Dental caries is a term for the process commonly referred to as decay of the teeth. Thus, a decayed tooth is properly termed a carious tooth. Dental caries or dental decay is a specific disease that causes dissolution and disintegration of the hard structures of the tooth, that is, enamel, cementum and dentin. (The word caries or decay refers to the disease; the word cavity refers to the lesion or hole in the tooth.) Dental caries is the most widespread disease affecting the human race. The incidence of caries is greatest during childhood and young adulthood. It attacks deciduous teeth the same as it attacks permanent teeth. Dental caries is progressively destructive. It usually begins in a minute area on the enamel or cementum and, if untreated, progresses to the dentin. The next step is penetration to involve the dental pulp. Infection and death of the pulp may follow, with possible extension of the infection into the tissues surrounding the apical portion of the root and the formation of an abscess. The control of dental caries is a very important problem that is receiving much attention in the fields of research and prevention.
In general, dental caries occurs because of improper or poor oral hygiene. The destruction of dental tissue by caries, however, is governed somewhat by the susceptibility of the teeth. Little is known about susceptibility or resistance to caries, but the degree of susceptibility may be influenced by certain factors, including diet and oral hygiene and some systemic diseases. Study of the direct cause of dental caries is very complex. Only two theories of its cause are considered here. According to the acidogenic (producing acid) concept, bacteria and their products accumulate in mucinous plaques, which are often invisible and adhere tightly to the teeth. The bacteria in the plaques metabolize (feed upon) carbohydrates in the diet and convert them to organic acids. These acids dissolve the enamel and allow deeper bacterial penetration into the tooth. The lesion is progressive. According to the proteolytic (effecting the digestion of proteins) concept, proteolytic bacteria attack the organic material in the enamel rods (which is mostly protein) along certain tracts called lamellae. Dissolution of the organic material in these lamella tracts eventually allows bacterial penetration to the underlying dentin. According to both concepts, dental caries is the result of microbial activity on the teeth. The process of dental caries may be a combination of both concepts, with the acidogenic concept accounting for dissolution of mineral content and the proteolytic concept accounting for destruction of organic content of the tooth.
1-17. CARIES IN ENAMEL (Figure 1-1)
|The organisms that produce acid are contained in mucinous plaques that adhere to the surface of the enamel. Common sites of plaque adherence are pits, fissures, interproximal areas, and along the free margin of the gingivae, particularly on the facial surface of the tooth. The enamel rods of a tooth are cemented together by a substance that dissolves more readily than the rods themselves, and thus, according to the acidogenic concept, the first effect in enamel caries is probably the dissolution of this cementing substance. The first visible evidence of caries is a slightly whitened area on the surface of the tooth (decalcification). This area is very easily overlooked, particularly when the teeth are wet. Drying of the tooth surface makes these areas far more visible. From the small areas on the surface of the tooth, caries continues its progressive destruction. As the acid dissolves the cementing substances, the enamel rods are left without support and break away. Since enamel contains a minimal amount of organic material, the primary acid effect on the enamel cementing substance results in loss of enamel structural support. Without support, the enamel rods break away, allowing progressive formation of a cavity within the enamel, until ultimately dentin is also involved. In summary, caries first penetrates the enamel and dentinoenamel junction. Then it spreads laterally and deeper within the dentin toward the pulp. Thus, what may appear to the patient as a small surface cavity may in fact be a very extensive involvement of the tooth structure. |
NOTE: Dental decay generally starts in areas that are not easily or normally cleaned.
Figure B shows primary areas of enamel decay, between the teeth and on the chewing surface. Spread of decay in dentin is shown in Figure C; note lateral advancement as well as progression of decay toward the pulp. With pulpal involvement, degenerative changes result in pathology within the pulp chamber (Figure D), resulting in eventual periapical granuloma or cyst development (Figure E).
Figure 1-1. Stages in the progress of dental caries.
1-18. CARIES IN DENTIN
From the small area on the surface of the tooth, caries continues its progressive destruction. As noted in the preceding paragraph, decay spreads easily within dentin after penetrating the enamel. The disease spreads laterally along the dentinoenamel junction and directly toward the pulp.
a. The Destructive Process. The destructive process of caries differs in dentin and enamel. In caries of enamel, the organisms cannot enter the substance of the enamel until the acid produced by the organisms has destroyed the enamel substance. This process is called demineralization. The reverse is true of the dentin, which is made of many hollow tubules. These tubules offer a natural pathway for penetration by bacteria and because the dentin contains a large proportion of organic materials, progression is faster in dentin than in enamel. When the dentin has been reached, acid-forming and proteolytic organisms can enter the dentinal tubules and produce acid or break down the organic matrix within the tissue itself. Since dentinal tubules tend to branch and communicate with each other at the dentinoenamel junction, the organisms penetrate the dentin laterally in all directions along this junction. Accompanying this lateral penetration is a penetration along the main tubules in the direction of the pulp. This lateral and direct involvement tends to form a cone-shaped area of decay. The apex of the cone is pointed toward the pulp of the tooth and the base at the dentinoenamel junction.
b. Limits to Dentin Destruction. Although dentin destruction in caries is normally faster than enamel destruction, the rapidity of dentin destruction both in depth and breadth will be governed by its structure. Because of the extensive organic matrix of the dentin, enough substance is left after the dissolution of the inorganic salts to retain its physical form until further destruction has taken place by other processes.
c. The Infected Layer and the Affected Layer. Caries in the dentin is described as having an infected layer and an affected layer. In the infected dentin, many microorganisms are present and most of the dentinal tubules have been destroyed through demineralization and decomposition (destructive process of proteins). The infected layer is soft on the surface but gets tough, leathery, or rubbery underneath. Below the infected layer is the affected layer of dentin. Few microorganisms are found in this area and the dentinal tubules are intact. Normal dentin is found under the affected layer. The difference in these layers plays an important role in the treatment of caries in the dentin.
1-19. ARRESTED CARIES
Arrested caries is the stage where the progress of the decay process has stopped. The softened dentin has been lost or worn away so that the discolored (either yellow, brown, or black), sound, hard dentin remains. The remaining dentin has a polished look.
1-20. PULPAL REACTION TO DENTAL CARIES
a. The Reason for Pain. When dental decay reaches a depth in the dentin that is near the pulp tissue inside of the tooth, the pulp tissue can become inflamed. The inflammation causes the blood vessels to swell and release fluid into the extracellular spaces. This swelling is limited by the hard walls of the pulp chamber and root canals and, as a result, severe pain may result because of the constriction. Pus can accumulate within the diseased pulp tissue that further accelerates the pathologic process.
b. The Process of Decay. The reaction of the pulp to dental caries varies. This reaction generally varies in accordance with the rate of advance of the carious process. Even before there is significant dentin involvement, the pulp tissue can become irritated and the irritation causes minor inflammation. This, in turn, stimulates the odontoblasts to produce secondary dentin in an effort to protect the pulp. If the rate of advance of caries is slow and the resistance of the patient is high, this deposition of secondary dentin may prevent the carious process from reaching the pulp tissues for a considerable time. If it were not for this protective reaction of the odontoblasts, a far higher percentage of carious lesions would reach the pulp chamber before detection, causing more injury to the pulp. If not treated or arrested, the carious process can eventually reach and involve the pulp tissue. As it nears the pulp, the irritation becomes more severe and direct bacterial invasion occurs. If the resulting inflammation is severe or of prolonged duration, the pulp tissue may die (necrose) if left untreated.