Dental Caries

Dental Caries

Definition:
− Dental caries is an irreversible progressive bacterial damage of hard
tooth structure exposed to the oral environment.
− Characterized by production of organic acids by specific strains of
bacteria causing demineralization of inorganic portion of the tooth
structure followed by destruction (breakdown) of the organic matrix.
− Break down of enamel and dentin creates a path for bacteria to reach
the pulp. Eventually inflammation of the pulp and, the periapical
tissues will occur.

Classification of dental caries:

I- According to site of attack:
1. Pit& fissure caries
• Occurs on occlusal of molars and premolars, on the buccal and
lingual surfaces of molars and lingual surfaces of maxillary
incisors.
2. Smooth surface caries
• Occurs on the interproximal surfaces below the contact area and
on gingival third of the buccal and lingual surface of the teeth
that are not self cleansing.
3. Root caries
• Occur when the root is exposed to the oral environment as a
result of periodontal disease.
4. Recurrent caries
• Occurs around the margin or at the base of existing restoration.
• It is due to in adequate or poor adaptation of the filling material
which produce leaky margin.

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II- According to rapidity (rate of attack):

1. Acute dental caries (Rampant caries)
• It is rapidly processing caries involving many or all of erupted
teeth.
• It occurs in children and young adults. Leads to early pulp
involvement because they have teeth with large pulp chambers and
wide and short dentinal tubules and open with no sclerosis.
• Baby Bottle caries is a form of rampant caries affect deciduous
teeth due to frequent and prolonged use of nursing bottle
containing milk, fruit juice or sweetened water. Commonly affect
the maxillary incisors followed by first molar. The mandibular
incisors usually escape because they are covered by the tongue.
2. Chronic dental caries
• It progress slowly and tends to involve the pulp later than acute
caries. Most common in adult.
• The slow progress of the lesion allow a sufficient time for both
sclerosis of dentinal tubules and deposition of secondary dentin.
• Pain is not a feature of chronic caries.
3. Arrested caries
• Precavity (white spot) interstitial caries may become arrested when
the adjacent tooth is lost so that the stagnation area is removed.
• The lesion may become remineralized by minerals from the saliva.

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Essential Requirements for Development Of Dental Caries:

1. Cariogenic (acidogenic) bacteria
2. Bacterial plaque
3. Time, where a sufficient length of time is needed for the
development of dental caries
4. Fermentable bacterial substrate (sugar)
5. Susceptible tooth surfaces.

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(A) Susceptible tooth

1. Position:

• Malposed, crowded teeth related to clasps and orthodontic

appliance are more susceptible to caries because of the creation
of stagnation or retention sites.

2. Morphology:

• Deep and narrow pits and fissures, contact area and undercut are
stagnation or retention, sites and are most susceptible to caries.

3. Structure:

• Enamel hypoplasia and enamel hypocalcification may affect the

rate of progression but not the initiation of caries.

4. Fluoride:

• Fluorides from drinking water and other sources are taken up by

calcifying tissues during development. When the fluoride content
of the water is 1 ppm or more the incidence of caries decreases.

The cariostatic effect of fluoride:

a) Increasing enamel resistance to caries:

• Fluoride replaces the hydroxyl group in the hydroxyapatite forming

fluoroapatite which is less soluble in acids than hydroxyapatite and
thus more resistant to acid demineralization.

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b) Enhancement of remineralization process of the carious lesion:

• The presence of fluoride in the oral environment (saliva and

plaque) facilitates the remineralization (repair) of the
demineralized carious lesion.

c) Inhibition of bacterial growth:

• Fluoride inhibits bacterial enzymes and thus stops bacterial

activities, e.g. Glucokinase, Fructokinase, Glucosyltranferase, etc.

(B) Carbohydrates

Carbohydrates are that they are the only component of the diet that can be
acted upon by plaque bacteria producing acids causing caries.

Factors affecting cariogenicity of carbohydrates:

1. Types of carbohydrate

• Monosaccharide and disaccharide are suitable substrate for oral

bacteria to utilize for energy and organic acids production mainly
lactic acids and pyruvic acids
• Sucrose, in particular is the "arch criminal" of dental caries.

Factors determining the cariogenicity of sucrose:

1. Sucrose most frequently consumed carbohydrate (table sugar, drinks,

jam, etc.) because of its low cost.

2. It promotes colonisation of teeth by Streptococcus mutans

3. Cariogenic bacteria (S.mutans) form extracellular polysaccharides

(dextran) of bacterial plaque faster from sucrose than from other
sugars. The disaccharide bond of sucrose contains enough energy to

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react with bacterial enzymes (glucosyltransferase) to form

extracellular dextran matrix of dental plaque.

4. Its small molecule allows it to diffuse readily into plaque

5. Bacterial metabolize sucrose rapidly with the production of organic

acids

2. Total amount of carbohydrate intake:

• Increased intake of fermentable carbohydrate is followed by

increased caries activity.

3. Frequency of carbohydrate intake:

• The frequent intake of carbohydrate at intervals (between meals)

will cause increased activity. That is because:

a) Increased period of availability leading to increased periods of activity

of microorganisms utilizing sugar and producing more acid.

b) The cleansing effect of other fibrous food elements is absent.

4. Consistency and texture of carbohydrate:

• Sticky carbohydrates are more cariogenic than solutions of sugars

because they are:

o Slowly washed by saliva.

o Attached to the tooth surface longer period of time

o Remains accessible to the oral micro-organisms, with more

acid production,

• Dried powdered milk is sticky and highly cariogenic while liquid

milk is not sticky and less cariogenic.

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5. Refinement of carbohydrate:

• It is the treatment of carbohydrate in industry to in order to make them

whiter, sweeter, improving its flavor and moving its fibrous material.

• Refinement of carbohydrate will increase its cariogenecity because:

a) Increased concentration of fermentable fraction of carbohydrate.

b) Removal of fibrous material so no cleansing effect.

c) Additional amounts of sugars are added when making cakes,

biscuits, etc.; this will increase concentration of fermentable
carbohydrate and also increase its adhesiveness.

• However, xylitol (a non fermentable sugar alcohol) is considered to be

a refined carbohydrate yet is non cariogenic. On the other hand, honey
is not refined but it is highly cariogenic.

(C) Micro-organisms

• The most potent acid producing strains is streptococcus viridians

(st.mutans, st.sanguis, st. salivaris, st. milleri) and some strains of
lactobacilli and actinomyces.

• The characteristic features of cariogenic bacteria include

the following:

1. Acidogenic property: Ability to produce acids from fermentable

carbohydrate. These acids are sufficient enough to drop the pH below
the critical level (pH 5.5) when demineralization of enamel starts and
caries is initiated.

2. Aciduric property: Ability to live, grow and function in high acidic

media i.e. a low pH level.

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 Dental Caries

3. Formation of abundant extracellular polysaccharide especially

dextran and levan for formation of plaque. So these bacteria can
produce smooth surface caries and pit and fissure caries in
gnotobiotcs.

4. Formation of intracellular polysaccharide (amylopectin):

· It resembles starch or glycogen.

· It is made up at glucose units.
· It is used by the organisms at the time of dietary
carbohydrate deficiency.
5. Micro-organisms should have attachment mechanisms for firm
adhesion to the surface and to each other.

Dextran Levan
1. Glucose polymer 1. Fructose polymer
2. Insoluble 2. Water soluble
3. Highly adhesive 3. Less adhesive
4. important in smooth surface 4. Act as a store of carbohydrate
caries
5. important role in forming the
bulk of the plaque, which gives
the plaque its diffusion limiting
properties, thus allowing the
retention of acids on the tooth
surface

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 Dental Caries

Saliva and Dental Caries

Since saliva is the medium in which bacterial plaque develops and works:
it is a critical regulatory factor in the carious process.

1) Formation of acquired enamel pellicle:

• Specific salivary glycoproteins form the acquired enamel pellicle

which initially protects the enamel surface from being colonized
by oral bacteria.

2) Washing effect of saliva:

• The flow of saliva has a cleansing effect on the mouth and teeth.
Human beings suffering from lack of salivary secretion
(xerostomia) usually show increased rate of dental caries.

3) Buffering effect of saliva:

• Buffering effect of saliva depends mainly bicarbonate and

phosphate content which can neutralize the pH fall (acidity) that
occurs when plaque bacteria metabolize sugar.

• The buffering capacity of saliva is increased with higher rates of

salivary flow.

• In mongolism decreased caries incidence may be due to increased

rate of salivary flow with its associated buffering element.

4) Remineralization of carious lesion:

• The inorganic components of saliva (calcium, phosphate and

fluoride) diffuse into the plaque reducing the solubility of enamel
and promoting the remineralization of the caries lesion.

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 Dental Caries

5) Salivary antibodies:

• Saliva contains secretory immunoglobulin A (sIgA) which is

produced by plasma cells found in salivary glands, the main role of
sIgA is

a. killing of bacteria,
b. Prevention of adhesion of bacteria to tooth surface.
c. Inhibition of bacterial metabolic activity.
d. Inhibition of specific bacterial enzymes such as
glucosyl transferase which are responsible for the
synthesis of extracellular polysaccharide from sucrose
6) Antibacterial substance:
• Several non-immunological components of saliva such as
lyzozymes, peroxides and lactoferrin have a direct anti-bacterial
action on plaque micro-organisms.

Dental Plaque

Definition:

1. Plaque is a tenaciously adherent deposit that forms on tooth surfaces.

It consists of an organic matrix containing a dense concentration of
bacteria.

2. It resists the friction of food during mastication, and can only be

readily removed by tooth brushing. However, neither tooth brushing
nor fibrous foods will remove plaque from inaccessible surfaces or
pits (stagnation areas).

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Composition:

3. Micro-organisms (60-70% by volume), mainly streptococci,

lactobacilli, veillonella (small gram -v e) and filamentous organisms.

4. An amorphous matrix (30-40% by volume) composed of:

• Proteins: (derived from saliva, gingival fluids and bacteria) and

include (glycoprotein, epithelial cells, amylase and
immunoglobulins).

• Carbohydrates: which include extracellular polysaccharides

(dextran and levan) and intracellular polysaccharides
(amlylopectin).

• Lipids: small amounts.

• Inorganic content: in which calcium, phosphate and potassium

seem to predominate

• Fluoride is the most important and effective cariostatic trace

element present in the plaque (5-50 ppm).

Role of plaque matrix:

The matrix is believed to have significant effect on caries through:

1. Acting as a diffusion limiting membrane thus retaining lactic acid in

high concentrations at particular sites where it can initiate caries.

2. The same diffusion limiting effect may also slow down the entry of
buffers from saliva, delaying their neutralizing action.

3. Contributes to adhesiveness, bulk and resistance to washing.

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 Dental Caries

Pathology of Dental Caries

I- Enamel caries

Smooth surface caries:

− Early smooth surface enamel caries (white spot lesion) is cone-shaped

with the base of the cone on the enamel surface and the apex pointing
towards the amelodentinal junction (ADJ).
− This early (initial) lesion is due to the action of acids resulting in
formation of submicroscopic pores, in ground sections this early
lesion consists of four zones.

Pit and fissure caries:

− The shape of the lesion differs because of different angulation of
enamel rods.
− The lesion starts as 2 cones (appearing as 2 smooth surface lesions)
with their bases on the lateral surfaces of the fissure and later they
coalesce to form one cone at the depth of the fissure.
− In early (initial) stages pit and fissure enamel caries has histological
zones similar to smooth surface caries lesions.
• Different phases and zones of enamel caries can be studied in ground
sections of smooth surface enamel caries lesion:
1) Phase of initiation
A. Translucent zone
B. Dark zone
C. Body of the lesion
D. Surface zone
2) Phase of bacterial invasion
3) Phase of destruction
4) Phase of secondary enamel caries

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1) Phase of initiation:
It is due to effect of bacterial acids upon enamel. Small initial caries
lesion shows four zones, beginning on the dentinal side of the lesion in
longitudinal ground section:

1) Translucent zone

• The first observed changes located on the advancing front i.e.

towards the dentine.
• This zone is due to initial demineralization.
• More porous than sound enamel.

2) Dark zone

• Lies superficial to the translucent zone.

• This zone is due to further demineralization.

3) Body of the lesion:

• It is the largest zone lies between the surface and the dark zone.
• This zone is due to progressive and greatest demineralization.

4) Surface zone:

• This zone which is 30 μ thick represents an interesting feature of

enamel caries where the surface zone remains intact appear
relatively unaffected. The greater resistance of surface enamel
zone is due to the precipitation of minerals derived from deeper
layers of the lesion as dissolved minerals diffuse outwards.

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Methods of detection of the four zones of initial carious lesion:

Zone 1 Zone 2 Zone 3 Zone 4
Translucent Dark Zone Body of Lesion Surface Zone
Zone Zone
Polarized Light 1% 2-4 % 5-25 % Decrease in
Detect % of enamel of the total E. Some are small 5%at volume of
submicroscopic volume others are larger. periphery of the submicroscopic
pores by volume The smaller lesion and pores.
(normal E. contain pores may be 25%at center
pores 0.1 % by due to of the lesion
volume). remineralization
which occurs in
the larger pores
in periods when
there is no acid
production.
Transmitted Light Translucent Brown or Dark Translucent Dark.
Using mounting • submicroscopic The smaller Sharply
media used in the pores filled with pores are so demarcated
section (quinoline) quinoline minute that from the dark
have the same • the normal quinoline doesn't zone.
refractive index as structural enter and air is
enamel features is lost allowed to pass
instead and is
scattered causing
the brownish
color of this
zone.
Microradiography Radiolucent More More more Radiopaque
Amount Radiolucent Radiolucent
&distribution of
mineral present
Microdessiction 1.2% 6% 24% Hyper
(magnesium and Mineralized
and Chemically
carbonate rich Zone.
Analysis minerals).

Detect mineral loss.

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 Dental Caries

2) Phase of bacterial invasion:

• When sufficient spaces are created by the action of acids, bacteria

begin to invade enamel
3) Phase of destruction

• When proteolytic bacteria begin to act on organic matrix of enamel

leading to complete destruction of the area.

4) Phase of secondary enamel caries:

• When the caries reach the dentino-enamel junction, it spread

laterally and in this way the enamel may become widely
undermined. Extension along the dentinoenamel junction results
in secondary enamel caries i.e. attack of enamel from beneath.

II- Dentin caries

− Caries in dentin involves both acid demineralization and the

breakdown of collagenous matrix by proteolytic bacteria.

− Processes in dentin caries

− Defense reaction of pulpodentinal complex
• Sclerosis
• Reactionary dentine formation
• Sealing of dead tract
− Carious destruction
• Demineralization
• Proteolysis  liquefaction foci &transverse cleft

− Histopathological studies of ground and decalcified sections of caries

in dentin are characterized by the presence of four zones:

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(1) Zone of sclerosis

(2) Zone of demineralization
(3) Zone of bacterial invasion.
(4) Zone of destruction.
1. Zone of sclerosis:
• The sclerotic or translucent zone (dentinal sclerosis) is located beneath
and at the sides of the caries lesion as a result of continuous deposition
of calcium salts within the walls of dentinal tubules gradually
obliterating them. This delays caries progression towards the pulp.

• With rapid lesion progression the odontoblastic processes are

destroyed without having produced dentinal sclerosis. These are called
dead tracts and are empty tubules.

2. Zone of demineralization:

• The diffusion of acids is ahead of the bacterial invasion resulting in

demineralized uninfected dentin. Minerals are removed from all
parts of the dentin but especially from the inner walls of the dentinal
tubules, which become wider, thus provide easier access to bacterial
invasion.

3. Zone of bacterial invasion:

The bacterial invasion probably occurs in two waves:

1) The first wave consists of acidogenic organisms (pioneers) mainly

lactobacilli produce acids which diffuse ahead into the demineralized
zone.

2) The second wave, mixed acidogenic and proteolytic organisms then

attack the demineralized dentin and causing the digestion of protein
matrix.

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• Proliferation of separate and distinct aggregates of micro-organism is

formed in within dentinal tubules separated by segments that are free
from microorganims forming beading.

• Later, adjacent beads coalescing with each other forming larger

distended segments of dentinal tubules filled with micro-organisms,
forming "liquefaction foci".

4) Zone of destruction:

• The neighboring liquefaction foci coalesce with each other forming

progressively larger and more irregular cavities filled with micro-
organisms and debris.

• In the same region were liquefaction foci are observed, other cavities
running at nearly right angle to the dentinal tubules are seen ;these are
termed: transverse clefts.

They are similar in their contents to liquefaction foci and may be due to:

1. Lateral spread of acids and bacteria along incremental lines or along

lateral branches of dentinal tubules.

2. Coalescence of adjacent liquefaction foci on adjacent tubules.

Reactionary dentin (or tertiary dentin):

• It is a defense reaction of the pulp against the acid attack. A layer

of reactionary dentin is often formed of the pulpal end of the dentin
lesion.

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