Zone of Dentine Caries: Development of Dentine Caries
Dentine differs from enamel in that it is a living tissue and as such can respond to caries attack. It also has a relatively high organic content, approximately 20 per cent by weight, which consists predominantly of collagen. In dentine caries it is, therefore, 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 (or tertiary) dentine and dentinal sclerosis. However, in progressive lesions the defense reaction is progressively overtaken by the carious process as it advances towards the pulp.
Caries of the dentine develops from enamel caries: when the lesion reaches the amelodentinal 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 amelodentinal junction. Larger lesions may show a broadening of the apex of the cone as it approaches the circumpulpal dentine. In caries of dentine, demineralization by acid is always in advance of the bacterial front, the subsequent bacterial invasion being followed by breakdown of the collagenous matrix. Because of the sequential nature of the changes, studies of ground and decalcified sections show a zoned lesion in which four zones are characteristically present (Fig.).
Zone of sclerosis
The sclerotic or translucent zone is located beneath and at the sides of the carious lesion. It is almost invariably present, being broader beneath the lesion than at the sides, and is regarded as a vital reaction of odontoblasts to irritation. Two patterns of mineralization have been described. The first is the result of acceleration of the normal physiological process of centripetal deposition of peritubular dentine which eventually occludes the tubules. In the second, mineral first appears within the cytoplasmic process of the odontoblasts and the tubule is obliterated by calcification of the odontoblast process itself. Sclerosed dentine therefore has a higher mineral content.
Dead tracts may be seen running through the zone of sclerosis. They are the result of death of odontoblasts at an earlier stage in the carious process. The empty dentinal tubules contain air and the remains of the dead odontoblast process and such tubules can obviously not undergo sclerosis. However, they provide ready access of bacteria and their products to the pulp. To prevent this the pulpal end of a dead tract is occluded by a thin layer of hyaline calcified material, sometimes called eburnoid, which is derived from pulpal cells. Beyond this, further, often very irregular, reactionary dentine may form following differentiation of odontoblasts or odontoblast-like cells from the pulp.
Zone of demineralization
In the demineralized zone the intertubular matrix is mainly affected by a wave of acid produced by bacteria in the zone of bacterial invasion, which diffuses ahead of the bacterial front. The softened dentine in the base of a cavity is therefore sterile but, in clinical practice, it cannot be distinguished reliably from softened infected dentine. It may be stained yellowish-brown as a result of the diffusion of other bacterial products interacting with proteins in dentine.
Zone of bacterial invasion
In this zone the bacteria extend down and multiply within the dentinal tubules, some of which may become occluded by bacteria (Fig). There are always, however, many empty tubules lying among tubules containing bacteria. The bacterial invasion probably occurs in two waves: the first wave consisting of acidogenic organisms, mainly lactobacilli, produce acid which diffuses ahead into the demineralized zone. A second wave of mixed acidogenic and proteolytic organisms then attack the demineralized matrix. The walls of the tubules are softened by the proteolytic activity and some may then be distended by the increasing mass of multiplying bacteria. The peritubular dentine is first compressed, followed by the intertubular dentine, resulting in elliptical areas of proteolysis-liquefaction foci. Liquefaction foci run parallel to the direction of the tubules and may be multiple, giving the tubule a beaded appearance (Fig). These changes are enhanced in the zone of destruction. The bacteria may show varying degrees of degeneration.
Zone of destruction
In the zone of destruction the liquefaction foci enlarge and increase in number. Cracks or clefts containing bacteria and necrotic tissue also appear at right angles to the course of the dentinal tubules forming transverse clefts (Fig.). The mechanism of formation of transverse clefts is uncertain. They may follow the course of incremental lines, or result from the coalescence of liquefaction foci on adjacent tubules, or arise by extension of proteolytic activity along interconnecting lateral branches of odontoblast tubules. Bacteria are no longer confined to the tubules and invade both the peritubular and intertubular dentine. Little of the normal dentine architecture now remains and cavitation commences from the amelodentinal junction. In acute, rapidly progressing caries the necrotic dentine is very soft and yellowish-white; in chronic caries it has a brownish-black colour and is of leathery consistency.