetyl glucosamine and N-acetyl
muramic acid, which constitutes the repeating units of cell wall
peptidoglcyans of bacteria.
 The enzyme also appears to alter the intermediary glucose metabolism in
sensitive bacteria and in some cases to cause aggregation perhaps
contributing to clearance of bacteria from the oral cavity.
 Sublingual and submandibular saliva contain higher levels of lysozyme than
parotid saliva.
 Lysozyme alone does not lyse prevent growth of pure cultures of
predominant bacteria in O.C. of man.
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 In presence of Na lauryl sulfate, a detergent lysozyme and alyse many
cariogenic and non cariogenic strepto cocci.
 Although lysozyme may not be effective specifically against cariogenic
microorganisms, it probably influences the ecological balance of the oral
mucosa by discriminating against transient organism introduced into the
mouth.
PEROXIDASE :
They are produced by the acinar cells of some major glands. Similar to
other peroxidases, the enzyme contains “hence’ and uses “thiocyanate” and
“hydrogen peroxide” produced by oral bacteria or present in glandular
secretions, to catalyse the formation of “hypothiocyanate” and possibly the
“cyano sulfurous acid”.
Hypothiocyanate oxidizes sulfhydral groups of oral bacteria resulting in
inhibition of glucose metabolism.
H2O2 is more toxic than hypothiocyanate to both oral bacteria and the
oral mucosa. Peroxidase thus protects the oral cavity from strong oxidizing
effects of the peroxide. Bacteria vary in their sensitivity to hyopthiocyante
with S.mutans with being among the more sensitive.
Lysozyme and peroxidase have been shown to inhibit adherence of
atleast one strain of S.mutans to saliva coated hydroxyapatite. The presence of
peroxidase, lactoferrin and lysozyme in the dental plaque appears to be related
to a change in composition of oral bacteria present in that plaque. The relative
importance of this change in plaque bacteria to caries incidence is not known.
The salivary glands secrete salivary peroxidase and thiocyanate ion
which act on water generated by certain bacteria.
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The oxidation reaction inactivates various enzymes of the glycolytic
pathway and thereby temporarily inhibit the growth, respiration and
metabolism of most species of oral bacteria.
α – AMYLASE :
 Is an enzyme that metabolizes starch and other polysaccharides. It is
produced by acinar cells of the major salivary glands, particularly those of
serous type.
 Amylase promotes the adherence of oral streptococci to hydroxyapatite.
 Its activity to bind to the tooth surface as a component of plaque and to
metabolize larger polysaccharides into glucose and mattose indicates that it
can provide substantiate for cariogenic bacteria.
 In addition it is known that S.mutans possess a glucosyl transferase ion in
their outer surface that can use maltose and maltodextrains (produced by α-
amylase) to generate other polysaccharides known as “glucans”.
 Glucan promotes adherence of streptococci and other bacteria to the tooth
surface, but glucans vary in their ability to promote adherence of oral
bacteria to the tooth surface, and therefore it is conceivable that a change in
substrate for bacterial glucosyl ion transferase would lead to change in
adherence of the bacteria.
 It is at present impossible to determine the net effect of α-amylase on dental
caries. At least some potential effects of amylase on the tooth surface can
be viewed as harmful. The net effect of combinations of α-amylase with
other components of the pellicle is not well understood however.
STATHERIN :
 It is an acidic peptide that contains relatively high levels of praline, tyrosine
and phosphoserine.
 It inhibits spontaneous precipitation of CaPO4 salts from supersaturated
saliva and prevents crystal growth. By doing so, it favours remineralization
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of tooth surface. It is able to function with other salivary proteins to protect
tooth surface from wear and from various physical forces.
 In addition to this, it can also bond to bacteria. In doing so it can enhance
the binding of cariogenic bacterial.
 This enhanced binding could indirectly promote caries activity, but the net
effect with bacterial binding with staltherin is not known.
HISTINS :
They are group of histidine rich proteins that are another acinar cell
product that affects the integrity of the tooth surface.
In addition to their demonstrated antifungal effects which do not directly
relate to the caries process histatins have antibacterial effects as well as the
ability to affect mineralization.
The major forms in the oral cavity are Histatin-1, Histatin-3 and
Histatin-5.
An important role played by Hsitatin, is its ability to bind
“hydroxyapatite” and prevent calcium phosphate precipitation from a super
saturated saliva and to inhibit crystal growth (thereby enhancing the stability
of hydroxyapatite present in tooth surface).
PROLINE-RICH PROTEINS :
They contribute significantly to protection of the enamel surface by
bonding with high affinity to hydroxyapatite. They constitute a large percent
of total protein in parotid and submandibular saliva and are products of acinar
cells secretion.
They are of two types (Saliva)
• Acidic proline rich
• Basic proline rich
Both are secretory products of major salivary glands.
The acidic praline rich proteins cases in a similar way as Histatin
i.e.bind tightly to hydroxyapatite and present precipitation of CaPO4 from the
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super saturated saliva, thereby protecting the enamel surface and preventing
demineralization.
The acidic and basic types bind to oral bacteria including streptococci.
As they bind to both bacteria and tooth surface this appear to have an important
influence on the bacterial composition of the enamel pellicle.
Secretion is enhanced by stimulation of β-adrenergic receptors in major
salivary glands. Because the level of stimulation is a determinant of the
amount of these proteins, drugs which act as the β-adrenergic receptor could
affect the degree of oral adherence of certain bacteria to the tooth surface.
CYSTATINS :
Group of cysterine-enriched protease inhibitors. As protease inhibitors,
they prevent act action of potentially harmful proteases on soft tissues of oral
cavity.
They bind to hydroxyapatite and inhibits the precipitation of CaPO4 and
protect the tooth by promoting supersaturation of saliva with calcium and
phosphate.
Most of cystaines are secreted by submandibular secretion.
MUCINS :
They are large molecular weight glycoproteins composed mainly of
carbohydrate and produced from acinar cells from submandibular, sublingual
and some minor salivary glands.
Major salivary mucins – MGI and MGZ.
MGJ absorbs tightly to the tooth surface. IT has the primary role of
contributing to the enamel pellicle, thereby protecting the surface from
chemical and physical attack including acid challenges.
Study of saliva and its tooth protective components reveal force
functions.
1. Buffering ability
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2. Cleansing effect
3. Antibacterial action
4. Maintenance of saliva supersaturated in CaPO4
The ability to aggregate bacteria appears to be shared by a number of
glycoproteins present in human saliva. These glycoproteins can be involved
both in adherence of bacteria to the tooth surface and in clearance from the oral
cavity.
FLUORIDE :
Fluoride is another important component of saliva. The ability of saliva
to deliver fluoride to the tooth surface, constantly marks salivary fluoride an
important player in caries protection largely by promotion remineralization and
reducing demineralization.
IMMUNOGLOBULINS :
The major immunoglobulin in saliva and other external secretions is
secretory IgA which differs from serum IgA. Secretory IgA is the product of 2
distinct cell types. Secretory IgA exists as a 11S dimmer constricting of 2 IGA
molecules joined by a J-chain plus a secretory component (SC). SC is a
receptor for polymeric immunoglobulin A containing J-chain; the IgA binds to
SC below the light junction of glandular epithelial cells and is then transported
across the luminal surface.
Salivary IgA are produced by plasma cells located in major and minor
salivary glands. It is then transported into saliva largely by the ductal cells of
the gland. IgA respective the principal immunoglobulin found in saliva. Ti
exists in saliva in approximate equal amounts of two isoforms, IgA, and IgA2.
The secretory component is added to the molecule by secretory cells and act as
part of the membrane receptor for IgA. The IgA complex allows IgA to be
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internalized and transported across the cell. The IgA receptor is cleaned off
during the secretion.
The secretory component protects IgA from proteolytic attack.
Secretory IgA has also been shown to inhibit the adherence to dental enamel
depending on the strain of the bacteria analyzed. Its presence in salivary
pellicle indicates that it is intimately related to the tooth surface. The ability of
secretory IgA to inhibit adherence appears to be relate to its ability to bind to
surface adhesives of bond as well as neutralize streptococci bacilli to bacterial
aggregation and removal from the oral cavity.
Secretory IgA molecular are multivalent antibodies and can prevent
adverse effect of bacterial toxins and enzymes.
The results of several studies attempting to correlate a protective effect
of IgA against dental caries have been conflicting and also in the role of IgA
and IgA2 in dental caries. It is not surprising that a characteristic correlation
between salivary IgA levels and degree of protection against dental caries has
not been readily shown in humans.
Saliva is well adapted to protection against dental caries. Salvias
buffering capability, the ability of saliva to wash the tooth surface to clean
bacteria, and to control demineralization and mineralization, salivary
antibacterial activities and perhaps other mechanisms all contribute to the
essential role in the health of teeth.
THE MECHANISM-ACID PRODUCTION :
The first step in the formation of the carious lesions is the increased
production of hydrogen ion in the bacterial plaque on the enamel surface.
These ions result from the process of glycolysis, by which simple sugars (mono
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and disaccharides) enter the bacterial cells and are metabolized by the glycolic
pathways until organic acids are produced.
While some simple sugars enter the mouth directly, much carbohydrates
are consumed in form of long chain polysaccharides, such as cooked and
uncooked starches. Here we find the first and unhelpful action of saliva caused
by the action of salivary enzyme amylase which begins the digestion of long
chains to produce the simple units needed by the bacteria.
Starch lodging in stagulation sites may be subjected to enzymatic
degradation and cooked starch which is partly degraded may become mildly
cariogenic as a result of prolonged amylase activity.
A more direct effect of salivary acid production is by bacterial inhibition
by a anti-bacterial effects of salivary enzymes lysozyme. Tactoperoxidase and
of lactoferrin and also other powerful inhibitor of plaque glycolysis derived
from both ingested fluids and saliva and that is the fluoride ion, which has an
inhibitory effect on plaque acid production.
ACID CLEARANCE :
Stephan, in his studies had demonstrated that following sugar intake,
acid production is rapid and within 5 minutes, the plaque will usually have
fallen below gingival overgrowth. The speed at which the plaque pH is
restored is dependent on many factors of which play and salivary buffering
capacity are among the important and most intensively searched.
While the buffering capacity of whole saliva rises on stimulation,
largely because of increased bicarbonate ion production, it remains half of the
whole plaque (which has cap of about 20 m equiv/lt).
Some 85% of plaque buffering capacity is due to hydrogen ions binding
by proteins of cell walls.
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As the bicarbonate ion concentration in stimulated saliva bathing the
dental plaque is so high, it is likely that the plaque ions are rapidly replenished
from saliva during acid production.
THE IONIC SEE-SAW :
When the saliva/ plaque buffering system can reduce the extent of the
fall in pH when sugars enter the mouth, prolonged and repeated glycolysis can
exhaust the ability of system to contain hydrogen ion removal.
The immediate effect of a falling plaque pH is to
a) Increase the free energy of the ionic species at the enamel – plaque
interphase.
b) Rate of migration of ions from both enamel and plaque.
As the pH falls below 6 the solubility limit of plaque fluid with respct to
hydroxyapatite increases.
When pH exceeds the limit (critical pH0 the calcium and phosphate
mineral ion products of plaque fluid leave enamel under a concentration
gradient.
However if the buffering action is effective and the pH rises, the
additional mineral ions in the plaque fluid will exceed its capacity to hold
themin solution when in contact with hydroxyapatite at the higher pH. This
state results in a vice-versa mechanism causing mineral ions to return to enamel
– remineralization.
Thus the repeated fluctuations in plaque pH produces a “see-saw” of
ions across the interface between the enamel surface and the plaque fluid. If
the see-saw actions produce a persistent deft for the enamel, then will occur.
The role of saliva in this mechanism is two fold.
It can replenish the buffer systems of the plaque fluid and there is
evidence of a relationship between saliva and plague fluid buffer components.
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It can donate mineral ions to the plaque increasing its degree of
saturation and reducing demineralization.
Finally, two other functions of saliva should be mentioned. The first is
the mechanism referred above, by which hypomineralized newly erupted
enamel, is raised to the status of “mature enamel” by deposition of mineral and
organic material from saliva into its initially porous structure. Without this
transformation teeth in many mouths would have little chance of escaping
carious attack and its explains the susceptibility of the newly erupted tooth.
Second process is continuation of first and is the confirmation of an
absorbed layer of protein and glycoprotein, the pellicle on the enamel surface.
SUMMARY OF THE ANTICARIES ACTION OF SALIVA :
 Aids in enamel maturation
 They inhibit plaque growth and metabolism
 May reduce glycolysis in plaque
 Spreads up sugar clearance by maintaining the plaque pH.
 Buffers pH fall in plaque
 Aids in remineralization by providing mineral
 Increases the rate of carbohydrate clearance
 Helps in increasing the thickness of enamel pellicle
 Aids remineralization by providing fluoride
MAJOR ANTIMICROBIAL PROTEINS OF HUMAN SALIVA : (Tenovuo
and Lagerlof 1994)
1. Non Immuno Globulin Proteins
- Lysozyme
- Lactoferrin
- Salivary peroxidase system
- Myeloperoxidase system
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2. Agglutinins
- Parotid saliva glycoproteins
- Mucins
- Secretory immunoglobulin A
- β -2 microglobulin
- Fibronectin
3. Histidine – Rich Proteins (Histatins)
4. Proline Rich Proteins (Staltherin)
5. Immunoglobulins
- Secretory IgA
- IgG
- IgM
IMMUNE FACTORS AND CARIES :
The soft and hard tissues of the oral cavity are protected by both” non
specific” and “specific” immune factors, which limit microbial colonization of
the oral surfaces and prevent the penetration of noxious substances and
ensuring damage to the underlying tissues.
Non specific immune factors in saliva are ;
- Lysozyme
- Lactoperoxidase system
- Lactoferrin
- Antibacterial compounds and
- High molecular weight glycoprotein’s
All these may act as bacterial agglutinins, unlike antibodies, these non specific
factors lack immunologic memory and are not subject to specific stimulation.
Major and Minor salivary glands constitute one of the major sources for
specific host immune factors Eg. IgA and IgM, IgG.
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IgA mediates its protective effect mainly through primary binding of
antigen. Binding can inactivate toxins, inhibit enzyme based system and effect
many other mechanism involved in microbial colonization. Thus binding of
several organisms result in their agglutination and consequent clearing from the
mouth.
An additional source of immune factors is the GCF. This contributes
more of IgG as well as some (monomeric) IgA.
The crevicular fluid also contains many of the complement components
and cell types that together with IgG and IgM antibody can “indicative’ or
“opsonize’ bacteria.
These specific host immune factors in whole saliva are assisted by the
phagocytozing non specific PMNL cells, migrating from the gingival crevice.
Numerous studies have shown that an increased antibody level of either
IgA or IgG to S.mutans can enhance its elimination and or interfere with its
cariogenic activity.
MICROFLORA :
By now it is agreed that caries cannot occur without microorganisms. As
early as Koch’s postulates, it was observed that for caries to occur, bacteria
played a definite role. The following factors further prove the role of bacteria in
caries
i) Caries will not occur in complete absence of microorganisms.
ii) Caries can occur in animals even if kept on single type of bacterial
growth.
iii) All oral organisms are not cariogenic, but histologically majority can be
isolated from carious enamel and dentin.
The part played by different micro organism at different sites is as
under.
a. OCCLUSAL CARIES :
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There are differences in occlusal caries and root caries and also in
smooth surface and pit and fissure caries. Ever since Clarke discovered the
species B.mutans, it is considered to be the significant microorganism out of all
the oral flora. Further studies on S.mitis and S.salivaris proved that this
organism plays a vital role in initiation of caries.
Main etiological microorganism in occlusal and pit and fissure caries is
S.mutans. S.mutans a) Ferments mannitol and sorbitol (synthesized insoluble
polysaccharide from sucrose) b) Are lactic acid formers which easily colonic
on tooth surface, c) Are more aciduric than other streptococci.
Few of these properties have also been shown by non cariogenic strains
such as enterococci, streptococci feacalis etc. Two properties, which make
them separate from other streptococci are ;
i) Acid accumulation by S.mutans is substance greater than that
of other oral streptococci.
ii) S.mutans contains lysogenic bacteriophage which has not
been isolated from non cariogenic strains.
DEEP DENTINAL CARIES :
As the environment is different in deep dentinal lesions, it is certain that
the flora of deep caries would be different. The predominantly present
microorganisms are lactobacilli which account for 1/3 of the oral flora. Certain
gram positive anaerobes and filaments are also present such as eubacerium,
actinomyces, bacillus, arachnia, bifidobacterium, eubacterium, propionic
bacterium. The incidence of gram positive facultative cocci is low.
CEMENTAL / ROOT CARIES :
As the name indicate, root caries starts at the cementum or CEJ and
appears only when the cementum is exposed. IT can occur at any tooth surface
but mandibular molars are more susceptible.
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The organism involved in root caries are different from those involved
in other smooth surface lesions. Predominantly actinomyces viscous have been
isolated other species of Actinomyces as A.naeslundi and no caries etc have
been isolated.
In experimental animals variety of organism such as A.viscosus,
A.naeslundi, S.mutans and S.salivarius have been shown to produce root caries.
Exact strains, which produce root caries is not clear but certainly the bacterial
flora is different in root caries as compared to others.
THE SUBSTRATE / DIET :
Diet refers to the customary food, which we take from time to time and
nutrition means the assimilated portion of diet, which affects the metabolic
process of body. Diet has shown to influence caries.
A variety of factors have been seen regarding the role of diet in caries
production.
a) PHYSICAL NATURE OF DIET :
It has been proved that the physical nature of diet affects caries direct.
The diet of primitive man consisted of raw food including sand and soil
coating, which led to attrition and cleansing the debris, thereby reducing caries.
Modern diet includes refined foods, soft drinks and etables, which lead to
collection of debris predisposing to more caries. Further it is observed that the
mastication of food reduces the number of microorganisms. Mechanically
rubbing and cleaning definitely has role in caries reduction.
b) CHEMICAL NATURE OF DIET :
By chemical nature we are mainly concerned with the nutrients present
in our meals, frequency of intake and also their cariogenic potential. The main
ingredient is carbohydrate, which is accepted as one of the most important
factor in dental caries process. Only refined carbohydrates are effective. For
caries production following factors are responsible.
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i) Type of carbohydrate eg. Monosccharides, Disaccharides or
polysaccharides.
ii) Frequency of intake
iii) Time of stagnation
The concentration of sugar in a food can be a key factor in the dental
caries process. Solution of sugar contains 0.3% of sugar in 1 liter of water.
Fosdick stated that the concentration of 0.8 M of sugar must be present
to pass through 1 mm of dental plaque and ferment to a harmful level (pH 5.2)
within a 5 minutes. Small amount of concentrated caloric sweeteners are just
as cariogenic as large amounts.
Time for caries lesion to develop and frequency of between meal snack.
It takes 18 months ± 6 months from the incipient attacking forces of organic
acids on the tooth enamel surface until a carious lesion can clinically be
detected. In case of xerostemic patients caries can be detected clinically within
3 months.
Caries prevalence is directly related to the frequency of between meal
snacking ¼ to 1/3 of total carolic intake of adolescents comes from between
meal snacks, but a major factor is their high dental caries susceptibility.
Cariogenic Potential of Foods :
Food is classified as cariogenic if when it comes into contact with
plaque bacteria, the pH falls below 5.5, which is the tooth demineralization pH.
Some of these foods which are cariogenic are applies, caramel, bread,
chocolate, cookies etc. Foods that non acidogenic like cheese generally
increases the pH after coming into contact with the tooth. These non cariogenic
not only increase the plaque pH above 6 but also contain relative high protein
content, a moderate fat content to facilitate oral clearance, contain minimal
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concentration of fermentable carbohydrate, exerta strong buffering action, have
high mineral content and stimulate salivary flow.
Sugar Alcohols :
These have little / no effect on plaque pH. Thus it is agreed that sorbitol
containing chewing gums may not contribute significantly for tooth decay.
Starch Rich Foods : They tend to retained on and around teeth for a prolonged
period of time and are ultimately degraded to organic acids and depress the
plaque pH for longer period of time contributing to demineralization phase of
dental caries process.
Sugar Rich Foods : There is a profound effect of readily fermentable carbon on
dental caries sucrose being the most cariogenic of the sugars and glucose,
fructose and lactose to a little lesser extent.
The physical form of sugar, that is in solution form it is much less
capable of causing netal caries when compared to other forms. Sticky sugars
develop more caries than when compared to sugars in non sticky form and
solution form.
Vitamin content of diet have reported to show significant effect on
dental caries. Vitamin D has been shown with greater relation to dental caries
because it helps in normal development of teeth, so def. causes malformations
and so increased caries incidence. Vitamin K has been tested as possible
anticaries agent by virtue of its enzyme inhibiting activity in the carbohydrate
degradation cycle. Vitamin B complex deficiency may exert a protective
influence on the tooth since these essential growth factors of the acidogenic
flora and also serve as components of co-enzymes involved in glycolysis.
Certain minerals such as calcium and phosphorous and trace elements
such as selenium and vanadium have some relation to dental caries. Role of
24

calcium and phosphorous is controversial. Def. of calcium during infancy and
IU. Life leads to poor calcification of teeth which may relate to occurrence of
caries. Caries incidence is significantly higher in people residing in
seleniferous areas and decrease in areas with increasing vanadium
concentration.
Fluoride in various forms also reduces the dental caries.
Basically following factors are responsible as for as diet and dental
caries is concerned.
i) Particle size and roughness of diet
ii) Pallatability of diet
iii) Eating and drinking pattern. After diet and within diet
iv) Retention and clearance of diet
v) Age at which diet is offered
ROLE OF PLAQUE IN DENTAL CARIES :
It is a gelatinous mass of bacteria adhering to the tooth surface.
The endogenous microorganism that are present in plaque are S.mutans,
S. sobrinus, lactobacillus species, Actinomyces species, nommutans
streptococci and yeast contribute the caries process.
Soft, translucent, and tenaciously adherent material accumulating on the
surface of teeth is commonly called plaque. Plaque is neither adherent food
debris, as is widely and erroneously thought, nor does it result from the
haphazard collection of opportunistic microorganisms. Actually accumulation
of plaque in teeth is a highly organized and ordered sequence of events. Many
of the organism found in the mouth are not found else where in nature.
Survival of microorganisms in the oral environment depend son their ability to
adherent to a surface.
25

Free floating organism are rapidly cleared from mouth by the salivary
flow and frequent swallowing. Only a few specialized organisms, primarily
streptococci, are able to adhere to oral surfaces such as mucosa and tooth
structure. These adherent bacteria have special receptors for adhesion to the
tooth surface. Once they are attached, these pioneering organism, proliferate
and spread laterally to form a mat like covering over the tooth surface. Further
group of bacteria produces a vertical growth away from the tooth surface
(external to). The resulting mixed streptococcal mat allows the adherence of
other organisms, such as filamentous and spiral bacteria, that otherwise are
unable to adhere directly to the tooth surface. Thus formation of a mature
plaque community involves a succession of changes and each change depends
on the preceding stage preparing the local environment for the next stage.
Plaque Communities and Habitats :
There are significant differences in the plaque communities found in
various habitats within the oral cavity. The oral mucosa is populated by
organisms with receptor specialized for attachment to the surface of epithelium.
The dorsum of tongue has a plaque community dominated by S.salivarius. The
teeth have a plaque community dominated by S.Sanguis and S.mitis. The
population size of MS on the tooth is highly variable. Normally it is a very
small percentage of the total plaque population but it can be as large as one half
the facultative streptococcal flora in other plaques.
White P and F on the crown may harbour a relatively simple population
of streptococci the root surface in the gingival sulcus may harbor a very
complex community dominated by filamentous and spiral bacteria. Facial and
lingual smooth surfaces and proximal surfaces also may harbour vastly
different plaque communities.
DEVELOPMENT OF PLAQUE :
26

The development of plaque is an etiological phenomenon. The plaque
community structure undergoes a succession of changes during periods of
unrestricted growth. These changes in the community structure consequently
change the overall metabolism and other characteristic of the plaque.
Community structural changes are predictable and are governed by general
principles of ecology.
The oral cavity is a well defined eco system being it has recognized
geographic limits and gather general composition of biologic community is
known. With the oral ecosystem are distinct habitats such as dorsum of tongue,
oral mucosa, gingival sulcus and various tooth locations including P and F and
various smooth surface areas. These habitates have unique environmental
conditions and harbour significantly different communities of microorganisms.
Within each habitual special combination of food and shelter are available to
support particular species of oral bacteria. This special combination of food
and shelter is termed as an “ecological niche”.
The growth of plaque is not _ of a random accumulation of opportunistic
organism passing through the oral cavity. Rather, an orderly sequence of
replacement communities occupies the tooth surface, each community
modifying the local environment of that site. The available niches, the limiting
factors and the environment conditions change as a result of the biologic
activity of each plaque community. This process of mutual change of the
community and its environment is called “Ecologic Succession”.
Plaque growth consist of surface attachment and their lateral spreading
as the attached organisms multiply. When the entire surface is covered growth
of colonies increases the thickness of the plaque. As the original colonizing
organisms proliferate, their progency produces vertical columns of cells called
“Palisades”. The palisades can be invaded by filamentous bacteria that
otherwise could not exist on the tooth surface.
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Early Stages of Plaque Succession ;
Within 2 hours of professional removal of all organic material and
bacteria from a tooth surface, a new coat of structure less organic film, the
pellicle can completely cover. The pellicle is formed primarily from the
selective precipitation of various components of saliva. The functions of
pellicle are ;
- Protect the enamel
- Reduce friction between the teeth
- Possibly provide matrix for remineralization.
The pellicle is formed from salivary proteins which include lysozyme, albumin
and immunoglobulin, IgA and IgG. The strong affinity of salivary proteins for
exposed hydroxyapatite is also of clinical important in operative dentistry,
because salivary contamination of a freshly etched enamel surface prevents
bonding of composite restorations.
The early stages of recolonization of the cleaned tooth surface involve
adhesion between the pellicle and the pioneering organisms. S.sanguis along
with actinomyces viscous, Actinomyces naeslundi and Peptostreptococcus are
the main pioneering species and are capable of attaching to the pellicle within 1
hour after tooth cleansing. The adhesion process sis very selective and requires
specific organism receptors capable of binding to certain areas on the
precipitated salivary proteins of the pellicle. Like for example the enzyme
glucosyl transferase maybe of critical importance in the adherence of MS to the
pellicle when sucrose is present because it enhances the polymerization of the
extracellular matrix that makes MS forms such tenaciously adherent.
Late Stages of Plaque Succession :
The late stages of plaque succession are responsible for causing either
caries / the periodontal disease. Early stages in plaque succession are generally
28

lacking in pathogenic potential because they are primarily aerobic communities
and lack sufficient number or proper types of organisms to produce sufficient
quantities of damaging metabolites.
However as plaque matures, the production of cells and matrix slow and
utilization of energy for the total community nut. Results in acid production
since mature plaque is primarily anaerobic, it reduces the available nutrients to
anaerobic metabolites that is fermentation products including weak organic
acids, amides and alcohol. Mature plaque communities rapidly metabolize
sucrose through glycolytic pathway to organic acids, primarily lactic acid. IN
cariogenic plaque, virtually all the available successor is metabolized to acid,
resulting in severe and prolonged drop in pH, thereby increasing the potential
for enamel demineralization. Demineralization of enamel occurs at pH of 5.0
to 5.5. A single successor exposure / rinse can produce pH depression lasting
upto 1 hour.
FACTORS THAT SERVE AS ECOLOGIC DETERMINANTS :
Ecologic determinants are factors that exert ecologic control over
habitats or nidus and ultimately determine the characteristics of dental plaque
community. Some of the determinants that control the overall composition of
the plaque community are shelter, pH, oxygen saturation and nutrient
availability.
Current Hypothesis to explain the role of plaque bacteria in the etiology of
dental caries :
There are two hypothesis concerning the pathogenecity of plaque.
Non-Specific Plaque Hypothesis :
This promotes the universal presence of potential pathogens in plaque
and therefore assumes that all accumulations of plaque are pathogenic.
Specific Plaque Hypothesis :
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It is based on the observation that accumulation of plaque is not always
associated with the disease. In this accumulation plaque can be considered
normal in the absence of the disease. Plaque is assumed to be pathogenic when
the disease is present.
This hypothesis provides a new scientific basis for the treatment of
caries that has radically altered caries treatment. Because only limited number
of microorganisms are capable of caries production specific plaque hypothesis
treatment is aimed at elimination of specific pathogenic organisms but not total
plaque elimination.
Ecologic Plaque Hypothesis (Harsh 1994)
Dynamic relationship exists whereby an environmental change in plaque
(eg. Low pH) drives a shift on the balance of the resident micro flora, thereby
shifting the balance towards enamel demineralization. caries can be prevented
not only by inhibiting the putative pathogens (eg. MS) but also by interfering
with the environmental change driving the ecologic shift. Eg. By reducing the
acid challenge to plaque by the use of alternative sweeteners / fluoridated oral
health care products
MICROBIOLOGY OF DENTAL CARIES :
The origin of oral microbiology coincides with the discovery of bacteria
by Lewenhock in 1683. Lewenhock studied the morphological types of
bacteria from the oral cavity. Many theories were proposed for the cause of
dental caries.
Erdl in 1843 put forth an another concept termed as the parasitic theory
of dental decay, which attributed dental caries to microorganisms or denticolon.
In 1850, Klencke described a parasites labeled protococcus dentalis as
the cause of dental caries for it could dissolve enamel and dentin.
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IN 1867, two German physicians, Leler and Rottenstein stated that
dental caries is started as purely chemical process but the living organisms
caused its progression into enamel and dentin.
Later in 1881, investigation of etiology of dental caries were made in
Koch’s laboratory in Berlin by B.D.Miller. he presented that concept of the
role of acid sand bacteria in dental caries productions. This theory was termed
as chemo parasitic theory.
Clarke in 1924, described a new streptococcus species, S.mutans, which
was isolated from carious lesions in the teeth of British Patients, later
lactobacillus acidophilus was identified.
Between 1920’s and 1940 number of studies was carried out to study the
existence of microorganisms responsible for dental caries by workers like
Arnold and MchChere and Becks, Jenser and Miller.
IN 1960, Fitzgerald and Keys isolate specific streptococci from rodent
carious lesions. Caries inducing streptococci are now considered members of
S.mutans group.
The most important factor in the pathogenesis of dental caries is the
capacity of a large number of oral bacteria to produce acid from the dietary
carbohydrates. Miller in his study conclude that no single group or specie
could be responsible for dental caries. Instead, several or all acidogenic
bacteria should be considered responsible.
Acidogenic bacteria usually found in large numbers are streptococci,
lactobacilli, actinomyces and yeasts. The ability of bacteria in plaque to
produce acids varies when first exposed to carbohydrates, all acidogenic
bacteria produce aids, but when pH decreases, more and more of the bacteria
31

loose their ability. When pH reduces to the critical level only few bacterial
species produce acids. These aciduric bacteria are of great importance
(lactobacillus and S.mutans) in the pathogenesis of caries.
Apart from S.mutans, S.sanguis, S.mitis Actinomyces viscous and
A.naeslundi produces extracellular insoluble glucans to various extent in the
presence of sucrose.
The cariogenicity of different plaque bacteria is to an extent determined
by the type of the interbacterial matrix they create. These insoluble extra
cellular glucans increases in plaque as the sucrose consumption increases. Thus
the glucans mechanically strengthen the plaque against the forces of
mastication and saliva washing, thus facilitating the aggregation of acidogenic
bacteria on the teeth.
Further several other groups of organisms in dental plaque such as
S.mutans, S.mitis, A. viscous, A.naesulundii and lactobacillus undergo
metabolism and produce intracellular polysaccharides which has the ability to
maintain acid production for prolonged periods in the absence of exogenous
sugar sources, thereby contributing significantly to enamel dissolution.
STREPTOCOCCUS MUTANS :
Of all the bacteria, streptococci have been studied most exhaustively.
Mucous membrane in the mouth and other parts of the body are characteristic
habitats for streptococci. The most prominent species of streptococci found in
oral cavity include S.mutans, S.mitis, S.mitior, S.Salivarius and S.milleri.
Although S.sanguis, S.milleri and S.salvarius have occasionally been found to
induce fissure caries. S.mutans like bacteria comprise the most important group
of streptococci implicated in caries etiology.
Ecology :
32

S.mutans does not colonize in the mouths of the infants prior to the
eruption of teeth. The same way it disappears from the mouth after extraction
of all the teeth. Infants most likely become infected from their parents. Studies
which are utilized lacteriocin typing and serotyping the “finger print”
individual strains have shown that strains isolated from newly erupted teeth of
infants are one identical to those present in the saliva of the mother.
S.mutans does not colonize teeth uniformly. The organisms may be
more frequently isolated from fissures and interproximal surfaces. It does not
spread readily from one tooth surface to the other. S.mutans may be spread to
other surfaces by the use of floss / dental exposures.
SUCROSE METABOLISM OF STREPTOCOCCUS MUTANS :
The most important substrate for the involvement of S.mutans in the
caries process is the disaccharide sucrose. Sucrose not only serves as a primary
energy source but also permits the initiation of additional biochemical agents
which are responsible for the cariogenic potential of this microorganisms.
There are three pathways involved by which S.mutans dissimilate
sucrose.
1. Conversion of sucrose to adhesive extrcellular carbohydrate polymers
by all bound and extracellular enzymes.
2. The transport of sucrose into the cell interior accompanied / followed by
direct phosphorylation for energy utilization through the glycolytic
pathway leading to lactic acid production.
3. The degradation of sucrose to free glucose and fructose by invertage.
STREPTOCOCCI OTHER THAN S.MUTANS :
STREPTOCOCCI SANGUIS :
This α-hemolytic streptococcus species was originally isolated from the
blood of patient with bacterial endocarditis. In humans, this organism habitats
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mainly in the oral cavity, especially in dental plaque. The specie do not
colonize the oral cavity until the first teeth erupt at about 6 months of age.
Serological studies of S.sanguis indicate the presence at least 3-4 types.
While the serology is complex. The organisms are easy to identify on sucrose
containing media, because it produces small, firm colonies. S.sanguisis found
both in carious and non carious sites. It ahs very low cariogenecity in
experimental animals with lesions limited to occlusal fissures.
STREPTOCOCCUS MITIOR :
Often called S.mitis this organism does not hydrolyse arginins and
ekulin as does S.sanguis. It produces soft round and black brown colonies on
mitis salivarious medium, which contain sucrose. A characteristic feature of
this organism is the absence of significant amounts of rhamnose in cell wall. It
produces extracellular glucan from sucrose, S.mitis is one of the most
commonly isolated bacteria in buccal mucosa. This along with S.sanguis are
among the most predominant organism in dental plaque. Its significance in
human caries is unknown and assumed to be very minor.
STREPTOCOCCUS SALIVARIUS :
This is found predominantly in tongue, soft tissue and in saliva but not
in high number in plaque. S.salivarius adheres well to epithelial cells but not to
hard tissues, especially pellicle coated enamel. Its low number in human
plaque suggests that its into of great significance in human caries initiation.
STRPETOCOCCUS MILLERI :
This was originally isolated from dental, brain and liver abscesses. It is
also found in gingival crevice, cervical plaque but not in other intraoral sites.
Although some strains induce fissure caries in experimental animals, but its
importance in dental caries in humans is not know at present.
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STREPTOCOCCUS SOBRINUS :
This along with S.mutans are now thought to be the main etiological
agent in dental caries. But further studies are needed to prove this.
OTHER BACTERIA ASSOCIATED WITH CARIES LACTOBACILLI :
In 1915, Kligler reported the presence of higher numbers of lactobacilli
in carious lesions. Lactobacilli are strong acid producers among the most
aciduric and acidogenic bacteria. These aciduric characteristic have been
utilized for the development of selective growth media for caries activity base
don lactobacillus count. They are found in carious lesions and their numbers in
plaque and in saliva correlate with caries experience. The restrictions of
dietary carbohydrate and restorations of teeth reduce the number of lactobacilli
population. These are often seen in deep dental caries because of their acid
resistance. They may not be directly associated with caries initiation but rather
become secondary invaders which contribute to the progression of already
existing lesion.
FILAMENTOUS BACTERIA :
Several types of filamentous organism have shown to initiate root
surface caries. Actinomyces and Rottia species have been found in human
dental plaque and dental caries. A viscous, an acidogenic bacterium that also
stores intracellular polysaccharides, is always among the predisposing flora of
plaque overlying the root lesions.
GRAM NEGATIVE COCCI :
Veilionella : Of the gram (-)ve cocci, this species is most commonly found in
plaque. These organism lack by enzymes involved in glycolysis and the
hexose morphosphate shunt and therefore do not utilize sugars as an energy
source. Veilionella utilizes lactic acid by converting it to pripionic and other
weak acids.
35

Thus is tells that there is decreased caries activity when the plaque has
veilionella in it. In other words it is the composition of plaque micro flora
rather than just the quantity of plaque that determines the pathogenecity.
SPECIFIC BACTERIA ASSOCIATED WITH ENAMEL CARIES :
Most commonly found bacteria are lactobacilli which was reported
earlier by Goadby as bacillus microdentalis. It was later identified as
lactobacillus species. Oral lactobacillus comprise a spectrum of species among
which L.casei and L.Ffermentium constitute the bulk of strains.
S.mutans was first described by Clarke in 1924, which is found
predominantly in the oral flora.
Lactobacilli and S.mutans are found nearly in all carious lesions and
their proportion in plaque and saliva is positively related with caries frequency
activity. S.mutans is more closely associated with initial caries lesions on
smooth buccal and lingual enamel surfaces than lactobacillus.
S.sanguis and S.mitis/ mitior are common in dental plaque and present
in numbers than found to be inversely relate dot caries activity. It is because
S.sanguis and S.mitis produce less acid than S.mutans.
S.salivarius is also able to induce caries, but this constitutes only a
small fraction of mature micro biota of dental plaque.
Actinomyces sp. Are present in plaque over carious lesion and necrotic
carious dentin. Although it was believed that Actinomyces specie does not
initiate enamel caries, but a recent study report indicates a relationship of
actinomyces odontolycius to the initiation of caries in approximal areas of
deciduous molar teeth.
Yeasts are also isolated from saliva, plaque and dental caries. These
organisms are aciduric but produce acid slowly. The primary oral reservoir of
yeast is the tongue and their numbers in dental plaque are low. They are
36

therefore not likely to contribute to the initiation of dental caries. Btu they may
be isolated from caries lesions because of their aciduric property, which
enables yeasts to increase in numbers on the various oral surfaces in the acid
environment exiting during high caries activity.
Several studies have shown than S.mutans and lactobacilli are related to
the development of dental caries on smooth enamel. In fissures, S.mutans and
lactobacilli are not found in higher proportion than S.sanguis the opposite is
true in caries free fissures. The initiation of caries tends to be preceded by
elevated number of both S.mutans and lactobacilli and to certain extent to
decreased number of S.sanguis.
In conclusion, S.mutans and species within lactobacilli are strongly
associated with the initiation of caries in enamel. These organisms have a
number of characteristic like ;
1. Both S.mutans and lactobacilli are acidogenic and have a high acid
production rate.
2. Specifically S.mutans, but also lactobacilli are able to produce insoluble
extracellular glucans.
3. S.mutans and species within lactobaicllius have the ability of intracellular
polysaccharides production.
4. Both the groups are considered as aciduric organism.
These characteristic specially, the combination of aciduric and strongly
acidogenic capability should be regarded as bestowing virulence to S.mutans
and lactobacilli.
Consequently, caries can be considered as a result of combined action of
all acid producing bacteria in plaque contributing to various degrees.
MICRO-ORGANISMS ASSOCIATED WITH ROOT SURFACE CARIES :
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A variety of bacteria colonize supragingival root surfaces. The genera
often found are actinomyces, streptococcus including S.sanguis, S.mitis and
veillonella. Recent studies show that two gram (-)ve genera cytophaga and
capno cytophaga strains of cytocapnophaga are specifically able to colonize
root surfaces. The gliding capacity of capno cytophaga makes its able to
extensively in vade dentinal tubules.
As in enamel caries, lactobacilli and S.mutans are associated with root
caries. Even caries other acidogenic bacteria like S.sanguis and actinomyces
specially found in large numbers also contribute in the pathogenesis of root
caries. A viscous is also one of the most dominant species in supra gingival
plaque, which may contribute in production of root caries.
Cementum and dentin are rich in organic frameworks. The clinical and
histopathological features of root surface caries are not the same as enamel
caries. In root caries, important microorganisms may be not only the highly
acidogenic and aciduric bacteria but also those possessing proteolytic and
peptidolytic activities.
MICROORGANISMS ASSOCIATED WITH DENTINAL CARIES :
When the caries lesion has penetrated into the dentin, the conditions for
microbial growth will change. The pH of carious dentin can be low specially
when enamel lesion is small and a thick layer of carious dentin exists. Further,
the large part of organic material in dentinal may favour gram (+)ve bacteria
and lactobacilli predominate the microbiota of carious dentin.
Less is known about the caries promoting capacity of various organisms
in carious dentin. However microbial products such as organic acids and
enzymes are found ahead of the bacterial front. These substances may
originate from the bacteria existing both in necrotic and the deeper part of the
carious dentin.
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Early studies concerned with the microfilaria of dental lesions showed
that the common bacteria found were positive allomorphic rods or gram
positive filaments. More different studies to identify the flora of an advanced
lesion in dentin have now been undertaken. The dominant organism are ;
Lactobacilli species : 33%
Arachnia species : 12%
Eubacterium species : 11%
Propionibacteirum species : 09%
Bifido bacterium species : 07%
Peptostreptococcus species : 06%
Streptococcus species : 05%
Actinomyces species : < 1%
There is no question that dental caries is an infection. The qualititative
nature of flora in plaque determines the metabolism and potassium for caries
production. This view is termed specific plaque hypothesis. The concept says
that certain plaques are more cariogenic than others because they contain
higher number of specification between species that cause cries specific
implicated most often in enamel caries are S.mutans and lactobacilli and in root
caries its actinomyces viscous. According to this hypothesis most, but not
necessary 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 this specific plaque hypothesis suggests the development and
implementation of prevention procedures that treat dental caries as a specific
bacterial infection.
DEMINERALIZATION AND REMINERALIZATION TOOTH SURFACE:
The physiochemical integrity of dental enamel in the oral environment is
entirely dependent on the composition and chemical behaviour of the
surrounding fluids i.e. saliva and plaque fluids. The main factors governing the
39

stability of enamel apatite are pH and the free active concentrations of calcium,
phosphate and fluoride in solution, all of which are derived from the saliva.
The carious process is initiated by the bacterial fermentation of
carbohydrates, leading to the formation of variety of organic acids and
therefore fall in pH. Initially the H+
will be taken up by the buffers in plaque
and saliva, when the pH continues to fall (H+ increases) however the fluid
medium will be depleted of OH- and PO3
4
which react with H+
to form H2O
and HPO2
4
.
On total depeletion of (OH- and PO3
4
) the pH can fall below the critical
value of 5.5, where the aqueous phase becomes undersaturated with respect to
hydroxyapatite. Therefore, whenever surface enamel is covered by a microbial
deposit, the ongoing metabolic process within this barrier results influctuations
in pH and occasionally steep falls in pH, which may result in dissolution of the
mineralized surface. The role of saliva in this process is highly dependent on
accessibility, which is closely related to the thickness of plaque.
So therefore, in principle dental enamel can be dissolved under two
different chemical conditions. 1) When the surrounding aqueous phase is
under saturated with respect to hydroxyapatite (HA). 2) Supersaturated with
fluorapatite (FA).
When HA is dissolved and FA is formed, the resulting lesion is a carious
lesion. Dissolving HA originates from the sub surface enamel and FA is
formed in the surface enamel layers. The higher the super saturation with
respect to FA, the more fluoride is taken up in the enamel surface the better
mineralized the surface enamel layer becomes and less dematerialized is the
surface body of the lesion.
40

On other hand, if there is undersaturation with respect to both HA and
FA, both apatites dissolve concurrently and layer after layer is removed and
this result sin an erosive lesion.
ROLE OF CALCIUM :
It is a bivalent ion excreted together with zygoma proteins, into the
lumen of the acini. The calcium found in saliva is dependent on the stimulation
rate of saliva. Depending on pH calcium is distributed in saliva as ionized and
bound forms.
The free, ionized calcium is especially important in the carious process
because it participates in establishing the equilibrium between the calcium
phosphates of the dentinal hard tissues and its surrounding. At pH values
closed to normal the ionized caries constitutes approximately 50% of the total
calcium concentration but it increases if salivary pH is lowered. Then bound/
unionized calcium is distributed in such a way that it is more / less firmly
bound to inorganic ions such as inorganic phosphate, bicarbonate and fluoride.
The tooth is usually separated from the saliva by an intermediate layer
of integuments in the form of a pellicle or / plaque. The total caries these
compartments is slightly higher, some times much higher than the salvia
because of high concentration of binding sites for calcium and because of
precipitated calcium slats. There is a strong correlation between both total and
ionized calcium in saliva and dental plaque, showing a flow of calcium over the
plaque saliva interface following existing diffusion gradients in ionized
calcium. This gradient will be large after sugar intake, liberating bound calcium
as the plaque pH slowly increases the concentrations of ionized calcium in
saliva, pellicle and plaque will slowly reach an equilibrium.
ROLE OF INORGANIC PHOSPHATE :
41

The concentration of these ions are dependent on the pH of the saliva.
The lower the pH the less concentration of the ions, indicating that the ion
production of H.A. decreases considerably with decreasing pH. The
phenomenon is the main cause of the demineralization of the tooth s with
calcium, the content of inorganic phosphate in saliva is prerequisite for the
stability of the tooth mineral in the oral environment.
About 10-25% of the inorganic phosphates depending on pH, is
completed to in organic ions such as calcium as is bound to proteins. A small
part, i.e. less than 10% is in the “disease form” which is a potent inhibitor of
the precipitation of calcium phosphate and influences the formation of calculus.
This is the rationale for the inclusion of pyrophosphates in tooth paste intended
to inhibit calculus formation.
ROLE OF FLUORIDE :
Fluoride in the fluids surrounding the enamel crystals has been shown to
have potential to reduce the rate of demineralization. When present in the
liquid phase of demineralization fluoride will be incorporated into the enamel
crystal and the enamel will become more resistant to demineralization.
Fluoride has also been shown to reduce the cid production in dental plaque.
The high initial fluoride concentration in the salivary film after fluoride
exposure will establish a concentration gradient between the dental
integument’s and the plaque. Fluoride will diffuse from saliva into the pellicle
and the plaque, rapidly elevating the concentration of fluorides in the plaque
fluid. Mineral CaF2 may form in saliva, pellicle and plaque fluid.
The limiting factor for the formation of CaF2 is the calcium content of
the oral fluids. Therefore the use of fluoride chewing gum after every meal as
a combined saliva stimulating and fluoride agent resulting in increased calcium
release from the saliva, foramen release and increased buffering effect, offers a
42

rational and administered measure for caries control during are just after the
fall in pH. CaF2 releases fluoride slowly. Fluoride diffusing into
microorganism also prevent participation of enzyme enolase in the glycolytic
pathway by binding magnet sum essential for optimal function of the enzyme.
CLINICAL PICTURE OF THE DENTAL CARIES PROCESS :
A plaque community of sufficient mass to become anaerobic at the tooth
surface has the potential to be cariogenic. A large pop of MS virtually, assures
this occurrence. A sucrose – rich diet gives a selective advantage to MS and
allows the organic to accumulate in large numbers in the plaque community.
The sucrose rich environment also allows MS to produce large quantities of
extracellular polysaccharides. There form a gelatinous meta. That produces a
diffusion – limiting barrier in the plaque. The combination of limited diffusion
and tremendous metabolism activity makes the local environment anaerobic
and every acidic and thus an ideal environment for dissolution of the subjacent
tooth surface. Once the tooth surface becomes cavitated, a more retentive
surface area is available to the plaque community. This allows filamentous
bacteria that have poor adhesion abilities such as lactobacilli, to become
established in the lesion.
In the absence of change in the host’s diet and oral hygiene practices,
the cavitations of the tooth surfaces produces a synergistic acceleration of the
growth of the cariogenic plaque community and expansion of the cavitations.
This results in a rapid and progressive destruction of tooth structure. One
enamel caries penetrates to the DEJ, rapid lateral expansion of the carious
lesion takes place because dentin is much less resistant to caries attack. This
shelted, highly acidic and anaerobic environment provides an ideal niche for
lactobacilli, which was earlier through to be primary etiologic agent. But MS
are problem the most important organic in the initiation of enamel caries and
A.viscous is the most likely organic to initiate root caries. After caries initiation
lactobacilli than become residents of the carious lesion, once their niche is
43

available. Because of their acidogenic potential and aciduric lifestyle,
lactobacilli are probably very important in the progression of dentinal caries.
CLINICAL SITES FOR CARIES INITIATION :
The characteristic of a carious lesion vary with the nature of the surface
on which the lesion develops. There are three distinctly different clinical sites
for caries initiation.
1) Recess of development pits and fissures of enamel.
2) Smooth enamel surfaces that shelter plaque
3) Root surface
Pits and Fissures :
The pit and fissures of newly erupted teeth are colonized by bacteria.
These early colonizes from a “bacterial plug” that remains for a long time,
perhaps even the life of the tooth. There are large variation in the microfilaria
found in P and F, suggesting that each site can be considered a separate
ecologic system. Large numbers of gram Positive cocci especially S.sanguis
are found in the P and F of newly erupted teeth, whereas large number of MS
are usually found inc various P and F.
The shape of Pit and Fissure contributes to their high susceptibility of
caries. There is considerable morphologic variation in these structures. Some
pit and fissure ends blindly, other open near dentin and others penetrate to
entirely through enamel.
Pit and fissure caries expands as it penetrate into the enamel. This the
entry site may appear much smaller than the actual lesion, making clinical
diagnosis difficult. Carious lesions of pit and fissure develops from attack on
their walls.
44

The progress of dissolution of the walls of a Pit and fissure lesion is
similar in principle to that of smooth surface lesion because there is wide area
of surface attacking extending inward, paralleling the enamel rods. The
occlusal enamel rods bend down and terminate on dentin immediately below
the development of enamel fault. Thus a lesion originating in P and F effect a
greater area of DEJ than does a comparable smooth surface lesion. In a C/s it
is a invested ‘V’ with narrow entrance and wider at DEJ.
SMOOTH ENAMEL SURFACES :
The smooth enamel surfaces of a teeth present a less favourable site for
plaque retention. Plaque usually develops on one those smooth surfaces that
are near the gingiva or under proximal contact. The proximal surfaces are
particularly susceptible to caries because of extra shelter provided to resident
plaque due to proximal contact area immediately occlusal to the plaque.
Lesions starting on smooth surface have a broad area of origin and a conical or
pointed, extension towards the DEJ. The path of ingress of lesion is roughly
parallel to long axis of enamel rods in the region. A C/s of enamel portion of
smooth surface lesion shows a V shape with a wide area of origin and the apex
of V directed towards the DEJ. After caries penetrates the DEJ softening of
dentin spreads rapidly laterally and pulpally.
ROOT SURFACE :
The root surface is rougher than enamel and readily allows plaque
formation in the absence of good oral hygiene. The cementum covering the
root surface is extremely thin and provides little resistance to caries attack.
Root caries lesions have less well defined margins, tend to be U shaped in C/s
and progress rapidly because of lack of protection from an enamel covering. In
recent years prevalence of root caries is increased because of the increasing
number of older persons who retain more teeth, experience gingival recession
and usually have cariogenic plaque on exposed root surfaces.
45

CLINICAL MANIFESTATIONS OF DENTAL CARIES PROCESS :
EARLY CHANGES :
The earliest stage of caries is the first time demineralization of enamel
after a plaque pH depression below the critical pH. This cannot be detected
clinically but through sophisticated experimental laboratory techniques.
WHITE SPOT LESION :
The first visual clinical presentation of dental caries is commonly
referred to as a “white spot lesion”. Although it is considered to be an incipient
lesion, it is actually a relatively late state of caries process. The lesion must
progress to a depth of 300-500 µm to be clinically detectable. The clinical
appearance of the white spot is caused by loss of sub surface enamel, resulting
in the loss of enamel translucency. The surface enamel over the white lesion
can appear as being clinically intact and smooth, generally indicating that the
lesion is not active. Those white spots with rough surface because of increased
porosity indicate that the lesion is active and may progress. Although
formation of white spots has been most extensively studies with smooth surface
caries, it appears that P and F and root caries also start with sub surface
demineralization.
At the white spot stage the lesion may be arrested or reversed by
modifying any of the causative factors on increasing preventive measures.
Although this stage is a reversible stage of clinical process, it can sometimes
leads to softening and loss of enamel surface due to high cariogenic potential.
The white spot stage can be considered as a gradually arrested lesion,
which may / may not progress to a frank cavitations. Therefore it is considered
as a pre cavitated lesion suggesting that it will eventually lead to cavitations but
not a cavitated lesion.
HIDDEN / OCCULT CARIES :
46

Concerns have been raised that there is an increased prevalence of caries
progressing into dentin on tooth surface with clinically intact surfaces.
Apparently, the increased use of topical fluoride may he the effect of
preserving the integrity of enamel surface, which may mask the progression of
dentinal caries lesions beneath the surface.
FRANK CAVITATIONS :
As the caries process progresses, the subsurface lesion eventually leads
to the collapse of surface layer and formation of cavitation requiring
restoration. AT this stage of caries process, tooth destruction progress more
rapidly because the cavitations favours plaque accumulation and reduced
salivary access.
ARRESTED LESIONS :
Caries lesions can theoretically become arrested at any stage of caries
process, either because the causative factors have changed or protective factor
are increased. A change in the oral environment can result in the arrest of
caries process.
ACUTE DENTAL CARIES :
It is that form of caries, which is a rapid clinical course and results in a
early pulp involvement by the carious process the process of rapid that there is
little time for the deposition of secondary dentin. The dentin is usually stained a
light yellow. Cavity is deep, undermining of enamel, pain is present, softening
of dentin.
CHRONIC DENTAL CARIES :
It is that form, which progresses slowly and tends to involve the pulp
much alter than acute caries. The slow progression of the lesion allows
sufficient time for both sclerosis of the dentinal tubules and deposition of
secondary dentin in response to the adverse irritation. The carious dentin is
47

often stained deep brown. The cavity is generally shallow one with a minimum
softening of dentin. There is little undermining of enamel and pain is not a
common feature.
NURSING BOTTLE CARIES :
It is a type of rampant caries effecting the deciduous teeth. There is
wide spread carious destruction of deciduous teeth, most commonly the four
maxillary incisors followed by first molars and then cupids. TI is the absence
of caries in maxillary incisors, which distinguishes this disease from ordinary
rampant caries.
Most of ions through carious enamel can result in third dissolution of the
underlying dentin before actual cavitations of the enamel surface. The acid
attack at the external ends of the dentinal tubules initiates a pulpal response
Because the straie from horizontal liens of greater permeability in the enamel,
they probably contribute to the lateral spread of smooth surface lesions. The
striae appear to be accentuated in early lesions due to the decreased mineral
content.
In the occlusal enamel, the striae of retzius and the enamel rod directions
are mutually perpendicular. On the axial surfaces of the crown, the striae
course diagonally and terminate on the surface as slight depression. Caries
preferentially attack the cases of the cords and the more permeable striae of
Retziuss which promotes lateral spreading and undermining of the adjacent
enamel.
CARIES OF ENAMEL :
As believed by most investigations, the formation of this caries is
preceded by the formation of a microbial (dental) plaque.
48

The process varies slightly depending upon the occurrence of the lesion
on smooth surfaces and P and F. So it is best to discuss separately.
SMOOTH SURFACE CARIES
PIT AND FISSURE CARIES
SMOOTH SURFACE CARIES :
The surface of enamel, at has newly erupted teeth, is covered by a
membrane composed of the primary and secondary cuticle. The significance of
this membrane in forestalling the development of a carious lesion is not known.
Caries prone patients usually have extensive deposits which must be
removed prior to clinical examination. On clean dry teeth earliest evidence of
caries on the smooth enamel surface of a crown is “white spot”. They are
chalky white, opaque areas that are revealed only when the tooth surface is
desiccated and are termed as incipient caries. These areas of enamel loose their
translucency because of the extensive subsurface porosity and caused by
demineralization. These incipient lesions will partially / totally disappear
visually when the enamel is hydrated.
The surface texture of this lesion is unaltered and is undetectable by
tactile examination with an explorer.
Clinical Characteristic of Normal and Altered Enamel.
Hydrated Desiccated
Surface
texture
Surface
hardness
Normal
enamel
Translucent Translucent Smooth Hard
Incipient
caries
Translucent Opaque Smooth Softened
Active caries Opaque Opaque Cavitated Very soft
Arrested caries
Opaque
dark
Opaque dark Roughened Hard
49

These incipient lesion sometimes can be seen radiographs as a faint
radiolucency, limited to the superficial enamel. It has been shown
experimentally and clinically that incipient caries of enamel can remineralize.
Non cavitated enamel lesions retain most of the original crystalline
framework of the enamel rods and the etched crystallites serves as mediating
agents for remineralisation. Calcium and phosphate ions from saline can
penetrate the enamel surface and precipitate on the highly reactive crystalline
surfaces in the enamel lesion. The supersaturation of saliva with calcium and
phosphate ions serves as the driving forces for the remineralisation process.
Furthermore, presence of trace amounts of fluoride ions during this
remineralisation process greatly enhance the precipitation of calcium and
phosphate resulting in remineralised enamel becoming more resistant to
subsequent caries attack due to incorporation of more acid resistant
fluorapatite.
Arrested / remineralised lesions can be seen clinically as intact, but
discoloured usually brown / black spots. The change in court is presumably
due to trapped organic debris and metallic ions within the enamel. These
discoloured remineralised arrested caries areas are intact and are more resistant
to subsequent caries attack than the adjacent unaffected enamel. They should
not be restored unless they are esthetically objectionable.
ZONES OF INCIPIENT LESION :
The ability to artificially produce natural enamel lesions has resulted in
identification of a detailed description of the early stages of caries in enamel.
The four required observed zones ;
a) Zone 1 : Translucent zone
b) Zone 2 : Dark zone
c) Zone 3 : Body of lesion
d) Zone 4 : Surface zone
50

TRANSLUCENT ZONE :
Deepest zone is this zone and represents the advancing front of enamel
lesion. TI is not always present. By means of polarized light it has been shown
that this zone is slightly more process than sound enamel, having a prone
volume of 1% compared to 0.1% in sound enamel, i.e. 10 times more than the
sound enamel. The chemical analysis shows that there is fall in the magnesium
and carbonate levels suggesting that rich minerals are dissolved in these zone.
The name refers to its structure less appearance when perfused with quinoline
solution and examined with polarized light. Here the pores/voids form along
the enamel prism boundaries presumably because of the ease of hydrogen ion
penetration during the carious process.
DARK ZONE :
This zone lies adjacent and superficial to the translucent zone and it is
known as dark zone because it does not transmit polarized light. The light
blockage is caused by the presence of many tiny pores too small to absorb
quinoline. These smaller air / vapour filled pores make the region opaque.
Pore volume is 2-4%.
Dark zone is not really a stage in the sequence of the breakdown of
enamel, rather it is formed by deposition of ions into an area of prev. only
containing large pores. Experimental remineralization has demineralized
increases in the size of dark zone at the expansive of body of lesion. There is
also a loss of crystalline structure in the dark zone, suggestive of the process of
demineralization and remineralization.
Size of dark zone is probably an indication of the amount of
remineralisation that has recently occurred. This zone is narrow in rapidly
advancing lesion and wide in more slowly advancing lesions.
BODY OF LESION :
51

This zone lies between the relatively unaffected surface layer and the
dark zone. It is the largest portion of incipient lesion and the area of greatest
demineralization. In polarized light the zone shows a pore volume of 5% in
spaces near the periphery to 25% in the centre of the intact.
The striae of Retius (Rest liens within enamel and containing more
organism content) are well marked in this indicating preferential mineral
dissolution along these areas of relative higher porosity.
Bacteria may lie present in this zone if the pore ridge is large enough to
permit their entity. Studies using TEM and SEM demonstrate the presence of
bacteria invading between the enamel rods (prisms) in the body zone.
SURFACE ZONE :
This zone is relatively unaffected by the caries attack. This zone when
examined by the polarizing microscope and micro radiography, appears
relatively unaffected. The greater resistance of the surface layer may be due to
greater degree of mineralization and / greater concentration of fluoride in the
surface enamel. It is about 40 µm thick. However removal of the hyper
mineralized surface by polish gin fails to prevent the reformation of a typical,
well mineralized surface over the carious lesion.
It has a lower pore volume than the body of the lesion (5%) and appears
radiopaque when compared to the unaffected adjacent enamel.
Thus the intact surface over the incipient caries is a phenomenon of
caries demineralization process rather than any special characteristic of the
superficial enamel. Nevertheless the importance of the intact surface cannot be
overemphasized, because it serves as a barrier to bacterial invasion. Arresting
the caries at this stage results in a hard surface that may at times be rough,
though cleanable.
52

PIT AND FISSURE CARIES :
The caries process does not differ much in nature from smooth surface
caries except as the variations in anatomic and histologic structures dictate.
Caries in the fissure does not start at the base but it develops as a ring around
the wall of a fissure. As the caries progresses, it extends towards dentin parallel
to enamel prisms and eventually coalesces at the base of the fissure. This
produces a cone shaped lesion with the base of cone toward dentin and not on
enamel surface as in smooth surface caries.
CARIES IN DENTIN :
HISTOLOGY OF DENTIN :
It is the hard portion of tooth covered by enamel on the crown and
cementum on the root. Dentin is a calcified product of the odontoblasts that line
the inner surface of the dentin. Each odontoblast has an extension (Tome’s
fiber) into a dentinal tubule. The tubules traverse the entire thickness of dentin
from the pulp to the dentino enamel junction. Filling the space between the
tubules is the intertubular dentin, a rigid bone like material composed of
hydroxyapatite crystals embedded in a network of collagen fibers. Walls of
tubules lined with smooth layer of mineral termed as peritubular dentin. A thin
membrane is always observed lining the tubule in normal dentin. There is
controversy regarding the nature of lining some say it is true plasma membrane
of odontoblast or the limiting membrane similar to that found on the surface of
bone. In either case the tubule allows fluid must and ion transport necessary
for the remineralization of intertubular dentin, apposition of peritubular dentin
and/or perception of pain.
CLINICAL AND HISTOLOGICAL CHARACTERISTIC OF DENTINAL
CARIES
Progression of caries in dentin is different from progression in the
overlying enamel because of structural differences of dentin. Dentin contains
much less mineral content and possess micro tubules that provide a pathway for
53

ingress of acids and ingress of mineral. The DEJ has least resistance to caries
attack and allows rapid lateral spreading once the caries has penetrated the
enamel. Caries advance in dentin more than enamel because dentin provide
much less resistance to acid attack because of less mineral content. Caries
produces a variety of responses in dentin, including pain, demineralization and
the remineralisation.
Often pain is not reported even when caries invades dentin except when
deep lesions bring bacterial infection close to the pulp. Episodes of short
duration pain may be felt occasionally during earlier stages of dentin caries.
These pains are due to stimulation of mechanoreceptors in pulp tissue by not of
fluid through dentinal tubules that have been opened to the oral environment by
cavitation.
The pulp dentin complex reacts to caries attacks by attempting to initiate
remineralization and blocking off the open tubules. These reactions result from
odontoblastic activity and the physical process of demineralization and
remineralization. These levels of dentinal reaction to dental caries can be
recognized.
1. Reaction to long term, low level acid demineralization associated with a
slowly advancing lesion.
2. Reaction to moderate intensity attack.
3. Reaction to serve rapidly advancing caries char. By very high acid level.
The dentin can react defensively (by repair) out low and moderate
intensity care attacks as long as the pulp remains vital and an adequate blood
circulation.
IN slow advancing caries : Vital pulp can repair demineralized
dentin by remineralization of the intertubular dentin and by apposition of
peritubular dentin. Dentin responds to the stimulus of it first caries
54

demineralization episode by deposition of crystalline material in the lumen of
the tubules and the intertubular dentin of affected dentin in front of the
advancing infected dentin of lesion. This repair occurs only if the pulp is vital.
Dentin that has more mineral content than normal one is called as
“Sclerotic dentin”. This S.D. formation occurs ahead of the demineralization
front of a slowly advancing lesion and may be seen under old restoration. S.D.
is shiny and darkly colored and function is to wall off a lesion by blocking
(sealing) the tubules.
There is crystalline precipitates which from in the lumen of the dentinal
tubules in the advancing front of demineralization zone (affected dentin) once
these affected tubules becomes completely occluded by the mineral
precipitates, they appear clear when tooth is sectioned. This portion of dentin is
called transparent dentin zone which is the result of both mineral loss in
intertubular dentin and precipitation of this mineral in the tubule lumen. This is
softer than normal dentin.
The second level of dentin response to moderate intensity irritants
results in bacterial invasion of the dentin. The infected dentin contains a wide
variety of pathogenic materials / irritants including high acid levels, hydrolytic
enzymes, bacteria and bacterial cellular debris. These materials can cause
degeneration and death of the odontoblasts and their tubular extensions below
the lesion, as well as mild inflammation of pulp. Groups of these empty tubules
are termed as dead tracts.
The pulp may be irritated sufficiently from high acid levels / bacterial
enzyme formation to cause the formation of replacement odontoblasts which
produce reparative dentin / reactionary dentin on the effected portion of the
pulp chamber wall.
55

Third level of dentinal response is to severe irritation. Acute, rapidly
advancing caries with very high levels of acid production overpowers the
dentinal defenses and results in infection, abscess and death of the pulp. Small
localized infection in pulp produce an inflammatory response involving
capillary dilation, local edema and stagnation of blood flow which results in
local anoxia and necrosis.
Maintenance of pulp vitality is dependent on the adequacy of pulpal
blood supply. Recently erupted teeth with large pulp chambers and short wide
canals with large apical foramina have much more favourable prognosis than
fully formed teeth.
ZONES OF DENTINAL CARIES :
Caries advancement in dentin process through three changes ;
i) Weak and organic acids dematerialize the dentin.
ii) The organic material of dentin particularly collagen degenerates
and dissolves.
iii) The loss of structural integrity is followed by invasion of
bacteria.
As the carious lesion progresses, various zones of carious dentin may be seen.
These zones are more clearly distinguished in slowly advancing lesions. Btu in
rapidly progressing lesions the difference between the zones become less
distinct. Beginning pulpally at the advancing edge of lesion adjacent to normal
dentin, these zones are as followed.
i) Zone 1 : Normal dentin
ii) Zone 2 : Sub Transparent Dentin
iii) Zone 3 : Transparent dentin
iv) Zone 4 : Turbid dentin
v) Zone 5 : Infected dentin
56

Zone 1 : Normal Dentin
It is the deepest area which has tubules with odontoblastic process that
are smooth, and no crystals are in the humans. The intertubular dentin has
normal cross banded collagen and normal dense apatite crystals. No bacteria in
the tubules. Stimulation of dentin produces a sharp pain.
Zone 2 : Subtranparent Dentin (Affected)
It has zone of demineralization of the intertubular dentin and initial
formation of very fine crystals in the tubule 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 dentin is capable of
remineralization.
Zone 3 : Transparent Dentin :
It is a layer of carious dentin that is softer than normal dentin and shows
further loss of mineral from the intertubular 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 template for remineralization of
intertubular dentin and thus region remains capable of self repair provided by
pulp remains vital.
Zone 4 : Turbid Dentin
This is a zone of bacterial invasion and is marked by widening and
distortion of the dentinal tubules, which are 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.
57

Zone 5 : Infected Dentin :
The outermost zone, infected dentin, consist of decomposed dentin that
is terming with bacteria. There is no recognizable structure to the dentin and
collagen and mineral seem to be absent. Great numbers 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 the
infection.
5. * * * *
Nature has provided us teeth to perform the functions of cutting,
grinding and admixing of food with saliva. The hard enamel cover along with
the periodontal ligament can withstand forces of for masticulation.
It is very strange that the hardest tissue of the body – the enamel, which
is indestructible otherwise, can disintegrate in the oral environment “Caries”
(Latin meaning ‘dry rot’) is the name given to the process of slow
disintegration that may affect any of the biological hard tissue as a result of
bacterial action.
Dental caries is peculiarly a local disease, which involves destruction of
hard tissues of the tooth by metabolites produced by oral microorganisms.
Many authors have rightly referred it to as “Civilization
Dystrophy”. Dental caries is a multifactorial disease which is the most
prevalent chronic disease affecting human race. It effecting humans of all ages
in all regions of the world.
It is the disease that may be never eradicated because of complex
interplay of social, behavioural, cultural, dietary and biological risk factors that
are associated with its initiation and progression. The interaction among risk
factors such as cariogenic bacteria, saliva, fermentable carbohydrates and
58

fluorides in the oral environment, influence bacterial colonization as well as
either demineralization / remineralization.
CARIOLOGY :
Dental caries and periodontal disease are probably the most common
chronic disease in world. Although caries has affected humans since
prehistoric times, the prevalence of this disease has greatly increase din modern
times on a world wide basis which is strongly associated with dietary change.
However evidence indicates that this triad peaked and began to decline in many
countries like U.S., Europe, New Zealand and Asutralia. The exact cause not
known but attributed to the addition of trace outs of fluoride in drinking water.
The decline in caries prevalence is also related to socio economic status.
That is people of higher and middle classes the decline is prominent but in
lower socio economic classes and rural residents there is higher prevalence of
caries. It is observed by NHANES (National Health and Nutritional
Examination Survey) that 80% of caries occurred of children which are of
lower socioeconomic status.
The limited segment of population experiences most of disease and this
effect is called as polarization. Prevalence of caries decrease is in developed
countries and increasing in less developed countries because of the cost of
caries to society is enormous.
Considering the magnitude and almost all universal impact of caries,
eradication of caries depends on availability of four things.
1) Potent eradicator weapon (Vaccine)
2) Strong and efficient public health service support
3) Popular support for the prognosis
4) An efficient surveillance system to monitor caries activity on
a population level.
59

Caries eradication is not achieved because these four basic requirements have
not been met.
DEFINITION OF CARIES :
Dental caries in simple terms can be defined “as the irreversible, slow
progressing decay of hard tissues of the tooth”.
It can be defined as the microbial disease of calcified tissues of teeth,
characterized by demineralization of the inorganic portion and destruction of
organic substances of the tooth – Shafer.
As a localized post eruptive, pathological process of external origin
involving softening of the hard tooth tissue and proceeding to the formation of
cavity – WHO.
Dental caries is an infectious microbial disease of the tooth that results
in localized dissolution and destruction of the calcified tissues – Sturdevant.
1. Incipient / Initial / Primary carious lesion : That describes the first attack
on a tooth surface.
2. Recurrent / secondary lesion : One occurred that is observed under /
around the margins or surrounding walls of an existing restoration.
3. Acute / rampant caries : Rapidly invading process that usually involves
severe teeth. Lesions are soft and light colored and are frequently
accompanied by severe pulp reactions.
4. Pit and fissure caries : Those originating in the pits and teeth and a
buccal, lingual and occlusal surfaces of posterior teeth.
5. Smooth surface carious lesion : Those carious lesions originating in and
around all surfaces and pits.
6. Forward backward : The first component of enamel to be involved in the
carious process is the interprismatic substances. The disintegrating
substances will proceed via this substance causing the enamel prisms to
be undermined. The resultant caries involvement in enamel will have a
cone shape.
60

In convex surfaces (P and F) base of cone will be away from DEJ, while in
concave surfaces. The base of cone will be away for the DEJ.
The first component to be involved in dentin is the protoplasmic
extension within the tubules. These extensions have their maximum spacing at
the DEJ but as they approach the pulp chamber and root canals the tubules
become more densely arranged with fever interconnection. One can therefore
in against caries cones in dentin will have a cone shape base of cone toward
DEJ.
Decay starts in enamel and then involves dentin. So whenever the caries
cone in enamel is larger or atleast the same size as that in dentin, it is called
forward caries.
However, if the carious process in dentin progresses much faster in
dentin than it doe sin enamel from its dentinal side. At this stage, therefore it
becomes back ward decay.
Chronic Carious Lesions : Variable depth, longer standing and tend to be fewer
in number. Dentin in this condition is hard in consistency and dark in colour.
Smile carious lesions : Caries associated with aging process ;
- Exclusively on root surface of teeth.
- Follow gingival recession.
Residual caries : Caries that is not removed during a restorative procedure
either by accident, neglect or intention.
Simple carious lesion : Involves only one surface of the tooth.
Compound carious lesion : Only 2 surfaces of teeth.
Complex carious lesion : 3 or more surfaces of teeth.
61

CLASSIFICATION OF DENTAL CARIES :
On the basis of clinical features, dental caries may be classified to 3
basic factors.
1. Morphology : According to the anatomical site of lesions.
2. Dynamics : According to severity an rate of progression of lesions.
3. Chronology : According to age patterns at which lesions predominate.
A. Classification Based on Morphology :
Classified Type I
Type II
I. Pit and fissure caries : Pit and fissures caries are limited to the occlusal
surfaces of molars and bicuspids the buccal pits of molars, and lingual surfaces
of maxillary anterior teeth.
II. Smooth surface caries
a) Interproximal lesions : Mesial / distal contact points.
b) Cervical lesions : On buccal / lingual surfaces near the dentin enamel
junction.
B. Black’s Classification (Therapeutic Classification)
Based on morphological classification of dental caries.
Class I : Structural defects of teeth such as pits, fissures and sometimes
defective grooves. They usually have 3 locations ;
a) Occlusal surfaces of molars and premolars.
b) Occlusal 2/3rd
of buccal and lingual surfaces of molars
c) Lingual surfaces of anterior teeth.
Class II : Found on proximal surfaces of bicuspids and molars.
Class III : Found on proximal surfaces of anterior teeth that donot involve or
necessitate removal of the incisal angle.
62

Microbiology of dental caries/ orthodontic course by indian dental academy

Microbiology of dental caries/ orthodontic course by indian dental academy

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