DENTAL CARIES PATHOLOGY, DIAGNOSIS AND PREVENTION

DDS YEAR II

DR. SHUROOQ SH. ABDULRAZZAK

CONSERVATIVE DENTISTRY

Dental plaque made visible with disclosing agent

INTRODUCTION AND DEFINITIONS

Dental caries: Is an infectious microbiologic disease of the teeth resultsing in localized dissolution and destruction of the calcified tissues by acid-forming bacteria found in dental plaque, in the presence of sugar.

Today, because of scientific advances and new technologies, dentistry is developing new strategies for managing dental caries. These strategies emphasize prevention and early intervention.

Dental plaque: Is a gelatinous mass of

bacteria adhering to the tooth surface.

The plaque bacteria metabolize sutable carbohydrates for energy and produce organic acids as a by-product causing the plaque pH to fall within 1–3 minutes. Unfortunately the plaque remains acid for some time, taking 30–60 minutes to return to its normal pH in the region of 7.

The buffering capacity of saliva is important in this return to neutrality.

Demineralization: loss of minerals from the tooth when the pH is dropping due to the effect of bacteria in the biofilm which are always metabolically active, causing minute fluctuations in pH.

Remineralization: is the process of gaining minerals when the pH is increasing.

If the biofilm is partially or totally removed mineral loss may be stopped or even reversed towards mineral gain.

Cyclic Process of Decay

Demineralization

Remineralization

Bacteria plus food

makes the saliva

very acidic within

5 minutes

Saliva is normal

30 minutes

after eating

Cariogenic: Organisms that cause caries.

Streptococcus mutans and lactobacilli have significant potential to cause caries.

MS are most strongly associated with the onset of caries while lactobacilli are associated with active progression of cavitated lesions

Cariogenicity potential: Is the degree to which a tooth is likely to become carious.

Caries: both the carious process that occurs in the biofilm at the tooth or cavity surface and the carious lesion that forms on the tooth tissue.

Carious lesion is the consequence of the carious process.

Dental caries

Plaque retention and susceptible sites:

1Pits and fissures on occlusal surfaces of molar and premolar teeth, buccal pits of molars and palatal pits of maxillary incisors.

2. Proximal enamel smooth surfaces just cervical to the contact area.

3. The enamel at the cervical margin of the tooth at the gingival margin. In patients with gingival recession, the area of plaque stagnation is on the exposed root surface.

4. The margins of restorations, particularly where there is a wide gap between the restoration and the tooth or those where the restoration overhangs the margin of the cavity.

Classification of Caries

Acc. to location

Pit/Fissure caries

- Smooth surface caries

- Root caries

Acc. to origin

- Primary

- Secondary/Recurrent

Acc. to tissues involved

- Enamel caries

- Dentinal caries

- Cemental caries

Acc. to rapidity of the process

-Acute/ Progressive

Rampant caries

Radiation caries

-Chronic

Arrested caries

Acc. to nature of progress

- Forward caries

- Backward caries

Acc. to age

- Nursing caries

- Senile caries

G. V. Black Classification

Forward – Backward Caries

Dental caries

Crown caries

Root caries

Root caries

Occlusal caries

Smooth surface caries

acute

arrested

Senile Caries: Aging process. Exposed root surfaces. Partial denture clasps.

Severity or rapidity of attack

In a mild case only the most vulnerable teeth and surfaces are attacked, such as occlusal pits and fissures.

A moderate attack may involve occlusal and approximal surfaces of posterior teeth.

In a severe attack buccal and lingual surfaces close to the gingival margin and anterior teeth also become carious.

Rampant caries A sudden rapid destruction of many teeth,

widespread, rapidly burrowing type of caries resulting in early involvement of the pulp and affecting those teeth usually regarded as immune to ordinary decay.

More than 10 lesions per year, it can be seen in the following:

Primary dentition of infants who continually suck a bottle or comforter containing sugar.

Permanent dentition of teenagers and is usually due to frequent cariogenic snacks and sweet drinks between meals.

Where there is a sudden marked reduction in salivary flow (xerostomia).

Rampant caries of the deciduous teeth

Rampant caries in a 19-year-old man

Arrested caries

A carious lesions which do not progress. It is seen when the oral environment has changed from conditions predisposing to caries to conditions that tend to slow the lesion down. Operative treatment is clearly not necessary.

The carious process in enamel

The earliest clinically visible evidence of enamel caries is:

white spot lesion

there is no cavity

Histologically: the shape of the white spot lesion is determined by the distribution of the biofilm and the direction of the enamel prisms.

Thus, Smooth surface lesion is conical shape with the apex of the cone pointing towards the DEJ.

The enamel overlying the white spot is hard (relatively intact surface zone).

Longitudinal ground section through a

carious lesion on a smooth surface

examined in water with polarized light.

The lesion is cone shaped.

Note the relatively intact surface zone

(SZ).

Sometimes the lesion is shiny and this

would indicate that good plaque control has been re-established and the outer demineralized enamel has been worn away. This lesion is arrested and sometimes it may appear brown due to exogenous stains absorbed by this porous region.

This erupting molar appears caries-

free but it is not.

A white spot lesion is now obvious at the

entrance to the fissures.

Then in active lesion:

Direct dissolution of the outer enamel surface.

Physical defect in the surface (cavitation) will take place.

Plaque formation continues within the cavity and this may not be accessible to cleaning aids. For this reason a cavitated lesion is more likely to progress, although it can still become arrested if the patient is able to clean.

Fissures and pits: The lesion forms at

the entrance to the fissure (non-cleansabl area), and the erupting tooth is particularly susceptible to plaque stagnation because;

1. children are not adept at removing plaque.

2. the erupting tooth is below the line of the arch and tooth-brushing misses it unless the brush is brought in at right angles to clean the surface specifically.

The correct position of the toothbrush on an

erupting second permanent molar.

The histological features of fissure caries are similar to those already described for smooth surfaces. The lesion forms around the fissure walls and gives the appearance in section of two small smooth surface lesions. The lesions again follow the direction of the enamel prisms and this anatomy gives the lesion the shape of a cone with its base at the DEJ.

A molar tooth with a white spot

lesion formed in an area of plaque

stagnation at the fissure entrance.

A hemisection of this tooth showing a

larger lesion than would be

expected from examination of the

outer enamel surface.

The carious process in dentine

Histologically, the carious process may be in dentine before an enamel cavity forms.

On an occlusal surface the lesion widens as it approaches the DEJ, guided by prism direction.

Eventually a cavity forms (filled with plaque) and demineralization spreads laterally along the DEJ, undermining the enamel.

Undermined enamel is brittle and will fracture if subjected to occlusal forces, producing a large cavity. In cavity preparation must often be removed to gain access to demineralized dentine beneath it.

A molar tooth with a cavity

whose base is in dentine.

A hemisection of this tooth showing the

cavity and lateral spread of the lesion

at the DEJ. There is extensive

demineralization of the dentine.

Pulp–dentine defence reactions

The important defence reactions are:

Tubular sclerosis within the dentine.

Reactionary dentine at the interface between dentine and pulp.

Inflammation of the pulp.

The state of the tissue at any time will depend on the balance between the attacking forces and the defence reactions.

Caries of peripheral dentine will result in pulpal inflammation and chronic inflammatory cells (macrophages, lymphocytes, and plasma cells) will infiltrate the pulp near the odontoblast layer.

Initial enamel caries Indeed, may show this chronic inflammatory reaction which is mainly due to the movement of bacterial toxins through the dentinal tubules.

After exposure; bacteria may enter the pulp. Polymorphonuclear leucocytes may now predominate, and acute inflammation can supervene and spread throughout the pulp, resulting in pulpal necrosis.

Then, inflammation may move apically until the entire pulp is necrotic.

This is followed either by spread of toxins into the periapical tissues at the root apex, producing the chronic inflammatory response of chronic apical periodontitis, or, if organisms pass into the periapical tissues, an acute apical abscess develops.

Degenerative or destructive changes in dentine

These include:

demineralization of dentine

destruction of the organic matrix

damage and death of odontoblasts.

These changes begin before cavitation of the enamel occurs and while the microorganisms are still confined to the tooth surface.

The rate of caries progress is highly variable and provided the biofilm is removed from the cavity surface the progress of the disease can be arrested.

Clinically; in actively progressing lesions,

the dentine is soft and wet, and, because of the speed at which some lesions develop, the defence reactions may not have time to be effective.

in arrested or slowly progressing lesions, the dentine, has a hard, leathery, or dry consistency. The defence reactions are well marked and the carious lesion accumulates minerals from the oral and from pulpal blood flow.

Root caries

Exposed root surfaces occur following gingival recession are susceptible to root caries and to mechanical wear and chemical damage more than enamel. Why? because the cementum on the root surface is softer than enamel and dentin

Histologically, demineralization appears to take place beneath a well-mineralized surface layer. Deep to the lesion there are often areas of tubular sclerosis and reactionary dentine.

carious lesions can be converted into arrested lesions by regular tooth brushing with a fluoride-containing dentifrice

Secondary or recurrent caries: is the same as primary caries except that it is located at the margin of a restoration.

it is most often localized gingivally where plaque is most likely to stagnate.

It can be arrested by regular disturbance of the biofilm with a fluoride-containing dentifrice.

Residual caries: The parts of the carious lesion that remain after cavity preparation

DIAGNOSIS OF

DENTAL CARIES

The prerequisites for caries diagnosis are:

Good lighting

Clean teeth

A three-in-one syringe so that teeth can be viewed both wet and dry.

Sharp eyes with vision aided by magnification;

Visual

Detectable explorer “stick”

Reproducible bitewing radiographs.

Laser caries detector

The diagnostic procedure

A film-holder and beam-

aiming device in use to take

a bitewing radiograph.

Laser caries detector

VISUAL & TACTILE EXAMINATION

A smooth surface lesion before and

after probing. Note the damage that

can be caused by a sharp probe.

Diagnosis of caries on occlusal surfaces

Clean the occlusal surface with a rotating bristle brush in the handpiece, on examination;

1. The enamel lesion that is only visible on a dry tooth surface is in the outer enamel.

2. The lesion visible on a wet surface is all the way through the enamel and may be into dentine.

3. Uncavitated enamel lesions are not visible on a bitewing radiograph.

4. Cavitated lesions may present as microcavities which are easily missed on visual examination but are usually visible in dentine on a bitewing radiograph

Diagnosis of caries on proximal surfaces

Usually the lesion forms just cervical to the contact area and vision is obscured by the adjacent tooth.

If the lesion is discovered clinically, it is usually at a relatively late stage.

Bitewing radiographs are important in diagnosing proximal caries in both enamel and dentine. once a lesion is visible in enamel on a bitewing radiograph it is usually in dentine when examined histologically.

It is not possible to judge the activity of a lesion from a single bitewing radiograph. also not possible to know whether a lesion is cavitated.

A proximal lesion on the root surface may be diagnosed visually if the gingival health is good. It is also is visible on a bitewing radiograph.

The radiographs record the progress of proximal caries over a period of 18 months

Suggested ranking for radiographic diagnosis of dental caries

(early proximal lesions) (Axelson)

a) No lesion. Enamel is

apparently sound. No

treatment is required

b) Lesion confined to outer

half of enamel.

c) Lesion penetrating

dentin enamel junction.

d) Lesion spreading laterally in

dentin.

e) Lesion penetrating dentin with the

possibility of pulpal involvement.

An orthodontic elastic separator

has been placed between two

premolars.

After 5 days the separator is removed

and now a probe can be used gently to

feel whether a cavity is present.

The operating light can help in diagnosis of proximal caries. It is reflected through the contact point with the dental mirror, and a carious lesion appears as a dark shadow following the outline of the decay.

Fibre-optic: a stronger lights, with the beam of 0.5 mm diameter, have been used. The light should be used with dry teeth. The advantages; can detect

enamel crazing, cracks and caries

Diagnosis of caries on exposed smooth surfaces

At the stage of the white or brown spot lesion, it is easily to be seen visually.

Uncavitated, active lesions are close to the gingival margin and have a dull surface.

Inactive lesions may be further from the gingival margin, white or brown in colour with a shiny surface.

Arrested lesions are hard and shiny, plaque-free, and some distance from the gingival margin.

Assessment of caries risk

Many factors are relevant to the assessment of caries risk:

1.Medical history; medical problems causing xerostomia

2. Dietary habits; ex: sweet drinks, sweets, and other sugar-containing snacks taken before bed.

3. Fluoride history; check using fluoride toothpaste

4. Clinical examination; a history of repeated restoration, multiple new lesions. Stagnation areas such as unsealed deep fissures, multiband orthodontic appliances, partial dentures, and poor restorative dentistry encourage plaque accumulation and increase caries risk.

5. Saliva; Where the dentist suspects from clinical examination that the mouth is dry, or where it is difficult to explain a high caries activity, salivary flow should be measured chairside. The stimulated salivary flow rate can then be expressed in millilitres (ml) per minute. The normal stimulated secretion rate in adults is 1–2 ml per minute.

Caries prevention

The relevance of the diagnostic information to the management of caries

There are three approaches to the management of active caries:

• Attempt to arrest the disease by preventive, nonoperative treatment

• Remove and replace the carious tissues (operative dentistry) and prevent recurrence by preventive, nonoperative treatment

• Extract the tooth.

Caries prevention

1

Reduce the pathogenic potential of

dental plaque

2

Increase the resistance of

tooth structure to caries attack

3

Augment salivary factors

Reduce the pathogenic potential of dental plaque

Mechanical plaque control 1

Chemotherapeutic method 2

Food intake restriction 3

Replacement sweetener 4

Sugar frequency reduction 5

Augment salivary factors

Sugar free chewing gum 1

Supportive life style 2

Elevate salivary quality 3

Increase saliva mineralization 4

Enhance F in saliva 5

Increase tooth structure resistance to caries attack

Community fluoride program 1

Professional fluoride 2

Self application fluoride 3

Sealant 4

Enamel treatment 5

Mechanical plaque control: Motivation about the correct way of tooth brushing

With children, pay particular attention to the occlusal surface of erupting teeth.

Tooth brush should be kept at right angle to the occlusal surface

When a proximal lesion in the outer enamel exist, the patient should be shown how to use dental floss.

Root surface lesions are as the same as coronal lesions to control by mechanical plaque control.

Pay particular attention to the proximal surfaces of teeth next to a denture.

Mode of Action

Bactericide

Crystallize

Remineralize

At the end of this lecture the students are able to:

Explain caries process and identify it’s etiology (C2)

Recognize the susceptible sites of plaque accumulation

Classify dental caries

Asses the severity of the caries attack

Describe caries process in the enamel

Describe caries process in the dentine

differentiate between different types of dental caries

Explain the pulp-dentin defense reaction against caries

Can diagnose caries in different sites of the tooth

Recognize factors that are relevant to the assessment of caries risk

List the steps of caries prevention

Describe the mechanical plaque control

• Pickard’s Manual of Operative Dentistry,

2003. Eighth edition. Edwina A. M. Kidd,

et al.

• Strudevant’s. Art and science of

operative dentistry. Fifth edition. 2006

• Fundamentals of operative dentistry. A

contemporary approach. Third edition.

2006.