ENAMEL CARIESKhubaib Ahmed Shaikh

3rd Year BDS StudentCEO: Young Social Reformers.

DEFINATION.• A bacterial disease of the calcified

tissue of the teeth characterized by demineralization of the inorganic and destruction of the organic substance of the tooth.

• Physiochemical as well as biological process because of interface between tooth and external environment and interaction of bacteria and tooth surface respectively.

DENTAL CARIES--Progressive bacterial damage

to teeth.--one of the most major causes

of all diseases and major cause of tooth loss.

--ultimate effect-to breakdown enamel and dentin and open a path for bacteria to reach pulp.

Consequences-inflammation of pulp and periapical tissues.

AETIOLOGY• Four major factors involved in etiology:-• Bacterial plaque.• Susceptible tooth surface.• Fermentable bacterial substrate

(sugar).• Time.

CARRIES

Diagrammatic representation of the parameters involved in the aetiology of dental caries.

Bacteriology of Dental Caries

Major organisms responsible for caries are:-

• Streptococcus mutans.• Lactobacilli.• Other strains of

streptococci.

Species strongly associated with carries • Mutans Streptococci specially S.Mutans. • Lactobacilli.Species that may be associated • Non mutans streptococci, e.g. mitis

group• Actinomycetes

Enamel Caries• Early lesion (white spot lesion) in smooth

surface enamel carries is cone shaped, with the base of the cone on the enamel surface and the apex pointing towards the amelodentinal junction.

Ionic Exchange In Enamel Caries.

• Ions see-saw across the plaque-enamel interface depending on pH.

• Ions in plaque can be rediposited into the enamel at a neutral pH or lost into the saliva.

• Enamel carries progresses when the net rate of loss of ions due to acid attack is greater than the net rate of gain due to remineralization.

•

Ionic Exchange In Enamel Caries.

• Fluoride ions encourage reprecipitation of minerals into enamel.

• Fluoride ions can replace hydroxyl ions in hydroxyapatite to form less acid soluble fluorapatite.

• It consists of series of zones, the optical properties of which reflect differing degrees of demineralization.

1. Translucent zone2. Dark zone3. Body of the lesion4. Surface zone

Translucent Zone• This is first recognizable histological

change at the advancing edge of the lesion.

• It is more porous than normal enamel and contains 1% by volume of spaces, the pore volume, compared with the 0.1% pore volume in normal enamel.

• Decrease in magnesium and carbonate when compared with the normal enamel.

• Dissolution of minerals occur mainly from the junctional areas between the prismatic and interprismatic enamel.

• The translucent zone is sometimes missing.

Dark Zone• This zone contains 2-4% by volume of

pores. Some of the pores are large, but others are smaller than those in the translucent zone, suggesting that some remineralization has occurred due to reprecipitation of mineral lost from the translucent zone.

• It is thought that the dark zone is narrow in rapidly advancing lesions and wider in more slowly advancing lesions when more remineralization may occur.

• Also called possitive or true zone as its always present.

Body Of The Lesion• This zone has a pore volume of between

5% and 25%, and also contains apatite crystals larger than those found in normal enamel.

• The lost mineral is replaced by unbound water and to a lesser extent by organic matter, presumably derived from saliva and microorganisms.

• There is increased prominence of the striae of the retzius in the body of the lesion.

• Form the bulk of the lesion.• Area of greatest demineralization.

Surface Zone.• This is about 40 micro meter thick and

shows surprisingly little change in early lesions. The surface of normal enamel differs in composition from the deeper layers, being more highly mineralized and having, for example, a higher fluoride level and lower magnesium level, and so understanding of possible chemical changes in this zone is difficult.

• The surface zone remains relatively normal despite subsurface loss of mineral, because it is an area of active reprecipitation of mineral derived both from the plaque and from that dissolved from deeper areas of the lesion as ions diffuse outward.

Histopathology.• Development of a subsurface

translucent zone, which is unrecognizable clinically and radiologically.

• The subsurface translucent zone enlarges and a dark zone develops in its center.

• As the lesion enlarges more mineral is lost and the center of the dark zone becomes the body of lesion. This is relatively translucent compared with sound enamel and shows enhancement of the striae of retzius, interprismatic markings, and cross striations of the prisms. The lesion is now clinically recognizable as a white spot.

• The body of the lesion may become stained by exogenous pigments from food, tobacco, and bacteria. The lesion is now clinically recognizable as a brown spot.

5. When the carries reaches the amelodentinal junction it spreads laterally, damaging the adjacent enamel, giving the bluish white appearance to the enamel as seen clinically. Although lateral spread can occur before cavitation, it is more common and more extensive in lesions with cavity formation.

• 6. With progressive loss of mineral a critical point is reached when the enamel is no longer able to withstand the loads placed upon it and the structure breaks down to form a cavity. Carries progression is slow process and it usually takes several years before cavitation occurs.

Remember Confusion Is Always Awesome.

(khubaib Shaikh).

Reference: Oral Pathology 4th audition by J.V Soams & J.C Southam.