caries part 1

7/29/2019 Caries Part 1

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CARIOLOGYSUBMITTED BYAKANKSHA PRABHA

Roll No. 03

BATCH 2011

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CONTENTS

DEFINITION

CLASSIFICATION

THEORIES OF DENTAL CARIES

HISTOPATHOLOGY OF CARIESENAMEL AND DENTINAL

CARIES

CARIES DIAGNOSIS

CARIES PREVENTION

CARIES TREATMENT

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DEFINITIONDental caries is defined as a

progressive, irreversible, microbial diseaseaffecting the hard parts of the tooth exposed to the

oral cavity ,resulting in decalcification ofinorganic constituents and dissolution of organiccomponents, there by leading to a cavity formation.

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CLASSIFICATION DENTAL CARIESA) On basis ofclinical features and patterns:1) Morphology i.e, according to anatomical site oflesions

a) Occlusal caries (Pit N Fissure Caries)b) Smooth surface caries

InterproximalCervical or gingival

c) Root cariesd) Linear enamel caries ( Odontoclasia)

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PIT N FISSURE CARIES CERVICAL CARIES INTERPROXIMAL CARIES

ROOT CARIES

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2) Dynamics i.e, according to severity and rate ofprogression of lesions:

Class 1: Very mild cariesClass 2: Mild cariesClass 3: Moderate cariesClass 4: Severe caries

Class 5: Very severe caries

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7INFANCY CARIES ADOLESCENCE CARIES

3) Chronology i.e, according to age patterns at which

lesions predominate:

a) Infancy cariesb) Adolescent caries


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4) Based on the pathway of dental caries: 1) Forward decay

2) Backward decay

8FORWARD CARIES

BACKWARD CARIES


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5). Therapeutic classificationBased on restoration design G.V. Black classified into:

a) Class 1: Pit and fissure cavities of posterior teeth,occlusal two- thirds of buccal and lingual surface of

molars & lingual surface of maxillary incisors.

b)Class 2 cavities: On proximal surface of posteriorteeth

c)Class 3 cavities: On proximal surfaces of anteriorteeth which do not involve the incisal edge.

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d) Class 4 cavities: Seen on proximal surfaces of anterior teeththat involve the incisal edge.

e) Class 5 cavities: Seen on gingival third of facial and lingualsurfaces of all teeth.

f) class 6 cavities: Seen on incisal edges of anterior teeth and

occlusal cusp heights of posterior teeth.

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g) Based on degree and rate of caries progression:1. Incipient

2. Arrested caries

3. Xerostomia induced caries [Radiation caries]

11XEROSTOMIA INDUCED CARIES ARRESTED CARIES


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6) Based on carious surfaces involved: simple [1surface]

compound [ 2 surface]

complex [3 or more surfaces]

7) Based on whether the lesion is a new one attacking apreviously intact surface or whether it is occurring aroundthe margins of a restoration:

primary [virgin] caries

secondary [recurrent] caries

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Based on site and size- G.J Mount

1997

A) Site

Site 1Pit and fissures of posterior teeth ; buccal, palatal grooves;erosion lesions

Site 2 Proximal surface

Site 3 Gingival third

B) Size

Size 0 Small

Size 1 (Mild)- Lesions which have progressed just beyondremineralisation

Size 2 (Moderate) Larger lesions with adequate tooth structure

Size 3 (Enlarged)Tooth structure and restoration are susceptible tofracture

Size 4 (Severe) Extensive loss of tooth structure

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Remineralisation

It occurs when the pH rises above 5.5.

Saliva & plaque fluid are super-saturated with calcium &phosphate ions.

Statherin, a proline-rich peptide, stabilises calcium &phosphate ions and prevents excessive deposition of theseions on the teeth.

This super-saturated state of saliva helps in remineralisationof enamel.

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EVIDENCE OF BACTERIAL ROLE IN CARIES ETIOLOGY

1. Germ free animal do not develop caries.

2. Antibiotics fed to animals are effective in reducing the incidenceand severity of caries.

3. Totally unerupted and unexposed teeth do not develop caries.4. Oral bacteria can demineralize enamel and dentin in vitro and

produce caries like lesions.

5. Micro- organism have been histologically demonstrated invading

carious enamel and dentin. They can be isolated and cultivatedfrom carious lesions

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ORAL MICRO-ORGANISMS CAUSING

CARIES

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HABITAT PREDOMINANT SPECIES ENVIRONMENTALCONDITIONS WITHIN

PLAQUE

Enamel Caries Streptococcus mutans Anaerobic

pH less than 5.5

Oxidation-reductionnegative

Dentin Caries Streptococcus mutans

Lactibacillus species

-----do----

Root Caries Actinomyces species -----do----


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NON-SPECIFIC PLAQUE HYPOTHESIS There is universal presence of potential pathogens in plaque.

All plaque is pathogenic.

SPECIFIC PLAQUE HYPOTHESIS Plaque is only pathogenic when signs of associated disease

are present.

Only a few micro=organisms are capable of cariesproduction.

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When local pH is higher than 5.5, calcium & phosphate ionsare present, demineralisation may be reversed.

Remineralisation of enamel and dentin results in theformationofarrested carieswhich is resistant to futurecariogenic challenge.

Remineraliation before cavitation results in brownishdiscoloration due to incorporation of exogenous pigmentedmaterial.

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If remineralization occurs after cavitation, theremaining exposed surface becomes harder andoften dark brown or black in color.

Eburnated dentinArrested caries on a dentinalsurface.

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HISTOPATHOLOGY OF DENTAL CARIES

ENAMEL CARIES

Light microscopic studies of carious lesions of

enamel without cavitation, have revealed fourdistinct zones, which represent varying degrees ofhard tissue transformation, beginning on thedentinal side of the lesion

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ZONE 1: TRANSLUCENT ZONE

It is the deepest zoneand represents the advancing frontof enamellesion.

The name refers to its structureless appearancewhen perfusedwith quinoline solution and examined with polarized light.

In this zone , pores or voids form along the enamel prism [rod]boundaries, presumably, because of the ease of hydrogen ionpenetration during the carious process.

The pore volume of this zone is 1% [10 times greater than normalenamel].

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ZONE 2: DARK ZONE

Lies adjacent and superficialto the translucent zone .

Called dark zone because it does not transmit polarized light .

This light blockage is caused by the presence of many tinypores too small to absorb quinoline.

The total pore volume is 2% to 4%.

It has been referred to as positive zone because it is usuallypresent.

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ZONE 3: BODY OF THE LESION

It lies between the relatively unaffected surface layer andthe dark zone.

It is the area of greatest demineralization.

It has the largest pore volume, varying from 5% at theperiphery to 25% at the centre.

The striae of retzius is well marked in this zone, indicatingmineral dissolution along these areas of relatively higherporosity.

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The first penetration of caries enters the enamelsurface via the Striae of Retzius.

The inter prismatic areas and these cross striationsprovide access to rod cores, which are then

preferentially attacked .

Bacteria may be present in this zone if the pore size islarge enough to permit their entry.

Studies using TEM and SEM demonstrated thepresence of bacteria invading between the enamelrods [prisms] in the body zone.

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ZONE 4: SURFACE ZONE This zone is relatively unaffected by the carious attack.

It has a lower pore volume than the body of lesion [less than5%]

and a radio opacity compared to the unaffected adjacentenamel.

It has been hypothesized that hypermineralisation andincreased

fluoride content of superficial enamel are responsible for the

relative immunity of enamel surface

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ZONES OF DENTINAL CARIES

Caries advancement in dentin proceeds through 3stages:

1. Weak organic acids demineralise dentin .

2. Organic material of dentin, particularly collagen,degenerates and dissolves; and

3. The loss of structural integrity is followed by

invasion of bacteria .

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ZONE 1 : NORMAL DENTIN :

The deepest area is normal dentin, which has tubuleswith odontoblastic process that are smooth, and nocrystals are in the lumen .

The intertubular dentin has normal cross bandedcollagen and normal dense apatite crystals .

No bacteria are in the tubules .

Stimulation of dentin [eg. by osmotic gradient , a bur,dessication from heat or air] produces a sharp pain.

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ZONE 2 : SUBTRANSPARENT DENTINThis is a zone of demineralization of inter tubular

dentin and initial formation of very fine crystals inthe lumen at the advancing front .

Damage to the odontoblastic process is evident .

However no bacteria are found in this zone.

Stimulation of dentin produces pain, and the dentinis capable of remineralization.

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ZONE 3: TRANSPARENT DENTIN It is softer than normal dentin .

Shows further loss of mineral from the inter tubular

dentin and many large crystals in the lumen of dentinaltubules .

Stimulation of this region produces pain .

No bacteria are present.

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ZONE 4: TURBID DENTIN It is the zone of bacterial invasion and is marked by

widening and distortion of dentinal tubules, filled with

bacteria .

There is very little mineral present, and the collagen in this

zone is irreversibly denatured.

The dentin in this zone will not self- repair this zone.

This zone cannot be remineralized and must be removed

before restoration.

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caries part 1

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