PRESENTATION BY:RAJESH JAINMDS 1ST YEAR

DEPARTMENT OF CONSERVATIVE AND ENDODONTICSITS DENTAL COLLEGE HOSPITAL AND RESEARCH CENTER

GREATER NOIDA

PRESENTED ON :-30th JULY 2012

MODERATOR –Dr.Rohit Kochhar

Introduction

Review of literature

History

Definitions

Theories of dental caries

Etiology

Classification

Histopathology

Diagnosis

Caries protection

Conclusion

References

Contents

Dental caries is the most common chronic disease (5 billion people worldwide)

It is costly in terms of time and work hours lost, money spent. In addition the expense incurred in education of health professional required to cope with this disease in terms of prevention, treatment and oral rehabilitation.

Introduction

Psoter WJ, Reid BC, Katz RV. 2005 stated that Enamel hypoplasia, salivary glandular hypofunction and saliva compositional changes may be mechanisms through which malnutrition is associated with caries, while altered eruption timing may create a challenge in the analysis of age-specific caries rates.

Hillman JD, Dzuback AL, Andrews SW(1976) concluded that streptococcus mutans was the main organism responsible for dental caries.

Dreizen S, Brown LR(1987)stated that there is a strong corelation between Xerostomia and dental caries.

Burke F.J.T (1998) states that presented trend in treating caries directed more towards prevention & minimal intervention rather than the traditional “drill and fill” dentistry.

Review of literature

Aristotle, Hippocrates and Shakespeare have all written on dental caries in their writings.

Some theories put forward are the Worm theory, Vital theory etc.

L. S. Parmly (1819)-first contributed to current understanding of caries mechanism

Emil Magitot experimented using Pasteur findings. He produced artificial carious lesions in extracted teeth.

W.D.Miller (1890) Chemo parasitic theory.

Gottlieb (1941) – Proteolysis theory.

Schatz & Martin(1955) –Proteolysis chelation theory.

HISTORY

Dental caries is a microbial disease of the calcified tissues, characterized by demineralization of the inorganic portion and destruction of organic portion of the tooth. (Shafer)

Dental caries is an infectious microbiologic disease of the teeth that results in localized dissolution and destruction of the calcified tissues. (Sturdevant)

Dental caries is defined as a progressive, irreversible multifactorial in nature affecting the calcified tissues of teeth, characterized by demineralization of the inorganic portion and destruction of organic portion of the tooth. (Soben peter)

Definitions

1. Worms Theory 2. Humor Theory 3. Vital Theory 4. Chemical theory 5. Parasitic at septic theory 6. Chemical Parasitic theory 7. Proteolytic theory 8. Proteolysis Chelation theory 9. Acidogenic theory 10.Levine’s theory 11. Bandlish theory

Theories of dental caries

a] Miller’s Chemo-parasitic / Acidogenic theory

b] The proteolytic theory

c] The sucrose-chelation theory

a)Acidogenic theory(w.d miller -1882)

Caries is a chemo parasitic process

Caused by acids produced by microorganisms of the mouth

Decalcification of the enamel which results in total destruction and decalcification of the dentin (preliminary stage)

Dissolution of the softened residue (final stage)

In a series of experiments following facts were demonstrated

Acid was present in deep carious lesions

Several types of bacteria could produce acid

Lactic acid was an identifiable product

Different kinds of food could decalcify the entire crown

Different kinds of microorganisms had potential to invade carious dentin

Draw backs

Phenomenon of arrested caries,caries on unerupted teeth is not explained

Smooth surface caries was not accounted

Particular type of organisms causing caries was not explained

b)Proteolytic theory (gotilleb,fresbie,pincus)

The organic or protein elements are the initial pathway of invasion by microorganisms

The organic component is most vulnerable and is attacked by hydrolytic enzymes of microorganisms ,this precedes the loss of inorganic phase

Critics organic matrix (small %) sufficient ??

lacks experimental support

c)chelation theory (schatz)

chelation; is a process involving the complexing of a metallic ion to a complex substance through a coordinate covalent bond which results in a highly stable, poorly disassociated or weakly ionized compound.

bacterial attack on the enamel initiated by microorganisms, consists in a breakdown of protein and other organic components in the enamel, chiefly keratin . This results in the formation of substances which may form soluble chelates with the mineralized components of the tooth and there by decalcifying the enamel even at a neutral or alkaline ph.

Draw backs

Organic matrix (small %) dissolution can produce sufficient amount of chelates .

Break down of organic matter by proteolysis in initiating caries lacks experimental support

I. PRIMARY FACTORS: 1.TOOTH a. Susceptible tooth surface b. biochemical characteristic of tooth 2.DENTAL PLAQUE 3.DIET 4.TIME

Mechanism of carious Mechanism of carious lesionlesion

Microorganisms found in various types of carious lesions

Pit and fissuresPit and fissures S.mutansS.mutans, , S.sanguis,lactobacilluS.sanguis,lactobacillus sp.actinomycess sp.actinomyces

Smooth surface Smooth surface cariescaries

S.mutansS.mutans, , S.salivariusS.salivarius

Root cariesRoot caries Actinomyces Actinomyces viscosus, viscosus, A.naeslundiiA.naeslundii, , s.mutanss.mutans, , s.sanguis,s.salivariuss.sanguis,s.salivarius

Deep dentinal cariesDeep dentinal caries Lactobacillus spLactobacillus sp, , Actinomyces Actinomyces viscosus, viscosus, A.naeslundiiA.naeslundii

II.MODIFYING FACTORS: 1. SALIVA 2. SYSTEMIC HEALTH 3. SEX 4. RACE 5. GEOGRAPHIC ENVIRONMENT 6. OCCUPATION

I. STURDEVANT

Based on - Location

- Extent

- Rate of progression

CLASSIFICATION

According to location:

a. Primary caries

b. Caries of pit and fissure origin

c. Caries of enamel smooth surface origin

d. Backward caries

e. Forward caries

f. Residual caries

g. Root surface caries

h. Secondary (recurrent) caries

According to extent: a. Incipient (reversible) caries

b. Cavitated (irreversible) caries

According to rate of progression: a. Acute (rampant) caries

b. Chronic (slow or arrested) caries

Class-I: - caries on the occlusal surfaces of molars and premolars

- occlusal 2/3 of the buccal and lingual surfaces of molars

- lingual surfaces of the anterior teeth.

Class II- restorations on proximal surfaces of posterior teeth.

Class III- restorations on anterior teeth that do not involve the incisal angles.

Black’s classification of tooth preparation

Class IV- Restorations on anterior teeth that involve the incisal angles.

Class V- Restorations on all gingival third of facial or lingual surfaces of all teeth (except pit and fissure lesions)

Class VI- restorations on incisal edge of anterior teeth or the occlusal cusp heights of posterior teeth.

1. Simple caries: one surface is involved

2. Compound caries: two surfaces are involved

3. Complex caries: three or more surfaces are involved

proposed by Simon

The shape and the depth of the carious lesion can be scored on a 4 point scale

D1 -Clinically detectable enamel lesions with intact (non cavitated) surfaces

D2 -Clinically detectable cavities limited to enamel

D 3 -Clinically detectable lesions in dentin (with and without cavitation of dentin)

D 4 – Lesions into the pulp.

WHO classification

Limited to the – occlusal surfaces of molars and premolars - buccal pits of molars - lingual surfaces of maxillary anterior teethPoor self-cleansing featuresUsually occurs before smooth surface cariesClinically - black or brown in color - slightly soft consistency - “catch” the tip of a fine explorerAdjacent enamel appears bluish white “Internal Caries”

PIT AND FISSURE CARIES

Develops on - proximal surfaces of the teeth - gingival third of the buccal and lingual surfaces (cervical caries)

Preceded by the formation of dental plaque.

Usually initiate just below the contact point.

Clinically- initially as faint white opacity or yellow brown pigmented area.

Adjacent enamel appears bluish white.

Smooth Surface Caries

Appears as crescent shaped lesion.

May extend proximally.

Almost always an open cavity.

Lack of oral hygiene on the part of patient.

Cervical Caries

Lateral spread of the lesion along the DEJ exceeds the caries in the contiguous enamel, caries extends into this enamel from the junction.

Backward Caries

Forward CariesForward Caries Caries cone in enamel is larger or at least the Caries cone in enamel is larger or at least the

same size as that in dentinsame size as that in dentin

Caries that remains in a completed cavity preparation

Not acceptable if - present at DEJ

- prepared enamel wall

Residual Caries

In old age patients

Initiates at the surface of a mineralized dentin and Cementum which have greater organic content

Usually have rapid clinical course

Root Surface Caries

Occurs at the junction of the restoration and the cavosurface of the enamelMay extend beneath the restorationIndicates unusual susceptibility to caries attack, poor cavity preparation, defective restoration.Also indicates presence of microleakage.

Recurrent (secondary) caries:

First evidence of caries activity in enamel

Clinically as white opaque region

Subsurface demineralization has occurred but no cavitation

May take up extrinsic stains

May undergo remineralization- called as “caries reversibility” or “consolidation” of early enamel carious lesion

Incipient (reversible) caries:

Lesion that has advanced into dentin with broken surfaceRemineralization is not possibleTreatment include cavity preparation and restoring with suitable material.

Cavitated (irreversible) caries:

Atypical form of dental caries in primary dentition

Lesion predominates on the labial surface of the maxillary anterior teeth in the region of neonatal zone

Lesion is crescent shape Increase caries susceptibility

of posterior teeth.

Linear enamel caries (odontoclasia):

Odontoclasia:

- variant of linear enamel caries

- results in gross destruction of the

labial surfaces of incisor teeth

- cause may be an inherent

structural defect

Rapid clinical course resulting in early pulp involvement

Frequently in children and young adults

Entry of lesion remains small while rapid spread along the DEJ

Clinically appears light yellow in colour

Pain is often present

Acute dental caries:

Common in adults

Large entrance of the lesion

Dentin is stained deep brown

Moderate lateral spread of caries at DEJ

Pain is not a common clinical finding.

Slowly progressive lesion that involves pulp much later

Chronic dental caries

Sudden and rapid onset and almost uncontrollable destruction of teethInvolves teeth that are ordinarily caries free (mandibular incisors)Ten or more new increments of carious lesion in one year

Rampant caries:

Rapidly progressing caries affecting primary dentition usually during first 2 years of life4 maxillary anterior are affected firstIf unchecked, maxillary and mandibular molars may also get involvedLower anterior are spared

(characteristic feature)

Nursing Bottle (Infancy or Soother) Caries

Acute caries attack at 11-18 years of ageLesion in teeth and surfaces that are relatively immune to cariesSmall opening in enamel with extensive underminingRapid clinical courseLittle or no secondary dentin formation

Adolescent caries:

Caries which becomes static or stationary and does not show any tendency for progressionAlmost exclusively occurs on occlusal surfacesBoth dentitions are affectedLesion appears as large open cavity with lack of food retentionSuperficially softened and decalcified dentin gets burnished and has brown stained polished appearance “Eburnation of dentin”

Arrested caries:

Complication of radiation therapy of oral cancer lesion

Radiation induced xerostomia produces caries conducive environment

Carious lesion develops as early as 3 months after onset of xerostomia

May be caused by other factors like salivary gland tumors, autoimmune diseases, prolong illness

Xerostomia induced caries (radiation caries)

Caries activity that spurts up during the old age.

They are located exclusively on the root surfaces of the teeth.

Also seen in association with partial denture clasps.

Causes: gingival recession, decreased salivary secretion, poor oral hygiene.

Senile Caries

• Loss of inter-rod substance

• prominent enamel-rods

• Appearance of transverse

striations of enamel rods due to

segmental demineralization

• Accentuation of incremental striae

of Retzius

Histological Features of early enamel caries

Histological Features of Advanced enamel caries

Classified on the basis of pore volume and mounting media

used

Zone 1 – Translucent zone

Zone 2 – Dark zone

Zone 3 – Body of lesion

Zone 4 – Surface zone

These zones are from the dentin towards

the outer enamel surface

NORMAL ENAMEL

DEJ

SURFACE LAYER

BODY OF THE LESION

DARK ZONE

TRANSLUSCENTZONE

TRANSLUCENT ZONE: -

Unrecognizable clinically & radiologically.

Occurs due to formation of submicroscopic pores at enamel rod boundaries and striae of Retzius.

This zone is slightly more porous than sound enamel having a pore volume of 1% compared to 0.1% of sound enamel.

DARK ZONE: -Lies superficial to translucent zone.

Called positive zone as it is always present.

Pore volume is 2 – 4%.

Increased porosity in this zone is due to greater degree of demineralization in this zone.

BODY OF LESION: -

Forms bulk of the lesion and lies between relatively unaffected surface zone and dark zone.

Area of greatest demineralization, having a pore volume of 5% near the periphery to about 25% in the center of body of lesion.

SURFACE ZONE: -

Interestingly, this zone not only remains intact during the early stages of attack by caries, but also REMAINS MORE HEAVILY MINERALIZED.

Pore volume of only 1%.

Ions for remineralization come either from those within plaque or from reprecipitation of calcium and phosphate ions diffusing outwards as deeper layers are demineralized.

Eventually, this zone is demineralized by the time caries penetrates dentin.

Once lesion spreads to DEJ, there is

lateral spread of caries

Surface enamel gets unsupported

enamel rods enamel # greater

cavitation

Zones of dentinal caries.

Zones start from pulpal side towards

dentinal side

Dentinal Caries

1. Zone of Fatty Degeneration of Tomes’ process

2. Zone of Sclerosis

3. Zone of Decalcification without Bacterial

Invasion

4. Zone of Decalcification with Bacterial Invasion

5. Zone of Decomposed Dentin / Infected dentin

543

2

1

Observing from the pulpal side at the advancing edge of carious lesion following different zones can be seen –

ZONE 1 – Zone of fatty degeneration of Tomes’ fibers

ZONE 2 – Zone of dentinal sclerosis

ZONE 3 – Zone of decalcification

ZONE 4 – Zone of bacterial invasion

ZONE 5 – Zone of decomposed dentin

Innermost layer of dentinal caries towards pulp

Due to deposition of fatty tissue in odontoblastic processes

Seen usually in rapidly progressing caries

No crystals or bacteria in lumen of tubules

Intertubular dentin normal

Fatty Degeneration of Tomes’ Process

As the microorganisms cause destruction to dentin, initially there is an attempt to stop the advancement of caries by depositing the minerals.There is a deposition of mineral in intertubular dentin.Zone is called “transparent zone”Odontoblasts are also start depositing dentin.At the periphery of sclerotic dentin, dead tracts are present.

Zone of Sclerosis/Sub-Transparent Dentin

Decalcification is by bacterial acid diffusion

Very narrow zone, softer than normal dentin

Further loss of minerals from inter tubular

dentin

Large crystals within lumen of dentinal tubules

Zone of Decalcification without Bacterial Invasion / Transparent Dentin

Initially only few tubules are involved & micro-orgs

also less

These are acidogenic, pioneer bacteria (initiators),

present long before lesion is clinically detected

Bacteria multiply within tubules & are seen in

advancing front of lesion

Zone of Decalcification with Bacterial Invasion / Turbid Dentin

Outermost zone, large scale

destruction of dentin

High concentration of bacteria

Removal of zone

Zone of Decomposed Dentin / Infected Dentin

DIAGNOSIS OF DENTAL CARIES

METICULOUS CLINICAL EXAMINATION TACTILE EXAMINATION RADIOGRAPHIC EXAMINATION TOOTH SEPARATION FIBEROPTIC TRANSILLUMINATION XERORADIOGRAPHY DIGITAL RADIOGRAPHIC METHODS COMPUTER AIDED RADIOGRAPHIC

METHODS DIGITAL FIBEROPTIC

TRANSILLUMINATION

METICULOUS CLINICAL EXAMINATION:

Careful examination under clean and dry condition with good illumination can reveal various signs of caries like:- - brown discoloration of pits and fissures - opacity beneath pits and fissures or marginal ridges - frank cavitation of the tooth surface

TACTILE EXAMINATION: • Use of dental explorer may help in detection of dental caries.•Tactile findings suggestive of caries are: - softness at the base of a pit and fissures and discontinuity of enamel surface - catch at the explorer tip - cavitation at base of pit and fissure•Cautions:excessive pressure with explorer can cause cavitation where was not present earlier infective m.org may be transferred to uninfected area

RADIOGRAPHIC EXAMINATION:

-Conventional , intraoral periapical and bitewing radiograph are employed to diagnose dental caries- bitewing is of more diagnostic value Uses of bitewing:• detecting proximal caries•Examining many teeth in one radiograph•Checking cervical margin of restoration•Monitoring the progress of arrest caries

Scoring the progress of caries on bitewing:

0= sound enamel1= radiolucency only in enamel2= radiolucency in enamel extending up to DEJ3= radiolucency in enamel and outer half of dentine4= radiolucency in enamel reaching inner half of dentine

TOOTH SEPARATION:

•To detect initial proximal caries, separation of the contacting teeth can be achieved using wedges or mechanical separator

•Once the proximal surface is accessible, visual examination and gentle probing may help in diagnosis of the carious lesion

FIBEROPTIC TRANSILLUMINATION:

•Carious lesion have lowered index of light transmission, when teeth are examined with the fiberoptic light source, caries appears as a dark shadow•After drying the tooth, a fiberoptic probe can be placed in the buccal or lingual embrassures directly beneath the contact area between two adjacent teeth.•If caries is present , dark shadow is seen beneath the marginal ridge•Non invasive•No radiation hazard•No permanent record •Difficulty in placing probe

XERORADIOGRAPHY:

•Image is recorded on an aluminium plate coated with a layer of selenium particles•These selenium particles are charged uniformly and stored in a unit called condition•When x-ray is passed onto the film , it causes selective discharge of the particles which forms a latent image.•This is converted into positive image by a process known as development in the process per unit•Less radiation exposure•No wet processing•Electric charge over the film may cause discomfort

DIGITAL RADIOGRAPHIC METHODS:

• offers more superior means of detecting caries•Can be obtained by 2 methods i)video recording and digitization of a conventional radiograph ii)direct digital radiography•The direct digital radiography system was RVG•It uses a charged couple device which works like a miniature video camera•This records images produced by conventional x-ray and stores it in the computer memory for image processing and viewing •Reduced radiation dose ,no need of dark room, no processing error, instant image visualization and can be magnified

COMPUTER AIDED RADIOGRAPHIC METHOD:

•This method uses the measurement potential of computers in assessing and recording the size of carious lesions.•Provides graphic visualization of the size and progression of the carious lesion especially a proximal caries.•Computer software have been developed for automated interpretation of digital radiographs in order to standardize image assessment•Helps in monitoring the carious process•Time consuming and expensive

DIGITAL FIBEROPTIC TRANSILLUMINATION:

•New technique which combines fiberoptictransillumination and digital CCD camera.•Images captured by the camera are sent to a computer for analysis, which produces digital images that can be viewed •This method overcomes the shortcomings of FOTI•Non invasive•Can detect incipient and recurrent caries very early•Does not measure the depth of the lesion

PREVENTION OF DENTAL CARIES

“An ounce of prevention

is worth a pound of dental

cure”.-Old Dental Public Health

Proverb

AIMS OF PREVENTION (Sturdevant):

1.Limiting pathogen growth & metabolism

2.Increasing resistance of tooth surface to demineralization

3.Caries control methods which include operative procedures

AIMS OF PREVENTION

According to SHAFER:

CLASSIFICATION OF METHODS FOR PREVENTION

Substances which alter tooth surface/structure• Fluorine• Bis-biguanides• Silver nitrate• Zinc chloride & potassium ferrocyanide

Interfere with carbohydrate degradation through enzymatic alterations• Vitamin K• Sarcoside

CHEMICAL MEASURES

Interfere with bacterial growth & metabolism

•Urea & ammonium compounds•Chlorophylls•Nitrofurans •Penicillin's•Other antibiotics•Caries vaccine •Ozone technology

Diet counseling

restriction of refined carbohydrates

Phosphated diets

Calcium phosphate rich diet.

Sugar substitutes

Non-caloric sweeteners-aspartame, saccharine

Caloric sweeteners-sorbitol, Xylitol, Mannitol

NUTRITIONAL MEASURES

Dental prophylaxis

Tooth brushing

Mouth rinsing

Dental floss

Oral irrigators

Chewing gum

Pit & fissure sealants

Preventive resin restorations

MECHANICAL MEASURES

Dental caries is an oral infection. Dental caries has a multi-factorial causation

involving the interaction of host factors (tooth surface, saliva, acquired pellicle), diet, and dental plaque (biofilm).

Besides these other modifying factors like socioeconomic status and behavioral patterns also greatly influence the caries process in a complex manner.

A good understanding of the caries process can help in formulation of better diagnosis, prevention and treatment of dental caries.

conclusion

1) Sturdevant's Art and Science of Operative Dentistry-5th edition pg74-110

2) Cariology Ernest Newbrun- 3rd edition

3) Diagnosis & Risk prediction of dental caries-Per Axelsson.

4) Textbook of operative dentistry-Ramya Raghu 2nd edition pg 50-70

5) Essentials of Preventive and Community dentistry- Soben Peter -2nd edition pg117-130

References