Intro to DENTAL CARIES

Operative Dentistry Exam 1

Dental caries

"biofilm-mediated, sugar-driven, multifactorial,

dynamic disease that results in the phasic demineralization and

remineralization of dental hard tissues

• Is the localized destruction of susceptible dental hard tissue by

  acidic by-products from bacterial fermentation of dietary

  carbohydrates.

  ▪ It is a bacterial driven, generally chronic, site-specific, multifactorial,

  dynamic disease process that results from the imbalance in the

  physiologic equilibrium between the tooth mineral and the plaque

  fluid; that is, when the pH drop results in net mineral loss over time

COMMON CHILDHOOD DISEASES (U.S.)

Carries is Number 1

CAUSING FACTORS of Dental Caries (4)

Host Types (5)

Tooth

▪ Saliva

▪ Muscular activity

▪ Habits

▪ Environment

Hard Tissue Composition Enamel

Hard Tissue Composition Dentin

SURFACE ENAMEL

Enamel is microscopically porous which makes it permeable

enamel rod

An enamel rod is the basic unit of tooth enamel. It is a tightly packed, highly organized mass of

hydroxyapatite crystals, which are hexagonal in shape and provide rigidity and strengthen the enamel.

Enamel Parts (3)

1. Enamel rods

2. Interrod enamel:

3. Rod sheath:

Interrod enamel

Located around the rod enamel

- Same composition as enamel rod

- Different direction

3. Rod sheath:

where enamel rods meet interrod

enamel

- More organic content

- Reduces stress on the rods

individual enamel crystal

About 20% of the crystal is carbonated hydroxyapatite. It is more easily dissolved

by acids

Dentin

Hydroxyapatite crystals are 30 times smaller, making

dentin somewhat softer than enamel.

Peritubular dentin

a relatively dense mineralized tissue that surrounds the tubules of

coronal tooth dentin. It is composed mainly of crystals of carbonated apatite together

with a small amount of collagen

intertubular dentin

The intertubular dentin, which lies between the tubules, is a less-calcified matrix that

consists of some apatite crystals embedded within a collagen matrix

WHY IS DENTIN MORE SUSCEPTIBLE TO CARIES THAN ENAMEL?

Less inorganic content

▪ Hydroxyapatite crystals are smaller

▪ More carbonated apatite

▪ Greater numbers of impurities in the crystals

▪ Critical pH is higher than enamel

▪ Tubules offer channels for diffusion of the

bacterial acids

The number and diameter of the tubules increase from DEJ to the pulp

DEMINERALIZATION

Loss of minerals

When pH drops

REMINERALIZATION

Reprecipitation of minerals

When pH rises

Remineralization vs Demineralization

Remineralization is a slower process than demineralization. When remineralization is given enough time, it can eliminate the

damage done during demineralization, but in the absence of this, the caries process will progress and a lesion will develop.

STAGES OF CARIES DEVELOPMENT

It is an ongoing process, characterized by alternating periods of

demineralization and remineralization

▪ Demineralization: is the dissolving of the calcium and phosphate

from the hydroxyapatite crystals

▪ Remineralization: is the calcium and phosphate being redeposited in

previously demineralized areas

▪ It is possible to have the processes of demineralization and

remineralization occur without any loss of tooth structure

Critical pH

The critical pH is the pH at which saliva and plaque fluid cease to be saturated with calcium

and phosphate, thereby permitting the hydroxyapatite in dental enamel to dissolve.

• It is the highest pH at which there is a net loss of from dental hard tissues, which is generally

accepted to be about 5.5 for enamel.

Critical pH values (4)

Enamel → 5.5

• Dentin → 6.0

• Cementum →6.7

• Fluorapetite →4.5

PROGRESSION OF DENTAL CARIES (5)

Normal enamel surface →first stages of demineralization →Enamel surface breaking down →

dentin is carious→ cavitation

Caries Progression in Enamel

Subsurface demineralization opposite plaque surface

• Some of the dissolved mineral gets re-deposited at the surface as

it exits the tooth

• Lesion can reach dentin without cavitation

• Remineralization is still possible (if not cavitated)

TOOTH FACTOR

Certain surfaces of a tooth are more prone to decay. Eg : In mandibular 1st molar

the most prone areas in order are occlusal, buccal, mesial, distal and lingual.

▪ Position of tooth on the arch: malaligned, rotation

▪ Surface enamel is more resistant to caries than sub-surface enamel because it is

highly mineralized

▪ Dentin is more vulnerable than enamel because of structural differences and

greater numbers of impurities in the crystal lattice

COMPOSITION OF SALIVA:

Water

▪ Inorganic

▪ Organic

▪ mucus

▪ Lipids

▪ Enzymes

INORGANIC COMPONENTS IN SALIVA

Calcium and phosphate

▪ remineralization and preventing demineralization.

▪ Phosphate also acts as a buffer

▪ Potassium, sodium, chloride as in other body

fluids

▪ Bicarbonate

Bicarbonate Function in Saliva

acts as a buffer

▪ pH 6.8 - 7.3

ORGANIC COMPONENTS IN SALIVA

Neumerous proteins and lipids

Enzymes

SALIVARY FUNCTION

Clearance

2. Antibacterial

3. Lubrication

4. Mineral exchange

CLEARANCE

• Saliva clears carbohydrates from the plaque

• Reduced saliva flow means less of all the components, less clearance, less protective effect

• Normal stimulated flow rate is about 1.0 ml/minute or more

• Stimulated flow rate of less than 0.7 ml/minute is a high risk factor for dental caries

Unstimulated vs Stimulated Clearance in saliva

Unstimulated: At rest

▪ Stimulated: When secretion is promoted by different stimuli

Types Of Enzymes

She said they dont matter

SALIVARY PELLICLE

Thin film on the surface of the enamel

▪ Comprised of strongly adsorbed specific proteins and lipids from the saliva

▪ Forms within mins/hours. Matures in days.

▪ Multiple layers

• If it mature becomres bad → will start plac formation

GOOD SALIVARY EFFECTS

Salivary proteins contribute to the pellicle to

protect the outer tooth surface

▪ Salivary proteins maintain supersaturation of

calcium phosphate

▪ Salivary calcium and phosphate inhibit

demineralization and enhance

remineralization

▪ Saliva carries fluoride around the mouth

▪ Salivary components buffer plaque acids

▪ Salivary proteins have antibacterial properties

BAD SALIVARY

EFFECTS

Pellicle formed allows bacteria to colonize on the

tooth

▪ Provides a sticky surface

▪ Provides nutrients for bacteria

▪ Precursor to plaque formation

▪ With low saliva, caries activity grows

exponentially

DECREASED

SALIVARY FLOW

Slow clearance of food particles

▪ Decrease buffering of acids

▪ Encourage growth of bacteria

▪ Inhibit remineralization because calcium

and phosphate ions are reduced

• Causes DRY MOUTH (XEROSTOMIA)

DRY MOUTH (XEROSTOMIA) CAN BE CAUSED BY

Many medications

▪ Radiation therapy to head and

neck

▪ Salivary gland disease

▪ Diabetes

▪ Decreased function with aging

Bacteria Criteria for Cariogenicity (In Caries) (4)

1. An organism must acidogenic (Produces)

2. An organism must be aciduric (tolerates)

3. An organism must exhibit tropism for teeth (sticks)

4. An organism must utilize refined sugar (sucrose)

Organisms responsible for dental caries (2)

Streptococcus mutans (MS): associated with the onset

of caries

▪ Lactobacilli: associated with active progression of

cavitated lesion

S.MUTANS IS THE PRIMARY CAUSATIVE AGENT OF INITIAL CARIES BECAUSE

It adheres to enamel (enzymes causes the formation of extracellular

polysaccharide which allows it to stick to smooth tooth surfaces)

▪ Acidogenic: It produces acid (it metabolizes sucrose to an end product of

lactic acid)

ACQUISITION OF MS

About 70% of children get S.Mutans from mom

- Significantly associated with maternal salivary levels

of bacteria

- Referred to as “vertical transmission”

Biofilms

Biofilms are a collective of one or more types of microorganisms that can grow on many different surfaces.

Dental plaque

Dental plaque is a structurally and functionally organized biofilm.

Dental plaque has been defined as the diverse community of micro-organisms found on a tooth surface as a

biofilm embedded in a matrix of polymers of host and bacterial origin

PLAQUE FORMATION (4 Stages)

SUBSTRATE (In Caires

Cariogenic foods

High-frequency exposure to fermentable

carbohydrates such as sucrose → produce

cariogenic biofilm

▪ Fermentable carbohydrates→ change

composition of biofilm→favors growth of

acidogenic bacteria

• Moderation is very important

Cariogenic foods

Are those that contain

fermentable substrates that can be

metabolized by oral bacteria to cause a

decrease in plaque pH < 5.5 and result in

demineralization of tooth enamel and

ultimately caries

Dietary advice for caries prevention is

based on three principles

CLASSIFICATION BASED ON HARD TISSUE AFFECTED

Enamel caries

▪ Dentin caries

▪ Cementum caries

BASED ON SURFACE AFFECTED

Pit and fissure caries

▪ Smooth surface caries

▪ Root surface

BASED ON RATE OF PROGRESSION

Acute/ rampant caries

2. Chronic caries

3. Arrested caries

Acute/ rampant caries

- Rapidly invading caries involving several teeth

- Appears soft or light colored

- If unattended causes early pulp involvement

2. Chronic caries

- Slowly progressing, long standing caries

- Hard consistency and dark colored

3. Arrested caries

Sometimes chronic caries lesion can become arrested

due to change in local environment

BASED ON EXTENT OF CARIES (2)

Incipient (non-cavitated) caries

Cavitated caries

Incipient (non-cavitated) caries

First evidence of caries activity in enamel

- Demineralized enamel not extended to DEJ

- Enamel surface is hard and still intact

- Can be remineralized

Cavitated caries

- Caries has spread beyond enamel into dentin

- Enamel is broken down and remineralization is not

possible

BASED ON ONSET

Initial / primary caries

Recurrent caries

Initial / primary caries

The original carious lesion of the tooth

Recurrent caries

- Caries seen around the margins of restoration

- Occurs due to microleakage and other

favorable conditions

BASED ON WHETHER CARIES IS COMPLETELY REMOVED

OR NOT

Residual caries

- Caries that remains in the prepared cavity even after the restoration is completed

- This may be left behind either by accident, neglect or intension

CLASSIFICATION SYSTEMS (2)

▪ GV black:

- Most commonly used

- Based on affected surfaces (location)

▪ ICDAS classification:

- Based on clinical representation and progression of the

lesion (extent)

CLINICAL CHARACTERIZATION OF CARIES

The characteristic varies vary with the nature of the surface on which the lesion

develops

There are 3 different clinical sites:

Pits and fissures (occlusal surface of posterior teeth)

2. Smooth enamel surfaces (buccal, lingual, facial, palatal)

3. Root surface

PITS AND FISSURES

Most susceptible surface to development of dental caries

▪ Cross section: Inverted V with narrow entrance and progressively wide area of

involvement closer to the DEJ

SMOOTH ENAMEL SURFACES

▪ The smooth enamel surfaces of teeth are less favorable site for plaque attachment.

▪ Cross section: V shaped with a wide area of origin and the apex of the v directed

towards DEJ

ROOT SURFACE

Root surfaces are rougher than enamel and readily allows plaque formation.

▪ Cementum covering the root surface is extremely thin and provides little

resistance to caries attack.

▪ Cross section: U shaped with less well defined margins .

ZONES OF ENAMEL CARIES

a) Surface zone: appears to be intact (reprecipitation, hypermineralization).

b) Body of lesion: subsurface, the largest portion of the lesion, mineral dissolution.

c) Dark zone: surrounds body of lesion, zone where caries is in progress, many pores

d) Translucent zone: represents the advancing front of the lesion (limiting zone)

.

A sharp explorer can easily penetrate the outer enamel and cause a small cavitation on an active lesion

ZONES OF DENTIN CARIES (3)

Soft Dentin

(infected dentin)

-Bacterial contamination

-Necrotic

-Irreversibly denatured collagen

-Cannot be remineralized

-Does not self repair

-Easily excavated

-Needs to be removed

Firm Dentin

(affected dentin)

- Demineralization of intertubular dentin

- Softer than hard dentin

- Intact collagen cross linking

- Leathery texture

- Can be remineralized

- Resistant to hand excavation, can only be removed by putting pressure

- Do not remove

Hard Dentin

- Cannot be easily penetrated with a blunt explorer

- Can only be removed by a bur or a sharp cutting instrument.

EXAMINATION AND DIAGNOSIS (4)

Good history

▪ Caries risk assessment

▪ Clinical evaluation

▪ Radiographic analysis

Incipient stages:

arrest and remineralize

Only when changes are irreversible: surgical treatment “drill and fill”

CARIES RISK ASSESSMENT

Clinicians treat the entire patient and not just individual teeth and caries lesions.

▪ Dental caries is a multifactorial medical disease process

▪ Individualize caries diagnosis and treatment or interventions for each patient

CAMBRA

Caries

Management

By

Risk

Assessment

.

represents a management philosophy that manages the caries disease process using a medical model.

CAMBRA Purpose

It is a process that provides an individualized evaluation of a patient’s pathologic

factors and protective factors and assesses the patient’s risk for developing future

disease.

▪ The risk assessment is then used to develop an individualized evidence- based

caries management plan that involves aspects of nonsurgical therapeutics and

dental surgical interventions

GOALS OF CAMBRA

Emphasis of the whole disease process

▪ Taking into account all factors that contribute to the

development of caries

▪ Pathological factors vs. Protective factors

▪ Shift focus from traditional restorative approach toward

the cause of the disease and the need to modify the

causes wherever possible

▪ Shift the caries balance towards the protective factors

Caries Management: The Medical Model

MAKE RECOMMENDATIONS BASED ON THE CARIES RISK

Increase the Protective Factors (4)

(a) Topical Fluoride delivery

(b) Saliva stimulation and supplementation

(c) Antibacterial treatment

(d) Minimally invasive restorative dentistry

General guidelines for caries management for a high- caries-risk patient

tep 1: Plaque control

• Provide prophylactic treatment followed by fluoride application

• See patient regularly to reinforce oral hygiene

Step 2: Treatment of existing caries lesions

• Treat noncavitated lesions as needed

• Restore cavitated lesions and seal surrounding pits and fissures as needed

• Salivary flow measurement to check for dry mouth and treat for xerostomia if needed

Step 3: Protection of surfaces at risk

• Seal all deep pits and fissures

• Apply fluoride varnish to exposed roots

Step 4: Maintenance care for prevention

• Review oral hygiene and dietary habits and advise patient to: Reduce the number of between-meal sweet snacks

• Substitute snacks rich in protein

• Advise patient to brush at least twice daily with high fluoride delivery toothpaste

• Advise patient to floss once daily

• Provide home treatment and/or other adjunctive therapy: Use over-the-counter fluoride rinse daily

• Chew or suck xylitol-containing gum or candies three times daily

• Recall patient every 3 months to: Reevaluate current caries risk

• Receive fluoride varnish treatment of all teeth

• Obtain bitewing radiographs every 3 to 6 months to check for lesions

eneral guidelines for caries management for a Moderate caries-risk patient

Step 1: Plaque control

• Provide prophylactic treatment followed by fluoride application

• See patient regularly to reinforce oral hygiene

Step 2: Treatment of existing caries lesions

• Treat noncavitated lesions as needed

• Restore cavitated lesions and seal surrounding pits and fissures as needed

Step 3: Protection of surfaces at risk

• Seal all deep pits and fissures

• Apply fluoride varnish to exposed roots

Step 4: Maintenance care for prevention

• Review oral hygiene and dietary habits and advise patient to: Reduce the number of between-meal sweet snacks

Substitute snacks rich in protein

• Advise patient to brush twice daily with over-thecounter fluoride toothpaste and floss once daily

• Provide home treatment and/or other adjunctive therapy: Use over-the-counter fluoride rinse daily

• Chew or suck xylitol-containing gum or candies three times daily

• Recall patient every 3 to 6 months to: Reevaluate current caries risk

• Receive fluoride varnish treatment of all teeth

• Obtain bitewing radiographs every 6-12 months to check for cavities

General guidelines for caries management for a Low caries-risk patient

Step 1: Plaque control

• Continue to reinforce oral hygiene

Step 2: Maintenance care for prevention

• Review oral hygiene habits

• Advise patient to brush twice daily with over-the-counter fluoride toothpaste

• Recall patient every 6-12 months to reevaluate current caries risk

• Obtain bitewing radiographs every 12-18 months to check for caries

OBJECTIVE OF PREVENTION

Decrease S.Mutans activity

▪ Realize that the removal of caries lesion and restoring it does not cure a caries

problem

▪ Increase protective factors

PREVENTION Antimicrobial

Chlorhexidine → Disrupts the bacterial cell wall with its positive charge

• Only for 2 weeks

Fluoride

topical, varnish, dentifrices, mouthwash

Casein phosphopeptide-amorphous calcium phosphate (CPP-ACP

Provides a

reservoir of calcium and phosphate →enhance remineralization of dental hard tissues

Other Provention Le

Sucrose limitation

▪ Xylitol: stimulates saliva, enhances remineralization and has an antibacterial effect

▪ Oral hygiene

▪ Sealants

▪ Restorations