Histology of Caries PDF

Histological and clinical appearance of dental caries Introduction The clinical appearance of caries is of great interest to the dental professional, because it tells something of the history of a caries lesion and provides valuable information for adequate noninvasive and invasive treatment. The hi...

Histological and clinical appearance of dental caries Introduction The clinical appearance of caries is of great interest to the dental professional, because it tells something of the history of a caries lesion and provides valuable information for adequate noninvasive and invasive treatment. The histology of the caries lesion provides fundamental understanding of the disease process; hence it supports the dental professional with information necessary to make the right treatment decision. Much of today’s histological knowledge of the caries process was discovered many years ago. Besides advances in oral biology, an understanding of the role of dental biofilm and the invention of the transmitted light microscope, particularly using polarized light, has fostered our knowledge of the caries process. Enamel Caries Smooth surface Caries It appear due to plaque formation on enamel. The earliest manifestation of incipient caries (early caries) of enamel is usually seen beneath dental plaque as areas of decalcification (white spots). The first change seen histologically is the loss of inter-rod substance of enamel with increased prominence of the rods. This is followed by the loss of mucopolysaccharides in the organic substance, presence of transverse striations of the enamel rods, accentuated incremental lines of Retzius as it goes deeper, the caries forms a triangular pattern or cone shaped lesion with the apex towards DEJ and base towards the tooth surface. Finally, there is loss of enamel structure, which gets roughened due to demineralization, and disintegration of enamel prisms. Pit And Fissure Caries lesion begins beneath plaque, with decalcification of enamel, pit and fissures are often deep, with food stagnation, enamel in the bottom of pit or fissure is very thin, so early dentin involvement frequently occurs. here the caries follows the direction of the enamel rods. It is triangular in shape with the apex facing the surface of tooth and the base towards the DEJ. when reaches DEJ, greater number of dentinal tubules are involved. It produces greater cavitation than the smooth surface caries and there is more undermining of enamel. The White Spot Lesion The first clinical signs (visible to the eye of the dental professional) of caries are the so-called “white spot” lesions. These lesions can be seen when plaque is removed from the enamel surface and this surface is dried with compressed air for a few seconds at a more advanced stage of disease, white spot lesions are visible also when the enamel surface is still wet. At this stage the caries process may have advanced through the entire enamel layer and into the dentin. Histology of enamel caries Traditional histology performed on thin sections perpendicular to the surface and through the enamel lesion describes four distinct zones within carious enamel that can be visualized using transmitted and polarized light microscopy.1. Translucent zone 2. Dark zone 3. Body of lesion 4. Surface zone Translucent zone: Unrecognizable clinically & radiologically. Occurs due to formation of submicroscopic pores at enamel rod boundaries. 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 centre 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. Dentin caries Dentine differs from enamel in that it is a living tissue and as such can respond to damage. It also has a relatively high organic content which consists predominantly of collagen. In dentine caries it is necessary to consider both the defence reaction of the pulpodentinal complex and the carious destruction of the tissue, which involves acid demineralization followed by proteolytic breakdown of the matrix. The defence reaction may begin before the carious process reaches the dentine, presumably because of irritation to the odontoblasts transmitted through the weakened enamel, and is represented by the formation of reactionary (tertiary) dentine and dentinal sclerosis. However, in progressive lesions, the defence reaction is overtaken by the carious process as it advances towards the pulp. Caries of the dentine develops from enamel caries: when the lesion reaches the amelo-dentinal junction, lateral extension results in the involvement of great numbers of tubules. The early lesion is cone shaped, or convex, with the base at the amelo-dentinal junction. Because of the sequential nature of the changes, studies of ground and decalcified sections should be taken. Histology of dentin caries: Early dentinal changes: With continuing demineralization of the enamel layer and increasing enamel porosity, acids and toxins of bacterial origin are able to reach and penetrate the underlying dentin. At this stage, the bacteria are still organized within the plaque covering the enamel surface and do not penetrate the enamel or dentin just yet or only in small numbers. we start by looking at the changes within dentin from the pulpal side toward the EDJ. Dentin reacts to caries before the demineralization process reaches the enamel–dentin junction (EDJ) and long before the enamel surface breaks down. The first sign of dentin reaction is tubular sclerosis. Usually, after the process of tubular sclerosis has begun, the odontoblasts start building a layer of reactive dentin, also referred to as reparative or tertiary dentin. At this stage no bacteria can be found in the dentin and, as long as the enamel surface is macroscopically intact, hardly any bacteria penetrate the enamel owing to the small size of the enamel porosities at the surface. Further on, in the direction of the EDJ, a layer of sclerotic dentin (earlier referred to as the translucent zone) is visible in thin sections using transmitted light microscopy. It is broadest (in the centripetal direction) close to the underlying layer of normal, unaffected dentin Sclerotic dentin shows occluded tubules with a thick peritubular layer, and a calcified tubular lumen. Keep in mind that these properties are true for a state of caries development where the enamel surface is porous, but still intact, and the dentin itself is hardly demineralized. The properties and shape of the sclerotic zone change with the progression of demineralization. The next zone toward the outside of the tooth appears relatively dark in transmitted light microscopy. Formation of this zone, referred to as “dead tracts,” is a consequence of tubular occlusion in the underlying zone consisting of sclerotic dentin. this zone is less resistant toward further progression of the caries process. Therefore, due to tubular occlusion within the sclerotic zone and retraction of the odontoblastic cellular processes, the dentinal tubules in the dead-tract zone appear empty and cut off from the living odontoblast. Between the dead tracts and the EDJ the so-called demineralized zone can be found, usually when carious enamel demineralization reaches the EDJ. It is caused by the penetration of organic acids of bacterial origin into the dentin. It has lower hardness than the sclerotic dentin. Advanced Dentin Reaction: Collapse of the intact enamel surface not only means that the enamel porosities have become so big, it also means that huge numbers of bacteria are able to penetrate the enamel lesion. With invasion of huge numbers of bacteria into the porous enamel, bacteria soon reach the EDJ and invade the dentin, forming the zone of penetration, which takes over the former zone of demineralization. Still at this point, the zone of demineralization precedes the bacterial invasion. This is of some clinical relevance, because it means that demineralized dentin does not necessarily contain bacteria and may be left during excavation. Also, irreversible pulpal inflammation is typically seen only at later stages, with the bacteria advancing as close to the pulp as around 0.5mm. With penetration of bacteria deeper into the demineralized zone, the demineralized zone itself moves toward the zone of sclerotic dentin at the expense of the dead tract zone. Further lesion development is most likely to occur. With invasion of huge numbers of bacteria into the porous enamel, bacteria soon reach the EDJ and invade the dentin, forming the zone of penetration, which takes over the former zone of demineralization With further progression of the bacterial front, the sclerotic dentin disappears completely, usually before the advancing front of bacteria reaches the pulpal wall. At this stage the enamel layer may have been broken down completely, thus exposing a large area of carious dentin. As long as the dentin surface, now opened up, stays covered by plaque, the complete degradation of dentin continues. While at the earlier stages of dentin involvement, demineralization by bacterial acids plays the major role, at the later stages hydrolytic and proteolytic enzymes successfully degrade the demineralized dentin matrix. The remaining soft material, consisting of remnants of demineralized dentin and dental plaque, is often referred to as the zone of destruction. Still, remnants of the sclerotic zone may be present enclosing the cariously affected dentin from the sides. With the zone of penetration reaching the dental pulp, irreversible pulpal inflammation cannot be avoided. Concept of infected and affected dentin: While dealing with caries, it is important to explain the concept of affected dentin and infected dentin. Fusayama reported that carious dentin has two layers, Outer layer (infected) and the inner layer (affected dentin). It is important to be able to differentiate between the two layers. Difference in reaction mechanisms between enamel and dentin: It is important to realize that there is a fundamental difference in reaction mechanisms between enamel and dentin. Enamel is a cell free tissue which does not show any cellular response in the case of caries attack; enamel reaction is based on chemical dissolution and precipitation phenomena. Dentin is different, because it has to be considered as vital tissue, since it contains living cellular processes from the odontoblasts lining the pulpo-dentinal wall. Root (cementum) caries 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 primary tissue affected in root caries is cementum. The destruction of cementum occurs parallel to the root surface, spreading along the cemental lines, and eventually forming ‘saucer-shaped’ carious lesions that may encircle the root. After decalcification of cementum, destruction of matrix occurs similar to dentin with ultimate softening and destruction of this tissue. nvasion of micro-organisms into the dentinal tunbules, finally leading to pulp involvement.