Cariology 2009

Cariology

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Dental caries

“It is an infectious microbiologic disease of the teeth that results in localized dissolution and destruction of the calcified tissues.”

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Classification

Anatomic site

Pit & fissure Smooth surface Proximal

Cervical

Root surface

Rate of progression Active or Acute

Arrested or Chronic

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classification

Hard tissue involved Enamel

Dentin

Cementum Etiology Radiation

According to age Nursing bottle Geriatric caries

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classification

According to researchers G.V. Black

Mount & Hume

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Rampant caries

Rampant caries

Few facts

Sucrose greatly stimulates plaque metabolism

Periods of demineralization & remineralization

Some 200 to 300 species of bacteria, yeast & protozoa present in oral cavity

MS----primary organism associated with caries in man

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Dental plaque

“A gelatinous mass of bacteria adhering to the tooth surface”

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Dental plaque made visible with disclosing agent.

Hypothesis concerning the etiology of caries

Nonspecific plaque hypothesis All plaque is pathogenic

Specific plaque hypothesis

Recognizes plaque as pathogenic only when signs of associated disease are present

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New Caries Treatment Based on the Medical Model

Etiology MS infection Symptoms Demineralization lesions

Treatment, symptomatic Restoration of cavitated lesions

Treatment, therapeutic Eliminate MS infection

Posttreatment assessment, Examine teeth for new lesions symptomatic

Bacteriologic testing for MS Post treatment assessment,

therapeutic

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Theories of Cariology

Acidogenic theory

Proteolysis theory

Microbiotic Secretions theory

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Acidogenic theory

Dental decay is caused by acids produced by microbial enzymatic action on ingested carbohydrates. These acids will decalcify the inorganic portion of the teeth; then the organic portion is disintegrated, creating cavities.

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Proteolysis theory

Organic portion of the tooth is attacked first by certain lytic enzymes, leaving inorganic portion without a matrix

support, causing it to be washed away, creating cavities

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Micrbiotic Secretions theory

Metabolic products of MO have the ability to chealate calcium from tooth substances, leaving the organic matrix

to be disintegrated

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1. A tooth surface without caries. 2. The f irst signs of demineralization.

3. The enamel surface has broken down. 4. A f illing has been made but the demineralization has not been stoppe

5. The demineralization proceeds and undermines the tooth. 6. The tooth has f ractured.

General Mechanism of DENTAL CARIES

Host ( tooth)

Parasites ( plaque mo) Medium ( carbohydrates)

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Etiology

bacteria food

tooth

Fig. 13-2 Dental caries.

Oral habitats

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Why do you need to restore teeth?

Restoration of damaged tooth structure Maintenance of pulpal vitality

Effective removal of the nidus of infection.

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Stephan’s curve

Demonstrates the acid production of bacteria (pH decrease) with a glucose swallow & the gradual rise due to salivary buffering.

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Stephan’s curve

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Tooth habitats for pathogenic plaque

Pits & fissures

The smooth enamel surfaces Root surfaces

Sub gingival areas

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Fissure anatomy

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Progression of caries in Pits & Fissures

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Smooth enamel surfaces

Presence of caries in these areas usually is indicative of a caries active mouth.

The proximal enamel surfaces immediately gingival of the contact area

Col In very young patients, the gingival papilla completely fills

the interproximal space under a proximal contact

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Initiation & progression on interproximal surfaces

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Smooth surface caries

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Cervical Burnout

Cervical Burnout

Root surface

Gingival recession

Root caries is alarming b/c rapid progression

Closer to pulp Difficult to restore

Following are more prone to caries Decreased salivary flow

Poor oral hygiene Decreased motivation

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Root Caries

Root Caries

Root Surface Caries

Subgingival areas

Gingival sulcus habitat is unique

Initial occupants of the sulcus are only an extension of the plaque community on the immediately adjacent surface of the

tooth

Immunologic materials may change some characteristics of the adjacent plaque by removing the most susceptible organisms.

Plaque changes progressively from cocci in the supragingival plaque to filamentous bacteria & spirochetes in subgingival

plaque

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Factors that serve as ecologic determinants

Oral hygiene

Available nutrients Sulcular fluid

Saliva Bacterial clearance

Direct antibacterial activity Buffers

Remineralization

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Enamel caries

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Incipient caries/white spot lesion

Initial carious lesion

limited to enamel intact surface but a porous subsurface. Chalky white, opaque Seen only when the surface is desiccated

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Earliest Sign of Decalcification

Earliest Sign of Decalcification

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Arrested lesion

It is an intact, but discolored, usually brown or black spot

Shiny surface, hard on excavation

Should not be restored unless esthetically objectionable

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Arrested caries

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Arrested caries

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Arrested caries

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Active lesions

White spot lesions that have a matte or visibly frosted surface or are plaque covered after drying or application of a disclosing agent. Cavitated lesions, including micro cavities as well as cavities exposing dentin.

Soft or leathery in consistency

Lesions visible in dentin on bitewing radiograph

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Active lesions

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Active lesions

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Active lesions

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ACTIVE ARRESTED

COLOR LIGHT DARK

CONSISTENCY MUSHY FIRM

MOISTURE WET DRY

SYMPTOMS SENSITIVE NONE

SHAPE DEPTH>WIDTH WIDTH>DEPTH

Recurrent Caries

Recurrent caries

“ Lesion observed under or around the margins or surrounding walls of an existing restoration”

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Recurrent caries

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Pre & Post-op treatment of recurrent caries

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Recurrent lesion

Residual caries

“ Lesion which is not removed during the restorative procedure, either by accident, neglect or intention”

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Residual Caries

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Dentinal caries

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Dentinal caries

Zone 1: Normal Dentin Deepest area

Normal odontoblastic processes No crystals are in the lumen

Intertubular dentin has normal cross banded collagen

Normal dense apatite crystals No bacteria

Stimulation of dentin produces a sharp pain

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Zone 2: Subtransparent Dentin

Demineralization of the intertubular dentin Initial formation of very fine crystals in tubule lumen

Damage to the odontoblastic process is evident No bacteria are found

Stimulation of the dentin produces pain Dentin is capable of remineralization

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Zone 3: Transparent Dentin

Zone of carious dentin softer than normal Shows further loss of mineral from intertubular dentin Large crystals in the lumen

Stimulation of this region produces pain No bacteria

This region remains capable of self repair provided the pulp remains vital.

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Zone 4: Turbid Dentin

Zone of bacterial invasion

Distortion of dentinal tubules which are filled with bacteria

Very little mineral present & collagen is irreversibly denatured

No self repair

Must be removed before restoration

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Zone 5: infected Dentin

Consist of decomposed dentin teeming with bacteria No recognizable structure to dentin & collagen Mineral seem to be absent

Removal is essential

Wet & mushy in appearance.

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Dentin

Infected dentin Contaminated with bacteria

Includes superficial granular necrotic tissue, & softened, dry, leathery dentin

Affected dentin

Comparatively hard, demineralized dentin that is not yet invaded by bacteria

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Infected Dentine

Affected Dentine

Pain (toothache) that may be associated with caries

♦Sweet -sharp, last seconds

♦Hot & cold -sharp, lasts seconds

♦Hot & cold -lingers, “throbbing”

♦Constant throb -pain starts off by itself

♦Painful on biting

Severity does not always relate to extent and “toothache” can present as any one of the above

Clinically, how would you treat the different types of carious dentin ?

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Caries diagnosis

Primary objectives of caries diagnosis are to identify those

lesions that require surgical treatment

lesions that require nonsurgical treatment persons who are at high risk of developing lesions.

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Clinical risk assignment for caries

High MS counts are found

Any two of the following are found Two or more active lesions

Large no of restorations Poor dietary habits Low salivary flow

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LOW RISK PATIENT

No cavitated lesions

May have inactive white spots (smooth shiny). Bacteria MS levels are low

Diet is normal sugar levels low Normal Saliva levels

Low DMF

MODERATE RISK PATIENT

No cavitated lesions

Some active white spot lesions (rough/chalky) Bacterial MS levels elevated

Moderate sugar use

Saliva normal or reduced (xerostomia) Moderate DMF

HIGH RISK PATIENT

One or more cavitated lesions

May have white spot lesions (active or inactive) Bacterial MS levels are very high

Sugar intake very high

Saliva levels low (xerostomia) High DMF

Assessment tools

Patient history

Clinical examination Nutritional analysis Salivary analysis

Radiographic assessment

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Medical history factors associated with increased caries risk

Age

Gender

Fluoride exposure Smoking

Alcohol

General health Medications

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Methods of caries treatment by the medical model

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Fluoride treatment modalities

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Antimicrobial Agents

Antibiotics

Vancomycin Kanamycin actinobolin Bis Biguanides chlorhexidine Halogens Fluoride

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Caries Prevention

General health

Fluoride exposure Immunization

Salivary functioning Antimicrobial agents Diet

Oral hygiene Xylitol gums

Pit & fissure sealant Restorations

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What can we do about caries?

1.Prevent ♦Frequency (and amount) of “substrates”(sugars)

♦Fluoride (water, tablets, mouthrinse, salt)

♦Regular visits to dentist, including placement of fissure sealants

♦Effective plaque removal

2.Treat ♦Drilling & Filling

♦Extract

Caries Management

Noncavitated caries Preventive measures Sealant, PRR, F-/Obs

Cavitated caries Restoration

Pulpitis, Apical RCT or Extraction Abscess

Think before ………………….

Two Difficulties

1) When to place an initial restoration?

Breakdown of the outer enamel is an important clinical indicator of the treatment

2) How to deal with severe caries?

Protection of dental pulp is the primary goal

Management of Fissured Surface

No Caries or Arrested Enamel Demineralization Cavitation or Caries in Fissures with or Questionable Caries in Caries in Dentin

Susceptible Morphology Dentin

Low High Low High Open fissures Caries Caries with round bur Risk? Risk?

enamel Demineralization dentin involve

No treatment Sealant Restoration Enamel PRR

Treatment Modalities

The results of diagnosis :

Pulp Exposure No exposure

Non-vital Conventional Vital (carious) restoration (traumatic)ex exposure

posure

RCT Direct pulp capping

Preventive Resin restoration

Etching in PRR

PRR-Composite

PRR-Final restoration

Caries control restoration

The goal is elimination of the source of cariogenic organisms by removal of caries from all deep lesions and placement of temporary restorations early in the treatment.

Caries Control Restoration

Cavity preparation is done quickly without definitive cavity preparation.

Undermined enamel be left to aid in retention of these treatment restorations, especially if restoratives are used that bond

to tooth structure.

Caries Control Restoration

Restorative materials used for caries control restoration.

CaOH

Reinforced Zinc Oxide-eugenol Glass ionomer

Amalgam

Deep Lesions

indirect pulp-capping procedure stepwise excavation

Indirect pulp capping

All infected dentin is excavated with large round burs and excavators, being careful not to expose the pulp. Basic fuchsin effectively identifies infected dentin.

A small amount of firm caries (affected dentin) is left over sites of potential exposure.

Indirect pulp capping

Calcium hydroxide liner is placed in the deepest areas. The high pH of the CaOH will neutralize acid, kill bacteria and stimulate formation of restorative

dentin.

The rein-forced ZOE, glass ionomer or amalgam restoration is placed

Stepwise excavation

Methods Of Caries Excavation

Classification of Various Tooth-Cutting Techniques

Ideal Properties Of Cutting Instruments

Comfort & ease of use

Discriminate & remove disease tissue Painless, silent, req. minimal pressure No heat or vibration

Affordable

Chemo-mechanical caries removal

a gel that selectively attacks denatured collagen in the carious dentine, thus making the carious dentine

softer. a set of specially designed

instruments used for removal of the

softened material.

Carisolv gel consists of two carboxymethylcellulose based gels:

a red gel containing : amino acids (glutamic acid, leucine and lysine), NaCl

NaOH Erythrosine (added in order to make the gel visible during use ).

and a second containing sodium hypochlorite

The gels are mixed & then applied onto the exposed carious dentine and left for 30 to 60 seconds then the

softened dentine is gently but firmly abraded away leaving a hard, caries-free cavity

A soft caries lesion Gel application. Let gel slide onto the lesion. Wait 30 seconds.

Re-applied gel stays clear. Cavity The lesion is gently scraped with is hard with a probe. a star instrument

The gel is removed with a Complete caries removal is dry pellet checked with an explorer

The cavity is cleaned with Finished cavity wet pellets

Advantages :

Conserve healthy tooth structure,

Virtually no risk of inadvertent pulp exposure, Reduce the need for anesthesia and allow for same-visit cavity preparations on multiple quadrants,

Designed to reduce post-operative sensitivity.

Sono abrasion

Sono abrasion technique is based on the removal of tooth material by an air- driven hand piece equipped with a diamond-coated working tip that removes tooth material by ultrasonic

kinetic energy.