1RVGDr.swapnil pakhale

“Dental caries is an irreversible microbial disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic portion and destruction of the organic substance of the tooth, which often leads to cavitations.”

It is a complex and dynamic process where multitude of factors influence and initiate the progression of disease.

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A detail of a tooth (to the right = enamel). It is covered by plaque, which consists mainly of bacteria. Plaque is often found close to the gum, in between teeth, in fissures and at other "hidden" sites. Demineralization:When sugar and other fermentable carbohydrates reaches the bacteria, they form acids which start to dissolve the enamel - an early caries lesion occurs due to loss of Calcium and Phosphates

Remineralization:When sugar consumption has ceased, saliva can wash away sugars and buffer the acids. Calcium and Phosphates can again enter the tooth. The process is strongly facilitated by fluorides

A CAVITY occurs if the Demineralization "wins" over the Remineralization43RVG

The first indication of tooth decay are white spots on the enamel caused by the loss of calcium.

If the demineralization process outruns the natural remineralisation process, the lesion grows and a cavity is formed. 

The bacteria may invade the pulp of the tooth, 

causing a consistent tooth pain, especially during the night.

The bacteria may also produce an

abscess,

Eventually the tooth may be extracted by

the dentist.

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It is believed to be preceded by the formation of microbial/ dental plaque.

The carious process varies slightly, depending upon the occurrence of the lesion on smooth surfaces or in pits or fissures.

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The earliest macroscopic evidence of incipient caries is the appearance of an area of decalcification beneath the dental plaque which resembles a smooth chalky white area.

The enamel surface overlying the white spot is hard and shiny.

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The first change is usually a loss of inter-prismatic or inter-rod substances of the enamel with increase prominence of the rods.

In some instances the initial change seems to consist of roughening of the ends of enamel rods.

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Another change in early enamel caries is the accentuation of the incremental Striae of Retzius.

There may also be accentuation of perikymata.

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As this process advances it will be noted, that smooth surface caries forms a triangular or cone shaped lesion, with the apex towards the DEJ, the base towards the surface of the tooth.

With fissure caries, the enamel lesion broadens as it approaches dentin.

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The small lesion has been divided into different zones based upon its histological appearance.

Four zones are clearly distinguishable, starting from the inner advancing front of the lesion.› Translucent zone› Dark zone › Body of the lesion› Surface layer

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It lies at the advancing front of the enamel lesion

It is the first recognizable zone of alteration from normal enamel

About half of the lesion demonstrate translucent zone.

The spaces or pores created in the tissue in this stage of enamel caries are located at prism boundaries and other junction site.

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

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Lies adjacent and superficial to the translucent zone.

This zone is formed as a result of demineralization and appears dark brown in ground section.

It has a pore volume of 2-4%. The dark zone shows positive birefringence

in contrast to negative birefringence of sound enamel, hence referred as positive zone.

It has been referred to as POSTIVE ZONE, because it is usually present.

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This zone lies between the relatively unaffected surface layer and the dark zone.

In polarized light the zone shows a pore volume of 5% in spaces near the periphery to 25% in the centre.

This lesion appears relatively translucent compared with sound enamel.

However striae of retzius within this region are well marked and appear enhanced, in contrast to the translucency of the area.

This region shows a region of positive birefringence. 54RVG

This zone indicates partial demineralization equivalent to about 1-10% loss of mineral salts and pore volume is less than 5% of spaces.

The porous subsurface zone is seen to be positively birefringence, the surface zone retains negative birefringence.

The greater resistance of the surface layer may be due to greater degree of mineralization and a greater degree of fluoride in surface layer.

55RVG

The lesion does not differ in nature from smooth surface caries except as the variation in anatomic and histological structure dictate.

The carious lesion more often starts at both the sides of fissure wall rather than the base.

Enamel in the bottom of the pit and fissure may be very thin so that early dentin involvement frequently occurs.

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The general shape of lesion is the opposite of that occurring on smooth surface.

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It produces greater cavitation than the smooth surface caries and there is more undermining of enamel.

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Caries in the enamel is clearly a dynamic process, but tissue is devoid of cells and is therefore incapable of reacting in a vital manner; whereas dentin being a part of dentin pulp complex is able to mount a reparative response.

Caries of dentin begins with the natural spread of the process along the DEJ and the rapid involvement of great number of dentinal tubules.

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The initial penetration of the dentin by caries is described as “dentinal sclerosis” or “transparent dentin.”

This dentinal sclerosis is a reaction of vital dentinal tubules and a vital pulp in which there is calcification of dentinal tubules that tends to seal them off

against further penetration by microorganisms.

Dentinal sclerosis 60RVG

The appearance of fatty degeneration of tomes dentinal fibers with the deposition of fat globules precedes even the early sclerotic dentinal changes.

The rate at which carious destruction progresses tends to be slower then in young persons because of generalized dentinal sclerosis that occurs as part of ageing process.

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In the earliest stages of caries microorganisms may be found penetrating these tubules. They have been termed as “pioneer bacteria”.

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This initial decalcification involves the walls allowing them to distend as the tubules are packed with microorganisms. Each tubule is seen to be packed with pure forms of bacteria, eg., one tubule packed with coccal forms the other tubule with bacilli.

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As the microorganisms proceed further they are distanced from the carbohydrates substrate that was needed for the initiation of the caries.

Thus the high protein content of dentin must favour the growth of the microorganisms.

Therefore proteolytic organisms might appear to predominate in the deeper caries of dentin while acidophilic forms are more prominent in early caries.

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The thickening and swelling of the sheath of Neumann may be noted at irregular intervals along the course of involved dentinal tubules.

Tiny “liquefaction foci” are formed by focal coalescence and breakdown of few dentinal tubules.

This “focus” is an ovoid area of destruction parallel to the course of tubules and filled with necrotic debris which tends to increase in size by expansion. 65RVG

The destruction of dentin by decalcification and then proteolysis occurs in numerous focal areas- leading to a necrotic mass of dentin of a leathery consistency.

Clefts present in the carious dentin that extends at right angles to the dentinal tubules, accounts for the peeling off of dentin in layers while excavating.

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Shape of the lesion is triangular with the apex towards the pulp and the base towards the enamel.

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Beginning pulpally at the advancing edge of the lesion adjacent to the normal dentin, these zones are as follows:

ZONE 1: Fatty degenration of tomes fibres due to degeneration of the odontoblastic process.

ZONE 2 : Dentinal sclerosis charachterized by deposition of calcium salts in dentinal tubules.

ZONE 3 : Decalcification of dentin, a narrow zone, preceding bacterial invasion.

ZONE 4 : Bacterial invasion of decalcified but intact dentin.

ZONE 5: Zone of decomposed dentin due to acids and enzymes. 68RVG

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It does not differ remarkably from the involvement of primary dentin except it is slower because the dentinal tubules are few in number and more irregular in their course, thus delaying penetration of microorganisms.

Sooner or later the involvement of pulp results with inflammation and necrosis.

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Root caries as defined by HAZEN, is a soft, progressive lesion that is found anywhere on the root surface that has lost its connective tissue attachment and is exposed to the environment.

The root surface must be exposed to the oral environment before caries can develop here.

Plaque and micro-organisms are essential for the cause and progression of the lesion – Actinomyces

Micro-organisms invade the cementum either along the Sharpey’s fibers or between the fiber bundles.

Spread laterally, since cementum is formed in concentric layers.

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After decalcification of cementum, destruction of matrix occurs similar to dentin with ultimate softening and destruction of this tissue.

Invasion of micro-organisms into the dentinal tunbules, finally leading to pulp involvement.

The rate is slower due to fewer dentinal tubules than crown area

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