Prof. d-r R.Kabaktchieva - 2020

What is Dental Caries?

It is a microbial disease of the calcified tissues of the teeth,

characterized by demineralization of the inorganic portion

and destruction of the organic substance of the tooth.

Dental caries is the localized destruction of the tooth and is often also described as a chronic disease or process that progresses very slowly.

It starts with enamel demineralization and if it does not stop the process affects dentin and cementum.

For a long time, this demineralization is partial and reversible.

When acidic episodes as a consequence of plaque metabolism become so frequent or prolonged as much as normal saliva defense mechanisms cannot compensate for them, demineralization starts to dominate.

If the situation persists, the dissolution of the enamel deepens, and finally, the changes become irreversible.

The carious lesion, is initially difficult to be

noticed,

but gradually grows and deepens.

The earliest visible sign of enamel caries is the „white spot lesion“.

To see the white spot lesion the plaque overlying it must be removed with a brush and the tooth thoroughly dried with air.

This can be done occlusally as well as buccally or lingually.

The active lesion is matt, chalky white spot.

A further increase in enamel porosity is due to the removal of mineral from the tissue under the outer surface.

A subsurface lesion starts to form.

The earliest visible sign of enamel caries is the

„white spot lesion“.

To see the white spot lesion the plaque

overlying it must be removed with a brush and the

tooth thoroughly dried with a syringe.

This can be done occlusally as well as buccally or

lingually.

The active lesion is matt, chalky white spot.

A further increase in enamel porosity is due to the

removal of mineral from the tissue under the outer

surface.

A subsurface lesion starts to form.

Loss of gloss and transparency of the enamel - the first and earliest

change possible for visual observation when unlocking the caries

process.

It is found under the dental plaque after cleaning and continuous

drying with air.

The lesion is the result of demineralization processes carried out in

the sub-surface layer of enamel by the action of plaque acids.

SEM observation showed that after 4 weeks of plaque accumulation there was a marked dissolution of sub-surface enamel.

This partly explains why the surface is matt.

It is, however, important that the intercrystallinespaces of the entire involved enamel surface are enlarged and hence contribute to the overall

increase in porosity of the enamel.

From this stage of lesion development, when the clinical changes can readily be seen without air-drying, the more extensive loss of mineral beneath the outer surface is constantly increasing.

The most striking feature of the

initial caries is that

demineralization changes affect

the sub-surface enamel layer

rather than the surface that is in

direct contact with the plaque's

acids.

Reasons for primary subsurface

demineralization

The explanation of this phenomenon is related to the specific structure of the surface enamel, as well as to the specific way of carrying out the demineralization processes.

They are the result of the forces of motion of acid diffusion, the kinetics of the process, and the establishment of an additional semi-equilibrium process between the surface and subsurface layers based on diffusion theory.

The dissolution of the enamel can be caused by two different processes: (1) carious lesion and (2) erosion.

Enamel is covered by plaque,

which consists mainly of

bacteria.

Plaque is often found:

- close to the gum,

- in between teeth,

- in fissures

- at other "hidden" sites.

A detail of a tooth

Demineralization:

When sugar and other

fermentable carbohydrates

reaches the bacteria,

they form acids which start

to dissolve the enamel

- early caries lesion

occurs due to loss of

Calcium and Phosphates

White enamel lesion

Observe without drying the enamel surface and before

cleaning the plaque.

Remineralization:

When sugar consumption

has stopped,

saliva can wash away sugars

and buffer the acids.

Calcium and Phosphates

can again enter the tooth.

The process is strongly

facilitated by fluorides.

ACAVITY occurs if the

Demineralization

"wins" over the

Remineralization over

time

Enamel cavitation - loss of superficial enamel in the

area of lesions observed. Cavitation is visible on 4

teeth with lost enamel layer and dentin entry.

1. A tooth surface without caries.

2. The first signs of demineralization.

3. The enamel surface has broken down.

4. A filling has been made but the demineralization has not been

stopped.

5. The demineralization proceeds and undermines the tooth.

6. The tooth has fractured.

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Terminology

Active caries lesion: a progressive carious lesion.

Arrested (inactive) carious lesion: A lesion that

may have formed years previously and then stopped

further progression.

Terminology1. Primary Caries: lesions on unrestored tooth surface.

2. Secondary (recurrent) caries: lesions that

developed adjacent to a filling.

3 Residual caries: demineralized tissue that has

been left behind

before a filling is placed.2

3

1

Terminology

White caries lesion ( White spot caries) :

the first sign of a caries lesion on enamel

that can be detected with the naked eye.

Also known as initial or incipient caries.

Terminology Rampant caries: the name is given to multiple active

carious lesions occurring in the same patient.

This frequently involves surfaces of teeth that

do not usually experience dental caries

(bottle or nursing caries, baby caries, radiation caries, or

drug-induced caries).

Pit and fissure caries

Smooth surface caries

CementumCaries

(Root caries)

CARIES OF ENAMEL

Smooth surface Caries:

It’ s develops as a result of plaque formation on enamel

The earliest manifestation of incipient caries (early caries) of

enamel is usually seen beneath the dental plaque

as areas of decalcification (white lesions).

First stage. The first visible signs

of the initial enamel caries

The first signs are located in the subsurface layer.

The surface appears to be apparently unchanged. ( fig1)

Initial demineralization of the subsurface layer is visible

under a microscope as a dark zone (spot) - there is an

underlying enamel structure - the rods, the interrods zones,

the striae of Retzius and the cross striations are clearly.

The enamel structure is preserved!

The initial demineralization is realized in the crystals found

on the rod borders and on the interrods areas, and

progressing along the lines of Retzius and cross striations.

Fig1 The first visible signs of the initial enamel caries are located in the

subsurface layer; B. Triangular in shape carious lesion with a tip pointing to the

enamel-dentine junction and a base to the enamel surface.

the loss of inter-rod substance of enamel

with increased prominence of the rods.

This is followed by:

- the loss of mucopolysaccharides in the organic substance;

- presence of transverse striations of the enamel rods;

- accentuated incremental lines of

Retzius

- disintegration of enamel prisms.

Conclusion:

The first change seen

histologically is:

Second stage.

As the demineralization progresses in the subsurface

zone, a triangular in shape carious lesion is formed.

It has a conical shape with a tip pointing to the

enamel-dentine junction and a base to the enamel

surface.

The cone tip is called an advancing front of the

carious lesion or of acid demineralization.

Third stage.

The process of demineralization gets deeper.

All of the features of the subsurface caries lesion

described by Silverstone have been formed.

There are 4 layers of the initial carious lesion, which

differ from each other by the degree of

demineralization and the amount and size of the

intercrystal pores (defects) in them.

As it goes deeper, caries forms a triangular pattern

(cone shaped lesion) with the apex towards DEJ and

base towards the tooth surface.

Finally, a loss was observed

of an enamel that becomes

rough, due to its demineralization and

the disintegration of enamel prisms.

Zones in enamel carious lesion

(according to Silverstone)

1. Surface zone.

2. Body of lesion.

3. Dark zone.

4. Translucent zone.

Surface zone

In the initial carious lesion: Remains relatively unchanged for a long time due to its continuous

remineralization.

- has a thickness of about 20-30 μm.

- It is made of hydroxylapatite (HA), fluorapatite (FA) and a large

amount of reprecipitated apatite.

- the presence of pores is about 1% (normally are about 0.1%)

- the mineral content is slightly reduced by ≈ 83% by volume

(in norm it is 86%)

* Pores - the size of newly formed intercrystal spaces

The reason for the weak involvement of the surface lesion

is the continuous reprecipitation of ions there, which are

extracted from the body of the lesion.

Body of lesion

This is the area immediately below the surface

layer and over the dark zone.

The changes begin the earliest and deepen the

fastest.

At the stage of developed carious lesion:

- demineralization of the crystals in the body is

significant,

- the pores are about

10% - up to 25%- 75%.

Body of lesion

Begins degradation of organic matter:

- Firstly the acid-soluble part is attacked,

- then the acid-insoluble part is involved.

With the formation of the body of lesion, the

process is clinically detectable as a white or

brown lesion.

Zone 2: Body of the lesion

- found between the surface and

the dark zone,

- it is the area of greatest

demineralization.

Zone 1: Surface zone

- relatively unaffected area,

- greater resistance probably

due to the greater degree of

mineralization and greater

Fluoride (F) concentration.

Dark zone

The area is located under the body of lesion and over the translucent area.

It is less affected than the area of the body lesion, but more strongly than the surface area and the translucent zone.

Chronic lesions have a darker zone.

the free spaces (pores) are about 2-5%.

In a rapidly developing lesion (acute process), the dark area is not formed.

They are filled with air that prevents passing the light

through them and therefore they look dark

Translucent area

This is the innermost area of the developing carious

lesion.

It represents the advanced front of the lesion.

The changes in this area are minimal and it is the first

area that is visibly different from sound enamel.

The pores are from 0.3 to about 1% and are located in

the areas of the rod`s boundaries, the lines of Retzius

and the cross striations.

The zones seen before complete disintegration of enamel are:

Zone 3: Dark zone

- this zone is usually present

and referred to as a positive zone

- formed due to demineralization.

- it is not always present

Zone 4: Translucent zone

-located at the advancing front of the lesion,

-slightly more porous than sound enamel.

A triangular pattern (cone-shaped lesion) with the

apex towards DEJ and base towards the tooth surface.

Carious

lesion

Dentin reaction

to caries

Cone-shaped lesion

Surface zone

Body of lesion

Body of lesion

Transclucent zone

Dark zone

Body of lesion

Surface zone

As the carious process progresses, the changes

deepen in each zone of the lesion.

The advancing front of the lesion enters deeper into

the enamel and reaches the EDJ.

The major changes are made into the body of the

lesion

can be seen only single crystals that have lost

their orientation around the organic matrix.

The intercrystalline spaces in the surface layer are

gradually expanding, allowing the penetration of

larger molecules of the plaque material.

Full demineralization occurs in the body of the lesion.

Then decomposition of organic matter occurs. First, the acid-soluble part is degraded.

Deepening changes allow the entry of the MO. With their proteolytic enzymes, degradation of the acid-

insoluble part of organic matter begins.

Thin crystals cannot withstand the chewing pressure. The body of the lesion has a soft consistency.

The subsurface layer cannot serve to support the surface layer.

It collapses, and the lesion is cavitated.

Finally, there is

loss of enamel structure, which gets roughened

due to demineralization and disintegration of

enamel prisms.

disintegration of

enamel prisms.

The lesions are cavitated.

Pit And Fissure Caries:

• The fissures have narrow entrance

and wide, folded bottom.

• Pit and fissures are often deep, with food stagnation;

• The narrow entrance allows the penetration of plaque

microorganisms to form a plaque on the fissure`s bottom.

• The lesion begins beneath plaque, with decalcification of

enamel; Caries follows the direction of the enamel rods

• Enamel in the bottom of pit or fissure is very thin, so

early dentin involvement frequently occurs.

The deep fissure retains a plaque until it is

filled

Тhe carious process begins on all the

surfaces of the fissure - both on the

bottom and on the walls.

Caries is triangular in shape with the apex facing the

surface of the tooth and the base towards the DEJ.

When reaches DEJ, the greater number of dentinal

tubules is involved.

It produces greater cavitation

then the smooth surface caries

and there is more undermining

of enamel.

Longitudinal cut of fissure carious lesion.

The formation of two mirror triangular caries lesions is

observed.

The fissure caries lesion has a cone shape but with a base

to the enamel-dentine junction and a tip to the surface

This is also the explanation for the usually small opening of

occlusal caries and the broad cavity in depth.

more undermining of enameldentinal tubules are involved

CARIES OF DENTIN

Begins with the natural spread of the process along the DEJ and

rapid involvement of the dentinal tubules.

The dentinal tubules act as tracts leading to the pulp

(path for microorganisms).

Early Dentinal Changes:

the initial penetration of the MO into dentine by caries leads to

dentinal sclerosis

calcification of dentinal tubules and sealing

against further penetration by microorganisms,

dentinal sclerosis - is more prominent in

slow chronic caries.

Dentinal sclerosisis

Behind the transparent sclerotic zone, decalcification of

dentin appears.

In the earliest stages, when only a few tubules are involved,

microorganisms may be found penetrating the tubules

Pioneer Bacteria.

This initial decalcification

involves the walls allowing

them to distend

as the tubules are packed

with microorganisms.

Each tubule is seen to

be packed with pure forms

of bacteria - one tubule

packed with coccal forms

the other tubule with bacilli.

As the microorganisms proceed further they are

distanced from the carbohydrates substrate

that was needed for the initiation of caries.

Тhe high protein content of dentin must stimulate the

growth of the microorganisms.

Therefore proteolytic organisms might appear

to predominate in the deeper caries of dentin, while

acidophilic forms are more prominent in early caries.

Advanced Dentinal Changes:

Decalcification of walls, the confluence of the dentinal tubules,

tiny caverns are formed by the local fusion and breakdown of dentinal

tubules.

These are ovoid areas of destruction parallel to the course of the tubules

Тhey are filled with necrotic debris

The adjacent tubules are distorted

and their course is bent due to this

expansion.

-ovoid areas of destruction

filled with necrotic debris

The destruction of dentin by decalcification and then

proteolysis occurs in numerous focal areas = leading to a

necrotic mass of dentin of a leathery consistency.

Clefts present in the carious dentin,

extends at right angles to

the dentinal tubules,

and help for the peeling off

of dentin in layers while excavating.

clefts extends at right angles to the dentinal

tubules

The shape of the lesion is triangular with the

apex towards the pulp and the base towards

the enamel:

The conical shape is a

consequence of the structure

and direction of dentine`s

tubules.

In the pulp direction, they are

more density, with narrow

intertubular species

in the opposite direction,

these spaces get bigger.

Thus, caries lesion will be:

more width on the surface

thinner in depth.

The first important moment clinically is the breakdown of

the outer enamel.

presumably created by mechanical injuries during

mastication,

microtraumas during interdental wear,

careless probing.

When this happened it may be difficult to clean the biofilm

out of the cavity - is going an ecological shift towards

anaerobic and acid-producing bacteria.

If the biofilm is sitting on the dentine,

demineralization can spread laterally

along the EDJ, undermining

sound enamel.

When a carious cone is formed, the following

layers are seen from the outside - inside:

1. Zone of destruction – the surface area of

completely decomposed dentine

2. A zone of bacterial invasion – zone of

penetration

3. Zone of demineralized dentin

4. A zone of formed sclerotic dentin

5. Zone of fatty degeneration

of the odontoblast processes.

Histological changes in dentine after cavitation of the carious lesion: 1 –

destruction; 2 – penetration; 3- demineralization; 4 – translucent zone;

5 – normal dentine; 6 – reactionary dentine

(1) Zone of destruction

It is the surface area of completely decomposed dentine

it is below the EDG - the most widely located and with significant destruction - the dentin structure is completely erased.

it is characterized by the complete demineralization of crystals and the destruction of organic matter -by the action of acids and proteolytic microorganisms.

The whole zone is a homogeneous mass with a soft consistency from degradation elements, plaque material, and MO.

(2.) A zone of bacterial invasion –

zone of penetration.

This area is just beneath the zone of destruction:

- the processes of demineralization are advanced but less than

superficial;

- Intertubular zones and peritubular (tubular walls) are affected -

they are thinned, and the lumen of the tubules themselves is

enlarged;

dentin tubules are filled with bacteria = the zone of penetration.

collagen fibers are irreversibly damaged;

in some places, enlargement of the dentinal tubules is so great

that there is a merger of several tubules - this leads to the

formation of caverns;

the caverns are filled with bacteria - there is a merging of

several caverns, from which are obtained areas with

complete deletion of the dentine structure.

Several separate zones of complete destruction can be seen.

In general, the area has a relatively safe dentin structure.

(3). Zone of demineralization

It is the next area in the direction of the pulp.

It is the border zone where there is partial

demineralization of the crystals in the peri- and

intertubular dentin.

The dentin structure is preserved and underlined, such as

dentinal tubules, lines of Ebner and Owen.

The underlined structure is the result of an increase in intercristal

spaces due to demineralization.

In some dentinal tubules, single microorganisms can be

seen.

Collagen fibers are preserved and can serve as a scaffold

for remineralization.

(4). Zone of sclerotic dentin formation

It is the defense reactions of tubular sclerosis and tertiary dentine formation continues as a response to these destructive processes.

It reduces the permeability of the dentine and contains irregular dentinal tubules.

This zone does not always exist. In a chronic process and good protection, this area can be

observed along the periphery of the carious dentine cone.

It seems transparent and homogeneous, due to the strong mineralization of all dentin structures.

In an acute process and lack of pulp-dentin complex protection, it may be missing.

In this area, bacteria are missing.

Zone of sclerotic dentin

Under good protection,

sclerotic dentin is formed

under the developing

process;

Sclerotic tubules do not

stain.

(5.) Zone of fatty degeneration of the

odontoblast processes.

It is the innermost area of dentinal caries and is the first

reaction to the advancing front of the acid invasion.

As a result of the meeting of acids with the odontoblast`s

processes in the dentin tubules, their damage begins.

Their transport function is broken.

Free space is released in the tubules, which allow free

acid diffusion and degradation products from the

overlying caries defect.

Process advancement in this zone leads to the next

demineralization and moving the carious dentine cone

to the pulp.

The defense of the dentine structures:

The defense takes place through the formation of the transparеnt/sclerotic protective dentin.

Odontoblast`s processes sure greater amounts of Ca, P and OH ions around the affected area:

they are used for further mineralization of the peri- and intertubular dentin as well as the lumen of the dentinal tubules.

a layer of super-mineralized dentin is formed, in which all dentin structures are deleted.

The function of this layer is to prevent the spread of the caries process by interrupting the highways for the movement of acids.

This layer is in dentin.

The protection of the pulp

It is carried out again by the odontoblastic cell

at the level of the pulp-dentin junction.

The odontoblasts produce a larger amount of

predentin only at the site corresponding to the

overlaying carious process and quickly mineralize

it.

Thus protective tertiary dentine is formed at the

expense of the pulp camber space.

It increases the thickness of the mineralized dentin

structure,

It slows caries development and protects the vital pulp.

Sclerotic protective dentin

A second way to protect the pulp A second way is hypermineralization of the peri- and

intertubular dentine and lumen of the dentinal tubules,

including the odontoblast process itself, just above the pulp.

This results in a sclerotic area immediately above the pulp:

the dentinal tubules above this zone remain without

protection due to the death of the odontoblast processes.

They form the so-called dead tracts in the dentin above

this area.

They are visible under the microscope as dark areas

extending from the pulp to the surface of the dentin.

Although formed as a defense mechanism, dead tracts are

rapidly overcome by the evolving carious process due to a

lack of protection in them.

“Dead tracts” in the dentin

The reaction in the pulp-dentin complex in a carious process:

Forms a sclerotic zone just above the pulp where the caries is located.

The odontoblast processes

above this zone remain without

protection and die.

„Dead tracts“ protect the pulp for short.

.

The mission of

oral care and oral prevention

focuses on the ability to help

individuals achieve and maintain

maximum oral health throughout

their lives.

Oral health is essential to the general health and well‐being of a human.

• Oral health means much more than healthy

teeth.

• Oral health is essential to general health.

Safe and effective disease prevention measures exist .

Everyone can voluntarily decide to improve oral health and prevent disease.

The patients should seek entry into well-planned preventive programs.

Purpose/goal of prophylaxis of oral diseases is

to maintain the health of teeth and periodont

throughout human life.

Prophylaxis of oral diseases is aimed to:

prophylaxis of caries;

prophylaxis of periodontal diseases;

prophylaxis of tooth-jaw deformities.

Prevention of caries and periodontal diseases is a

priority of pediatric dentistry.

Preventive care can be defined and

classified into three different levels.

1. Primary prevention

2. Secondary prevention

3. Tertiary prevention

Primary preventionuses strategies and agents to prevent the onset of disease, reverse the

progress of the disease, or arrest the disease process before

secondary preventive treatment becomes necessary.

The general approaches to the primary prevention of dental caries and

periodontal diseases involve the following measures:

• Professional oral assessments.

• Patient involvement in the control of plaque,

- a naturally acquired bacterial biofilm that develops on the teeth.

- this process is called self‐care and is accomplished by brushing

and flossing teeth and using other preventive products.

• Professional periodontal debridement

- removal of soft and hard deposits from the teeth using manual or

ultrasonic dental instruments.

• Community water fluoridation

- addition of fluoride to a water supply.

Other measures:

• Use of products for self‐care and for professionally

initiated remineralization procedures

- i.e., replacement of lost minerals in teeth.

• Use of antimicrobial agents to reduce plaque biofilm.

• Use of dental sealants.

• The practice of nutritionally healthy habits including

sugar discipline

- limitation of the amount of sugar in the die

to prevent a nutrient source for oral bacteria.

Secondary prevention uses routine treatment methods to terminate a disease process and/or restore tissues to as nearly normal as possible. This level can be termed restorative care.

Tertiary prevention uses measures necessary to replace lost tissues and rehabilitate patients to as nearly normal as possible. This level can be termed reconstructive care.

When prevention is not practiced, disease and infection frequently cause the undesirable effects of pain and discomfort.

The shift from primary to tertiary prevention results in an extremely rapid increase in the cost of health care, with a proportional decrease in patient satisfaction

According to Axelsson, 2000 the oral

prophylaxis is now divided into five categories:

1. "Primary" primary prevention.

It includes all preventative measures aimed at pregnant

women. They provide conditions for the proper development of

all oral structures, prevention of early postnatal transmission of

cariogenic microorganisms and prevention of poor oral habits in

the child.

2. Primary prevention.

Maintaining an intact dentition and periodontium, i.

prevention of caries, gingivitis, and periodontitis to achieve

100% oral health.

3. Secondary prevention.

Prevention of disease recurrence (caries, gingivitis,

and periodontitis) following their successful symptomatic

treatment.

4. Tertiary prevention.

Symptomatic treatment of dental caries, gingivitis,

and periodontitis, which is achieved with restorations,

cleaning and scaling of gingival and periodontal pockets

and periodontal surgery.

5. Pain relieve.

It is aimed at pain relieving in the treatment of caries,

endodontic treatment, and extractions.

Oral prophylaxis strategies

The main strategies of oral prophylaxis are: creation of resistant structures;

prevention of early transmission of cariogenic microorganisms by the parents to the child;

reduction of the pathogenic situation.

The creation of resistant structures can be accomplished with the combination of nutritional and fluoride prophylaxis, mineralization and remineralization, a prophylactic seal of the fissure, oral health training and oral health promotion.

Prevention of early transmission of cariogenic microorganisms occurs with oral health training/education, creation of appropriate nutrition habits, oral hygiene, nutritional prophylaxis, and oral health promotion.

The reduction of the pathogenic situation is accomplished by oral hygiene, nutritional and fluoride prophylaxis, mineralization, and remineralization of enamel, prophylactic seal of a deep fissure, oral health promotion and caries risk assessment.

Forms of dental prophylaxis

Dental prophylaxis has the following forms:

1. Oral hygiene.

2. Endogenous fluoride prophylaxis.

3. Exogenous/Local fluoride prophylaxis.

4. Prophylactic seal of deep fissures.

5. Nutritional prophylaxis.

6. Remineralization as non-operative treatment of caries.

7. Oral health promotion.

Based on the purpose, dental prophylaxis

may be public, group, and individual.

Public prophylaxis is a massive application of prophylactic methods and means for the whole society.

This form of prophylaxis is organized and financed by the state,

organized by professionals and carried out with the help of

specialists, educators, teachers and public organizations.

Group prophylaxis is targeted at society groups that are with special priority.

Such groups are the infants, children in the early childhood

group, pre-school and school-age, and others. Such a group is

that of pregnant women or children with developmental

disorders and defects or with general disorders.

Individual prophylaxis is targeted at every individual regardless of age, social status and health.

It is mandatory for every child from the moment of birth.

It is done by the dentist.

Dental prophylaxis may be complex or selective.

Complex prophylaxis is related to the multifactorial

etiology of caries and periodontal diseases.

In order for these diseases to be effectively prevented,

it is necessary to co-administer all types of prophylactic

methods and means.

Only the complex application of prophylactic measures

can lead to a real result.

Selective is this prophylaxis, where appropriate means

or methods are selected according to the needs of a

particular group of children.

end