CARIOLOGY

SUBMITTED BY AKANKSHA PRABHA Roll No. 03 BATCH 2011

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CONTENTS
DEFINITION

CLASSIFICATION THEORIES OF DENTAL CARIES HISTOPATHOLOGY OF CARIES ENAMEL AND DENTINAL CARIES CARIES DIAGNOSIS CARIES PREVENTION CARIES TREATMENT
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DEFINITION Dental caries is defined as a progressive, irreversible, microbial disease affecting the hard parts of the tooth exposed to the oral cavity ,resulting in decalcification of inorganic constituents and dissolution of organic components, there by leading to a cavity formation.

CLASSIFICATION DENTAL CARIES A) On basis of clinical features and patterns: 1) Morphology i.e, according to anatomical site of lesions a) Occlusal caries (Pit N Fissure Caries) b) Smooth surface caries Interproximal Cervical or gingival c) Root caries d) Linear enamel caries ( Odontoclasia)

PIT N FISSURE CARIES

CERVICAL CARIES

INTERPROXIMAL CARIES

ROOT CARIES

2) Dynamics i.e, according to severity and rate of progression of lesions: Class 1: Very mild caries Class 2: Mild caries Class 3: Moderate caries Class 4: Severe caries Class 5: Very severe caries

3) Chronology i.e, according to age patterns at which lesions predominate: a) Infancy caries b) Adolescent caries

INFANCY CARIES

ADOLESCENCE CARIES

4) Based on the pathway of dental caries: 1) Forward decay 2) Backward decay

FORWARD CARIES

BACKWARD CARIES
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 5). Therapeutic classification Based 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 posterior teeth c)Class 3 cavities: On proximal surfaces of anterior teeth which do not involve the incisal edge.

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

e) Class 5 cavities: Seen on gingival third of facial and lingual surfaces 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]

XEROSTOMIA 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 a previously intact surface or whether it is occurring around the 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 1 Pit 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 beyond remineralisation Size 2 (Moderate) Larger lesions with adequate tooth structure Size 3 (Enlarged) Tooth structure and restoration are susceptible to fracture 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 these ions on the teeth. This super-saturated state of saliva helps in remineralisation of 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 incidence and 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 cultivated from carious lesions

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ORAL MICRO-ORGANISMS CAUSING CARIES

HABITAT PREDOMINANT SPECIES ENVIRONMENTAL CONDITIONS WITHIN PLAQUE
Anaerobic pH less than 5.5 Oxidation-reduction negative -----do---Enamel Caries Streptococcus mutans

Dentin Caries

Streptococcus mutans Lactibacillus species Actinomyces species

Root Caries

-----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 caries production.

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 When local pH is higher than 5.5, calcium & phosphate ions are present, demineralisation may be reversed. Remineralisation of enamel and dentin results in the formationof arrested caries which is resistant to future cariogenic challenge. Remineraliation before cavitation results in brownish discoloration due to incorporation of exogenous pigmented material.

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 If remineralization occurs after cavitation, the remaining exposed surface becomes harder and often dark brown or black in color. Eburnated dentin Arrested caries on a dentinal surface.

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HISTOPATHOLOGY OF DENTAL CARIES ENAMEL CARIES

Light microscopic studies of carious lesions of enamel without cavitation, have revealed four distinct zones, which represent varying degrees of hard tissue transformation, beginning on the dentinal side of the lesion

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ZONE 1: TRANSLUCENT ZONE

It is the deepest zone and represents the advancing front of enamel lesion. The name refers to its structureless appearance when perfused with 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 ion penetration during the carious process. The pore volume of this zone is 1% [10 times greater than normal enamel].

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ZONE 2: DARK ZONE

Lies adjacent and superficial to the translucent zone . Called dark zone because it does not transmit polarized light . This light blockage is caused by the presence of many tiny pores too small to absorb quinoline. The total pore volume is 2% to 4%. It has been referred to as positive zone because it is usually present.

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ZONE 3: BODY OF THE LESION

It lies between the relatively unaffected surface layer and the dark zone. It is the area of greatest demineralization.

It has the largest pore volume, varying from 5% at the periphery to 25% at the centre.
The striae of retzius is well marked in this zone, indicating mineral dissolution along these areas of relatively higher porosity.
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 The first penetration of caries enters the enamel surface via the Striae of Retzius.
The inter prismatic areas and these cross striations provide access to rod cores, which are then preferentially attacked .

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

Studies using TEM and SEM demonstrated the presence of bacteria invading between the enamel rods [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 than 5%] and a radio opacity compared to the unaffected adjacent enamel. It has been hypothesized that hypermineralisation and increased 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 3 stages: 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 tubules with odontoblastic process that are smooth, and no crystals are in the lumen . The intertubular dentin has normal cross banded collagen 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 DENTIN

This is a zone of demineralization of inter tubular dentin and initial formation of very fine crystals in the 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 dentin is 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 dentinal tubules . 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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