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SEMI NAR BY Dr . KARTHI K MOHAN. I Postgraduate Student



INTRODUCTION Dental caries is a most interesting but different process to study microscopically because of the technical problems involved in penetration of the tissue for examination. The principal manner in which caries of the enamel has been studied is through the use of ground sections of teeth. The decalcification process necessary for cutting thin sections usually results in complete loss of enamel unless special methods are used. This has materially impeded the investigation of dental caries at the microscopic level, although surprising advances have been made in the face of adverse conditions.

Histology Of Enamel: Enamel is composed of very tightly packed hydroxyapatite crystallites, organized into long columnar rods (prisms). The rods are somewhat key-shaped in cross section. Individual enamel rods are formed by the activity of ameloblasts. Each rod starts at the DEJ and extends as a wavy, continuous column to the surface of the crown. The mineralization process is apparently somewhat discontinuous and is characterized by altering phases of high and low activity. Periods of low activity create “rest� lines within the rods. These rest lines, in combination with similar lines in neighboring rods, form a structure visible on mounted cross sections of

enamel and are named the striae of Retzius. The striae are regions characterized by relatively higher organic content. Both the striae and the inherent spaces in the prism boundaries provide sufficient porosity to allow movement of water and small ions, such as hydrogen ions. Thus enamel is capable of acting as a molecular sieve by allowing free movement of small molecules and blocking the passage of large molecules and ions. The sieve like behavior of enamel also explains why insipient caries of enamel can produce a pulpal response prior to penetration of bacteria. The movement of ions through carious enamel can result in acid dissolution of the underlying dentin before actual cavitation of the enamel surface. This acid attack at the external ends of the dentinal tubules initiates a pulpal response by unknown mechanisms. Since the striae form horizontal lines of greater permeability in the enamel, they probably contribute to the lateral spread of smooth surface lesions. The surface manifestations of the striae are the imbrication lines of Pickerel.

Histology of Dentin: The dentin is the hard portion of the tooth that is covered by enamel on the crown and cementum on the root. Dentin is the calcified product of odontoblasts, which line the inner surface of the dentin within the periphery

of the external pulp tissue. Each odontoblast has an extension (termed Tomes fiber) into the dentinal tubule. The tubules transverse the entire thickness of the dentin from the pulp to the DEJ. Filling the space between the tubules is the inter-tubular dentin, a rigid bone like material composed of hydroxyapatite crystals embedded in a network of collagen fibers. The walls of the tubules are lined with a smooth layer of mineral termed peri-tubular dentin.

The recent application of transmission and scanning electron microscopy to the study of dental caries has added greatly to our understanding of this disease, as has utilization of other techniques, including histochemical studies and the use of radioactive isotopes. For ease of understanding, the histopathology of dental caries is considered under:

1. Caries of enamel, 2. Caries of dentin, 3. Caries of cementum.

Caries of the Enamel: Caries of the enamel is believed by most investigations to be preceded by the formation of a microbial (dental) plaque. The process varies slightly, depending upon the occurrence of the lesion on smooth surfaces or pits or fissures. For this reason it is best to discuss enamel caries under o Smooth surface caries. o Pit and Fissure caries.

Smooth surface caries: The surface of the enamel, at least in newly erupted teeth, is covered by a membrane composed of the primary and secondary cuticle. The significance of this membrane in forestalling the development of a carious lesion is not known, but it is probably not clinically important because it is lost early in postoperative life.

The earliest manifestation of incipient caries of the enamel is 1. The appearance beneath the dental plaque of an area of decalcification, which resembles a smooth chalky white area.

That this is a critical point in the development of this disease is understood by the convening of a symposium, “Incipient Caries of Enamel�, which was held at the University of Michigan in November 1977 and edited by Rowe. Study of early lesions by the transmission electron microscope, particularly by Scott and his associates, had revealed that: o The first change is usually a loss of the interprismatic or inter-rod substance of the enamel with increased prominence of the rods. o In some instances the initial change seems to consist of roughening of the ends of the enamel rods, suggesting that the prism may be more susceptible to early attack. o The work of Sognnaes and Wislocki on the mucupolysaccharide present in the interprismatic organic substance of the enamel revealed that the degradation of this substance occurred very early in the caries process. o Very early in the process also, there is the appearance of transverse striations of the enamel rods, dark lines or bands occurring at right angles suggesting segments. o Another change in early enamel caries is the accentuation of the incremental striae of Retzius. This appearance is an optical phenomenon due to loss of minerals, which causes the organic structures to appear more prominent.

As the caries process advances and involves deeper layers of enamel, it takes a distinctive shape: o It forms a triangle of a cone shaped lesion with the apex toward the dentino-enamel junction and the base toward the surface of the tooth.

There is eventual loss of continuity of the enamel surface, and the surface feels rough to the point of an explorer. This roughness is caused by disintegration of the enamel prisms after decalcification of the interprismatic substance and the accumulation of debris and microorganisms over the enamel.

Before complete disintegration of the enamel, several zones are seen, beginning on the dentinal side of the lesion:

Zone 1: The translucent zone lies at the advancing front of the enamel lesion. It is not always present. This zone is more porous than sound enamel, having a pore volume of 1% compared with 0.1% in sound enamel, as seen by polarized light.

Zone 2: The dark zone lies adjacent and superficial to the translucent zone. It is also known as Positive zone, because it is usually present. This zone is formed as a result of demineralization.

Zone 3: The body of the lesion lies between the relatively unaffected surface layer and the dark zone. It is the area of greatest demineralization. In polarized light the zone shows a pore volume of 5% in spaces near the periphery to 25% in the center of the intact lesion.

Zone 4: The surface zone when examined by polarizing microscope and micro radiography, appears relatively unaffected. The greatest resistance of the surface layer may be due to a greater degree of mineralization and/or a greater concentration of fluoride in the surface enamel.

It has been implicated that enamel lamellae act as pathways for invasion of proteolytic microorganisms and subsequent development of caries, bur there is no direct evidence to indicate that the enamel lamellae play any significant role in the development of caries.

Pit And Fissure Caries: The carious process in pits and fissures do not differ in nature from the smooth surface caries except as the variations in anatomic and histologic structure dictate. o Here too the lesion begins beneath the bacterial plaque with decalcification of enamel. o Pits and fissures are often of such depth that food stagnation with bacterial decomposition in the base is to be expected. The enamel at the bottom of the pit of fissure may be very thin, so early dentin involvement occurs frequently. o Some pits and fissures are shallow and have a thick layer of enamel covering their base.

In both types the enamel rods flare laterally in the bottom of the pits and fissures. When caries occurs here: o It follows the direction of the enamel rods and characteristically forms a triangle or cone-shaped lesion with its apex at the outer surface and its base toward the dentino-enamel junction.

Note that the general shape of the lesion here exact opposite of the lesion occurring on smooth surfaces. o Because of this shape a greater number of dentinal tubules are involved when the lesion reaches the dentino-enamel junction. o Pit and fissure caries, particularly of the occlusal surfaces, usually produces greater cavitation than proximal smooth surface caries.

CARIES OF DENTIN: Caries of dentin begins with the natural spread of the process along the dentino-enamel junction and the rapid involvement of a great number of dentinal tubules, each of which act as a tract leading to the dental pulp along which the microorganisms may travel at a variable rate of speed, depending upon a number of factors.

In some instances carious invasion appears to occur through an enamel lamellae so that little if any visible alteration in the enamel occurs. Thus, when lateral spread at the dentino-enamel junction occurs with the involvement of underlying dentin, a cavity of considerable size may actually form with only slight clinically evident changes in the overlying enamel except for its undermining.

EARLY DENTIN CHANGES: o The initial penetration of dentin by caries results in alterations in the dentin previously described as “Dentinal Sclerosis or Transparent Dentin”. This dentinal sclerosis is a reaction of the vital dentinal tubules and a vital pulp in which there results a calcification of the dentinal tubules that tends to seal them off against further penetration of microorganisms. The formation of sclerotic dentin is minimal in rapidly advancing caries and most prominent in slow chronic caries. The term “transparent dentin” has been applied because of the peculiar transparent appearance of the tooth structure when a ground section is viewed by transmitted light. By reflected light sclerotic dentin appears dark. o The appearance of fatty degeneration of Tomes dentinal fibers, with the deposition of fat globules in these processes, precedes even the early dentin sclerotic changes. This can be demonstrated only by the application to fresh dentin of special stains such as Sudan red, which selectively stains fat. The significance of this phenomenon is not known, although it has been suggested that the fat contributes to the impermeability of the dentinal tubules.

o Except in unusual cases of arrested caries, continued destruction of dentin occurs despite the attempts at walling off on the part of the tooth. The rate at which the carious destruction progresses tends to be slower in older individuals than in young persons because of generalized dentinal sclerosis that occurs as part of ageing process. o Close examination of the dentin behind a zone of sclerosis of dentin formed in response to caries will reveal decalcification of the dentin, which appears to occur slightly in advance of the bacterial invasion of the tubules. o In the earliest stages of caries when only a few tubules are involved, microorganisms may be found penetrating these dentinal tubules before there is any clinical evidence of the carious process. These have been termed “Pioneer Bacteria�. o This initial decalcification involves the walls of the tubules, allowing them to distend slightly as they become more packed with masses of microorganisms. o Careful study of individual tubules will usually show almost pure forms of bacteria in each one. Thus one tubule may be filled with coccal forms, while the adjacent tubules may contain only bacilli or thread forms.

o These microorganisms as they penetrate farther and farther into the dentin, become separated more and more from the carbohydrate substrate upon which the bacteria responsible for the initiation of the disease depend. o The high protein content of the dentin would favor the growth of those microorganisms which have the ability to utilize this protein in their metabolism. Thus proteolytic organisms would appear to predominate in deeper caries of the dentin, while acidogenic forms are more prominent in early caries. o The observation that the morphologic type of bacteria in deep carious dentin is different from that of the bacteria in initial caries substantiates the hypothesis that “Initiation and Progression� of dental caries are two distinct processes. The evidence indicates that the organisms responsible for the initiation of caries are subsequently replaced by others as the environmental conditions occasioned by the advancing carious lesion are altered. Nevertheless many organisms do have both acidogenic and proteolyic properties.

ADVANCED DENTINAL CHANES: The decalcification of the walls of the individual tubules leads to their confluence, although the general structure of the organic matrix is maintained for some time. o A thickening and swelling of the sheath of Neumann may sometimes be noted at irregular intervals along the course of the involved dentinal tubules, in addition to the increase in diameter of the dentinal tubules due to packing of the tubules by microorganisms. o Tiny “liquefaction foci” described by Miller, are formed by coalescence and breakdown of a few dentinal tubules. This “focus” is an ovoid area of destruction, parallel to the course of the tubules and filled with necrotic debris, which tends to increase in size by expansion. o This produces compression and distortion of adjacent dentinal tubules so that their course is bent around the “liquefaction foci”. o In areas of globular dentin, decalcification and confluence of tubules occurs rapidly. The presence of considerable amounts of globular dentin accounts for the rapid spread of caries in so called malacotic of soft teeth.

o The destruction of dentin through a process of decalcification followed by proteolysis occurs at numerous focal areas, which eventually coalesce, to form a necrotic mass of dentin of a leathery consistency. Clefts are common in this softened dentin, although they are rare in chronic caries.

As carious lesion progresses, various zones of carious dentin may be distinguished which grossly tend to assume the shape of a triangle with the apex toward the pulp and the base toward the enamel. Beginning pulpally at the advancing edge of the lesion adjacent to the normal dentin, the following zones are seen: o Zone of fatty degeneration of Tomes fibers. o Zone of dentinal sclerosis characterized by deposition of calcium salts in dentinal tubules. o Zone of decalcification of dentin, a narrow zone, preceding bacterial invasion. o Zone of bacterial invasion of decalcified but intact dentin. o Zone of decomposed dentin.

SECONDARY DENTIN INVOLVEMENT: The carious involvement of secondary dentin does not differ remarkably from involvement of the primary dentin, except that it is usually somewhat slower because the dentinal tubules are fewer in number and more irregular in their course, thus delaying penetration of the invading microorganisms. Occasionally caries will spread laterally at the junction of the primary and secondary dentin and produces a separation of the two layers.

ROOT CARIES: Root caries has been defined by Hazen and his colleagues as “soft, progressive lesion that is found anywhere on the root surface that has lost connective tissue attachment and is exposed to the oral environment”. Enamel may be secondarily involved if it is undermined during the caries process. Dental plaque and microbial invasion are essential part of the cause and progression of this lesion.

Microorganisms appear to invade the cementum either along the Sharpey’s fibers or between the bundles of fibers. Since cementum is formed in









microorganisms tend to spread laterally between the various layers. Irregular mineralization on this cemental surface may often be seen at the same time, probably representing beginning calculus formation. After decalcification of the cementum, destruction of the remaining matrix occurs similar to the process in dentin, with ultimate softening and destruction of this tissue.

As the caries process continues, there is invasion of microorganisms into the underlying dentinal tubules, subsequent matrix destruction and finally pulpal involvement.


1. Clifford M Sturdevant et al “ The Art And Science Of Operative Dentistry”, Mosby 3rd edition 1997: 91-99. 2. Shafer, Hine, Levy, “A Textbook Of Oral Pathology”, Saunders, 4 th edition:437-447.

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