DEPARTMENT OF CONSERVATIVE AND ENDODONTICS

COLLEGE OF DENTAL SCIENCES, DAVANGERE.

SEMINAR ON

DENTAL CARIES

Presented By

Dr.Meena Reddy P.G. Student

ree Ganeshaya NamahaMULTIFACTORIAL 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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DiseaseGenetic 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

2. Agglutinins

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- 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

22

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.

23

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 :

24

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.

25

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

26

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 :

27

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.

28

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

29

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 :

30

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

31

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.

33

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

34

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 :

35

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.

36

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

37

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 PO34 which react with H+ to form H2O

and HPO24.

On total depeletion of (OH- and PO34) 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.

38

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 :

39

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

40

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

41

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.

42

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.

43

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 m 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 :

44

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

45

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.

46

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

47

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

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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 :

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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 m 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.

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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

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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

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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.

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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

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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.

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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

56

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.

57

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.

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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.

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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.

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Class IV : Found on the proximal surfaces of anterior teeth and involve /

require the removal and restoration of incisal angle(s).

Class V : Found at the gingival third of the facial and lingual surfaces of

anterior / posterior teeth.

Class VI : Were not originally included in Black’s classification. They are also

found on molar and premolar cusp tips, axial angles of teeth, or any highly

cleansable areas.

C) Classification related to degree and rate of progression of caries

1. Infancy (Sooth / Nursing Bottle) caries

It’s a form of rampant caries effecting the deciduous dentition. This is

due to prolonged use of ;

- Nursing bottle (Mil / Milk formula, fruit juice)

- Breast feeding

- Sugar / Honey sweetened pacifiers.

2. Adolescent caries

3. Geriatric / Senile caries

According to Sturdevant – Base don location, extent and rate.

Location of Caries :

1. Primary caries : Original carious lesion of the tooth.

a) Caries in enamel P and F

b) Smooth surface

c) Root surface

i) Backward caries : Spread of caries along the DEJ exceed the caries

in the contiguous enamel, caries extends into this enamel from DEJ.

ii) Forward caries : Caries where the caries cone in enamel is larger or

at least same size as that of dentin.

iii) Residual caries : Caries that remains in a completed cavity

preparation either accidentally or by the operator.

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2. Secondary caries

Extent of Caries :

1. Incipient caries (Reversible)

2. Cavitated caries (Non reversible)

Rate of caries :

1. Acute (rampant) caries

2. Chronic (slow / arrested) caries

NEW CAVITY CLASSIFICATION :

Given by Graham J. Mount W. Rosy Hume (Australian Dental Journal

1998)

This classification is designed to simplify the identification of lesion and

to define their complexity to provide benefits for the profession and their

patients. It has been proposed according to SITE and SIZE of the lesion.

The three sites of carious lesion :

It can occur in three sites on the crown / root of a tooth, that is in those

areas subject to the accumulation of plaque. These are ;

Site 1 : P and F and enamel defects on occlusal surfaces of posterior teeth and

on other smooth surfaces, such as cingulum pits on anteriors (includes all

lesions of black class I but also other smooth surfaces).

Site 2 : Approximal surfaces immediately below the areas in contrast with

adjacent teeth (all lesions associated with contact areas) includes all anterior

and posterior teeth. Includes all lesions of Black’s class II, III and IV lesions.

Site 3 : Describes cervical 1/3 of crown following gingival recession either in

enamel or dentin or exposed root around full circumference of tooth. Includes

Black’s class V and also extends to root surface for recession.

The above three sites are then grades as 4 sizes according to extent of

progress and gives the guidance for management of any stage.

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Size 1 (Minimal) : Minimal involvement of dentin just beyond treatment by

mineralization alone.

Size 2 (Moderate) : Moderate involvement of dentin still sufficient amount of

enamel present supported by dentin and not likely to fail under occlusal load.

That is remaining tooth structure is sufficiently strong to support the

restoration.

Size 3 (Enlarged) : Enlarged and more extensive lesion. Remaining tooth

structure is weakened to the extent that cusps or incisal edges are split or are

likely to fail if felt exposed to occlusal load / incisal load. The cavity design

will have to be modified and enlarged to the extent that the restoration will take

the main occlusal load and protect the remaining tooth structure.

Size 4 (Extensive) : There is extensive loss of tooth structure, such as loss of a

cusp.

SizeMinimal

1Moderate

2Enlarged

3Extensive

4SitePit / Fissure 1 1.1 1.2 1.3 1.4Contract Area 2 2.1 2.2 2.3 2.4Cervical 3 3.1 3.2 3.3 3.4

THEORIES ON ETIOLOGY OF CARIES :

Dental caries is a multifactorial disease. The process by which a tooth

can be destroyed easily in oral cavity, which is indestructible otherwise, is very

difficult to understand. Till today no single theory can explain the

phenomenon of caries.

In view of unique characteristics of the tooth vis-à-vis caries, the caries

does not fall into any of the common pathological lesions of oral cavity.

Dental caries is not inflammatory in origin, nor a degenerative in nature and

neither it is neoplasm. It is a local disease which involves destruction of hard

tissues of tooth by metabolites produced by microorganisms.

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Numerous reference to dental caries, including early theories to explain

mechanism of caries have been found. Before we undertake correct concept of

caries etiology lets diseases in brief the early theories.

THEORIES – EARLY CONCEPT

- CURRENT CONCEPT

EARLY CONCEPT

a) Worm theory

b) Humoral theory

c) Vital theory

d) Chemical / parasitic theory

e) Septic theory

CURRENT CONCEPTS :

a) Acidogenic theory (Chemico-Parasite Theory) – Miller, 1890.

b) Proteolytic theory – Gottlieb (1944), Frisbic (1944), Pincus (1946).

c) Proteolytic cheltion theory – Schatz, Martin 1954.

d) Sucrose – Chelation theory – Eggars – Luna (1967)

e) Levine’s theory – Levine 1977

f) Phosphate – Sequestration theory

g) Autoimmune theory

h) Genetic theory

EARLY THEORIES :

a) Worm Theory (500 BC)

The earliest reference of tooth decay and tooth arched, probably

appeared around 14 cent B.C. when oracle love inscriptions were excavated

from the ruins of the Ying Dynasty, showed the character meaning ‘caries’.

According to the concept of that time, the cause of caries was thought to be

“invasion of worms into teeth. Therefore the character of caries was shown as

a worm over tooth surface. The association of systemic disease and teeth was

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probably obtained from writings of a physician around 668 B.C. The physician

ahs mentioned that the inflammation in his legs and arms was due to tooth and

that it must be extracted.

The legend of worm was discovered on ones of the many day tablets

excavated near the Niffer, Ur and other countries with the Euphrates valley of

lower Mesopotamian. The early history of India, Egypt and Writings of Homer

also makes reference to the worm as the cause of tooth ache.

b) Humoral Theory :

According to Galem the ancient Greek physician considered that a

persons physical and mental constitution was determined by the relative

proportions of the four humours of the body namely ;

Blood : Sanguine

Phlegm : Phelgniate

Black bile : Melanocholic

Yellow bile : Choleric

All diseases including caries could be explained by an imbalance of these

humours. According to Galen dental caries was produced by internal action of

acids and corroding humours.

Certain authors such as Hippocrates favoured this concept and also

added that the accumulated debris around the teeth help to corroding action.

He further stressed that stages of juices over the tooth surface caused tooth

ache.

c) Vital Theory :

The vital theory, regarded dental caries as originating within the tooth

itself, analogous to bone gangrene. This theory, proposed at the end of 18 th

century, remained dominant until the middle of 19th century. A clinically well

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known type of caries is clear, extensive penetration into dentin, even into the

pulp, but with a barely detectable catch in the fissure.

d) Chemical / Acid Theory :

In 17th and 18th centuries, there emerged a concept that teeth were

destroyed by acids formed in the oral cavity. The exact nature and exact

mechanism of acid formation was not known.

Robertson (1935) proposed that dental decay was caused by acid formed

by fermentation of food particles around the teeth.

Different postulates were given : one suggestion was that putrefaction of

protein gave rise to ammonia, which was subsequently oxidized to nitric acid

and another was that food was decomposed to sulphuric acid. Till then activity

of bacteria was not recognized

c) Parasitic / Septic Theory :

In 1843, Erdl described filamentous parasites in the “surface membrane”

(plaque) of the tooth. Shortly thereafter, Ficinus (1847), a Dresden physician,

observed filamentous microorganisms, which he called denticoloar in material

taken from the carious cavities. They said that these bacteria caused

decomposition of enamel cutile.

CURRENT THEORIES :

The etiology of dental caries is generally agreed to be a complex

problem, complicated by many indirect factors, which obscure the direct

cause / causes. There is no universally accepted opinion n the etiology of

dental caries.

ACIDOGENIC THEORY / MILLER’S CHEMICO-PARASITIC THEORY :

This theory is a blend of the above two theories (chemical and parasitic)

because it states that caries is caused by acids produced by microorganisms of

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mouth. And the writings of Millers W.D. helped to establish this concept firm

basis. Work of Willoughley D.Miller (1853-1907) had a most profound effect

on the understanding of caries etiology and subsequent caries research. Miler

concluded that “no single species of microorganisms caused caries but rather

that the process was mediated by an oral organism capable of producing acid

and digesting protein.

Miller hypothesized that “dental caries / decay is a chemico-parasitic

process consisting of two stages ;

1) Decalcification of enamel which results in the total destruction

and decalcification of dentin as a preliminary stage.

2) Dissolution of the softened residue.

The acid which effects this primary decalcification is derived from the

fermentation of sugars lodged in the retaining centre of the teeth.

Further weight was added to this theory by Williams (1897) who

observed dental plaque on the enamel surface. Plaque was considered to be a

means of localizing organic acids formed by microorganisms in contact with

the tooth surface. The plaque partially prevented dilution and neutralization of

organic acids by the saliva.

The theory has been accepted by the majority of investigators in a form

essentially unchanged since inception. The bulk of scientific evidence does

implicate carbohydrates, oral microorganism and acids and for this reason

decreases further consideration.

PROTEOLYTIC THEORY (GOTTLIEB AND DIAMOND AND

APPLEBAUM, 1994) :

The classical chemicoparasitic theory is not universally accepted.

Instead, it ahs been proposed that the organic / protein elements are the initial

pathway of invasion by microorganisms. The human tooth contains only about

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1.5 – 2% of organic material of which 0.35 – 0.4% is protein. According to

this theory the organic component is most vulnerable and is attacked by

hydrolytic enzymes of microorganisms. This precedes the loss of the inorganic

phase.

Gottleib (1944) said that the “initial action was due to proteolytic

enzymes attacking the lamellae, rod sheaths, tufts, and walls of the dentinal

tubules. The yellow pigmentation which was seen was attributed to pigments

produced by the proteolytic organisms.

Frusbie (1944) described cares as, caries is initiated by at slightly

alkaline pH produced by the proteolytic activity involving depolymerisation

and liquefaction of the organic matrix of enamel.

Once the organic part sets free after the dissolution of inorganic part,

these salts are dissolved subsequently by acidogenic bacteria.

Pincus (1949) contended that proteolytic organisms attacked the protein

elements, such as dental cuticle and then destroyed the prism sheaths. The

loosened prisms then fell out mechanically. He also suggested Nasmythis’

membrane and the enamel proteins are mucoproteins which acted upon by

sulphatase enzymes of gram negative bacilli yielding sulfuric acid. The

released sulfuric acid could combine with the calcium of mineral phase.

Though enamel contains 10 to 1.5% of organic matrix out of which

0.6% is protein, initiation of caries with breakdown of this small amount of

protein is highly questionable. Till date significant loss of enamel tissue then

proteolytic activity has not been proved experimentally. Moreover enzyme

system capable of attacking keratin has also been not demonstrated. Therefore

this theory by and large lacks experimental support.

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Frisbier (1944) described caries as a proteolytic process involving

depolymerisation and liquefaction of the organic matrix enamel. The less

soluble inorganic salts could then be freed from their organic bond favouring

thrice solution by acidogenic base that secondarily penetrate along widening

paths of ingress.

PROTEOLYSIS – CHELATION THEORY :

Chelation is a process involving the complexing of a “metallic ion” to a

“Complex substance” through a coordinate covalent bond which results in a

highly stable, poorly dissociated or weakly ionized compound (Chelar law).

This theory proposed by Schatz et al (1955) implies a simultaneous

microbial degradation of the organic components (hence proteolysis0 and the

dissolution of minerals of the tooth by the process of chelation.

Numerous naturally occurring chelating agents exists, the most common

of these being the citrates. Amino acids are also known to act as chelators, as

well as hydroxyl and ketoesters of eyerhaf emben system pathway,

phosphorylated and nonphosphorylated compounds in the hexose

monophosphate shunt, polymorphates including these involved in

phosphpsylate, certain antibiotics lipids carbohydrates, enzymes, vitamins,

oxalates etc.

Chelation ha been proposed as an explanation for tooth decay whereby

the inorganic components of enamel can be removed at neutral / alkaline pH.

The proteolysis – chelation theory considers dental caries to be a bacterial

destruction of teeth where the initial attack is essentially on organic

components of enamel. The beak down of this organic matter have chelating

properties and thereby dissolve the minerals in the enamel. Thus both the

organic and inorganic constituents of enamel are simultaneously demolished.

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According to this theory, decalcification is mediated by a variety of

complexing agents such as acid anions, amines, peptides, polyphosphates and

carbohydrate derivatives. These substances are microbial breakdown products

of either the organic components of enamel / dentin / of food that is ingested

and diffuses through the plaque. Oral keratinocyte bacteria are thought to be

involved in the process. Difference in keratin content of the enamel in children

with high caries and low caries experience are considered important. It should

be noted that only a small fraction of enamel mass any resemblance to the

keratin of hair.

Several reconciliations must be made if proteolysis – chelation theory is

to be accepted. These include ;

1) The observation of increased caries incidence with increased sugar

consumption. This is because increased sugar / carbohydrate consumption

leads to ;

a) Stimulating / increasing proteolysis.

b) Producing conditions under which keratinous proteins are less stable.

c) Compelxing calcium

2) The observation of increased lactobacillus counts with high caries activity.

This is because of the result of carious process rather than the cause thus Schatz

suggested that ;

a) Proteolysis may provide ammonia which presents a pH drop that would tend

to inhibit growth of lactobacilli.

b) The release of calcium from hydroxyapatite by chelation might encourage

the growth of lactobacilli, since calcium has been reported to produces this

effect.

c) Calcium exerts a vitamin spacing action on some lactobacilli.

3) The observation of decreased caries incidence following topical / systemic

administration of fluoride.

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a) This may occur through formation of fluroapatite which strengthens the

linkages between the organic and inorganic phases of the enamel thereby

preventing a reducing complexing.

IV. LEVINE’S THEORY :

Levine established the chemical relationship of enamel plaque and the

factors which determined the movement of minerals from Saliva / plaque to

enamel and vice versa which he termed as “Ionic See-Saw mechanism”.

In this mechanism be emphasize that demineralization are

remineralization of enamel is a continuous process. IF in a given interval of

time, more ions have the enamel than enter it, then there is a net

demineralisation which amounts to start of the carious process. It has been

proved that passage of ions is not a one way process and that ions are

constantly being exchanged between enamel and plaque. At times, the chemical

condition at enamel plaque interface may favour outward most of ions and at

other times the situation may be reversed. This delicate balance of ion is

dependent on many factors. The three most important factors which are

respectively are ;

a) pH of plaque

b) Calcium and phosphate ion concentration at the interface

c) Fluoride ion concentration

If pH falls below 5 (critical pH0 eg. During carbohydrate in take,

mineral ions are liberated from the hydroxyapatite crystals of enamel surface

and diffuse into plaque within 20 minutes salivary buffer neutralize the acid.

At this stage, the plaque is super saturated with ions some of the ions are lost

and others are deposited onto the enamel. With such repeated episodes, overall

demineralization occurs which leads to caries.

For this phenomenon to occur the, actual mineral ion concentration of

saliva is important. IF free calcium and phosphate ions are higher in saliva

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because of dietary and other sources, there would be a greater tendency of ions

to move from plaque to enamel. Reverse is true if ion concentration is saliva is

low.

Another factor which plays an important role in see-saw mechanism is

fluoride. Fluoride favours movement of ions from plaque to enamel. The initial

deposit appears to be in the form of calcium fluoride. Fluoride concentration as

low as 5 ppm can but the see-saw mechanism.

OTHER THEORIES :

According to him oral fluids protect the enamel by providing a

protective covering on the enamel surface attrition makes fissures wider and

removes the superficial layer of enamel along with initial carious lesion, if

present. The new layer of enamel becomes protective again with the help of

oral fluids. In areas where the oral fluids cannot reach eg. Contact area cannot

be made protective against the carious attack.

Caries starts in contact areas where the protective action of oral fluids is

not there i.e. the perimeter of the contact alia. Smaller the area, more is the

perimeter /unit area; as the area becomes large, the perimeter / unit area falls.

Similarly smaller the contact area the perimeter / unit area as the contact

becomes more (may be physiologic / attrition) the perimeter / unit area falls.

The effect of acid attack depends on perimeter/unit area.

Greater the perimeter stronger the attack. As the length of perimeter /

unit area falls with increase in size of contact area, the carious lesion progress

faster in a smaller contact area.

According to Dr.Bandlish the meticulous contact through brushing and

cleaning reduces the caries not by removing plaque but removing enamel.

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PROTEOLYTIC THEORY

CHELATION :

Chelate results from combining an inorganic metal ion with at least 2

electron rich functional groups in a single organic molecule.

Chelating agent is a molecule capable of seizing and holding a metal ion

in a claw like grip and forming a heterocyclic ring. The atoms holding the

metal ion are called ligands and are usually O2 , N2 sulphur.

In biology there are well known chelates including haemoglobin

(containing iron) chlorophyll, Vitamin B-12, enzymes cytochrome oxidase

(Iron and Copper) and carboxy peptidase – A (Zinc).

Example of chelate structures are lactate or citrate and calcium. Calcium

is held covalently by two oxygen’s of the carboxyl groups and in a coordinate

covalent bond involving mushard electrons of the alcohol groups.

Citrate can effectively form chelates of calcium and may be important

for the physiological mobilization of calcium from skeleton and transport of

complexes calcium to serum. Lactate is of negligible importance as an organic

chelator of calcium.

Chelation has been proposed as an explanation for tooth decay whereby

the inorganic components of enamel can be removed at neutral or alkaline pH.

This prot-chel theory considers. Dental caries to be a bacterial

destruction of teeth where the initial attack is essentially on organic

components of enamel.

The break down products of this organic material have chelating props

and thereby dissolve the mineral in the enamel. Thus both organic and

inorganic constitutes of enamel are simultaneously demolished.

Accumulation to this theory, decalcification of enamel is mediated by a

variety of complexing agents, such as acid anions, amines, amino acids,

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peptides, polyphosphates and carbohydrate derivatives. These substances are

microbial break down products of either organic components of enamel / dentin

of food that is ingested and diffuses through the plaque.

OTHER THEORIES :

Phosphate – Sequestration Theory :

Postulated that steady state equilibrium exists between inorganic

phosphate of saliva and mineral phase of enamel.

According to this theory, as bacteria take up phosphate, inorganic

phosphate must be removed from enamel to maintain the equilibrium.

Bacterial – Phosphatase theory :

Found that bacterial alkaline phosphatase was found to release

phosphate from enamel in vitro. It was speculated that this enzyme could

participate in caries destruction by acting on phosphoproteins of enamel.

Difficulty with this theory is that this enzyme is an intracellular enzyme

so lysis of cells has to occur to free the enzyme.

THEORIES :

CHEMO-PARASITIC THEORY – MILLER’S :

Blend of above 2 theories because ;

6. States that caries is caused by acids produced by microorganisms of mouth.

7. It is customary to credit this theory to W.D.Miller who helped to establish

this concept on firm basis. But however contributions were given by many.

a) Pasteur : Discovered that microorganism transform sugar to lactic acid

in the process of formation.

b) Another French man Emil Magitot, demineralized that fermentation of

sugars caused dissolution of tooth mineral in vitro.

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c) In Berlin, Lefer and Rottenstien (1867) gave additional experimental

evidence implicating that acids and bacteria are the causative agents of

caries.

They described a specific micro organism, hepato thrix bacillus, in the tubules

of carious dentin and thought that it was respectively for enlarging the tubules

and facilitates rapid penetration of acids.

Then work of an American, W.D. Miller (1853-1907) at University of

Berlin had a most profound effect on the under standing of caries etiology and

subsequent caries research.

Miller demonstrated the following factors ;

1. Acid was present with in the deeper carious lesions, as shown by reaction

on litmus paper.

2. Different kinds of food (bread, sugar etc) mixed with saliva and incubated

at 37o C could decalcify the entire crown of a tooth.

3. Several type of oral bacteria (at least 30 types) could produce enough acid

to cause dental caries.

4. Different microorganism invade carious dentin. Then HC concluded;

a) No single species of microorganism caused caries.

b) Rather the process was mediated by an oral microorganism capable

of producing acid and digesting protein.

DENTAL DECAY :

It is a chemo-parasitic process consisting of 2 stages ;

1. Decalcification / softening of tissues (for enamel Decalcification

signifies its total destruction).

2. Dissolution of softened residue

Further it was added to this by Williams (1897) who observed dental plaque on

enamel surface plaque was considered to be a means of localizing organic acids

formed by micro organisms.

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In saliva, chief buffer systems are HCO3 and HPO4. Bicarbonate is by far the

most important salivary buffer due to several reasons.

1. It can buffer rapidly by losing CO2 (compared with blood).

2. Its pK (Point at which pH changes the least (acid-base) is close to that

encountered in plaque, therefore it is more effective in that range.

3. As flow rate increases, the HCO3 (bicarbonate) concentration increases,

whereas HPO4 falls slightly with increased flow rate.

4. After removing of HCO3 by a current of CO2 free air at pH5, the

buffering capacity of saliva is reduced markedly.

Dialysis of saliva which removes both HCO3 and HPO4 but not protein – leads

to total loss of salivary buffer capacity. This indicates that salivary proteins

can be disregarded as buffers.

Urea is continuously secreted in saliva, plaque microorganism can

convert urea to other introgenous products and ammonia. The NH3 thus

formed can also serve as buffer.

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