Primary Preventive Dentistry 6th Ed. (2004)
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Objectives ^ 1. Name the four general types of carious lesions that are found on the different surfaces of the teeth. 2. Describe the histologic characteristics of enamel and dentin that facilitate fluid flow throughout a tooth. 3. Describe the four zones of an incipient caries lesion. 4. Describe the conduits (pores) that directly conduct acid from the bacterial plaque to the body of the lesion. 5. Name the two bacteria most often implicated in the caries process, and indicate when each is present in the greatest numbers during the caries process. 6. Describe the series of events in a cariogenic plaque and subsurface lesion from the time of bacterial exposure to sugar until the pH returns to a resting state. 7. Discuss the characteristics of root caries and explain the differences and similarities to coronal caries. 8. List measures to prevent and to remineralize root and coronal caries. 9. Explain why so much time is taken by the profession in treating secondary caries. 10. Explain the relationship between pH and calcium and phosphorus saturation in caries development. 11. Discuss the protective relationship of calcium fluoride to hydroxyapatite and fluorhydroxyapatite during an acidogenic attack. Introduction Understanding Caries: Concepts Every day there is a normal, but minute, demineralization of the hard tooth structures caused by bacterial acid production, as well as consuming acid foods such as fruit juices, vinegar, and soft drinkseven from the abrasion of toothbrushing.1,2 So long as the demineralization is limited, the body's remineralization capabilities can replace the lost minerals from elements such as calcium, phosphate, fluoride and other elements that are found in the saliva. The physiologic demineralization does not become pathologic until the demineralization outstrips the remineralization over an indefinite period of time that leads to the onset of cavitation. A favorable balance between de- and remineralization is necessary to maintain the homeostasis needed for a lifetime of intact tooth retention. When a cavity occurs, it can be defined as a localized, post-eruptive pathological process involving bacterial acid demineralization of hard tooth tissue, which if continued without a compensatory remineralization, results in the formation of a cavity. The history of dental caries is as long as history itself. Probably one of the oldest and most whimsical theories of caries and toothache was that of the tooth worm which allegedly lived in the center of the tooth.3 Many early barber-surgeons reported sighting the "worm," but none seemed to be able to capture the creature, nor could explain how it got into the tooth in the first place. In the late 1700s the worm theory was largely replaced by the vital theory, a theory that postulated that inflammation arising from within a defective tooth eventually caused a surface lesion. Robertson in 1835-England, and probably one of the first preventive-oriented dentists believed and published, that food impaction and fermentation might be the cause.4 By the end of the 19th century, others in Europe began to indict bacteria as the culprit. In 1890 W. D. Miller, an American dentist teaching in Germany, published his chemicoparasitic theory of caries which (with many modifications) is still accepted in concept today.5 As a result of his experimentation, Miller believed that the extraction of the "lime salts" from the teeth was a result of bacterial acidogenesis and was the first step in dental decay. Miller's work however, failed to identify dental plaque as the source of the bacteria and the bacterial acids. The chemicoparasitic theory became more cogent when taken in conjunction with the finding of other contemporary dental researchers, including G. V. Black (the "Grand Old Man of Dentistry") who described the "gelatinous microbic plaque" as the source of the acids.6 Caries lesions occur in four general areas of the tooth: (1) pit and fissure caries, which are found mainly on the occlusal surfaces of posterior teeth as well as in lingual pits of the maxillary incisors and buccal surfaces of lower molars; (2) smooth-surface caries, that arise on intact smooth enamel surfaces other than at the location of the pits and fissures; (3) root-surface caries, which might involve any surface of the root; and (4) secondary or recurrent caries that occur on the tooth surface adjacent to an existing restoration. Smooth-surface caries can be further divided into caries affecting the buccal and lingual tooth surfaces, and approximal caries, affecting the contact area of adjoining tooth surfaces (i.e., mesial or distal surfaces). Dental caries is a multifactorial disease process, often represented by the three interlocking circles and an arrow depicting the passage of time (Chapter 1, Figure 1-4). For caries to develop, three conditions must occur simultaneously: (1) there must be a susceptible tooth and host; (2) cariogenic microorganisms must be present in quantity; and (3) there must be excessive consumption of refined carbohydrates. When exposed to a suitable substrate (usually sugar or sugar-laden snacks or desserts), cariogenic bacteria present in the plaque produce acid. If this occurs over a sufficiently long period of time, a caries lesion develops. Each of these main factors includes a number of secondary factors and can be introduced to either protect or further damage the tooth. For example, fluoride incorporated into dental enamel increases tooth resistance (see Chapter 8 and 9). Conversely, a reduction in the saliva flow (xerostomia) greatly increases the caries risk.
^ Before discussing the carious process further, it is necessary to briefly review the embryology and histology of enamel. Without this review it is very difficult to understand how de- and remineralization can occur in such a highly mineralized tissue as enamel. The enamel is made up of billions of crystals that in turn make up millions of individual rods. The enamel rods, when viewed in cross section with an electron microscope, appear not as rods, but as keyhole-shaped structures, approximately 6 to 8 microns in diameter, with the enlarged portion of the keyhole called the head and the narrow portion the tail. With this configuration, each head fits between two tails. The tail is always positioned toward the apex. In the head of the rod the long axes of the crystals, called the C axis, are parallel to the enamel rod. However, as the periphery of the rod is approached, the crystals assume an angle to the more central crystals; in fact, in the tail this angle may be around 30. (Figure 3-1). Each rod that extends from the dentoenamel junction (DEJ) to the tooth surface is completed start-to-finish by one ameloblast. The final enamel is approximately 95% inorganic, and 5% organic material and water. This 5% porosity forms a network of channels for fluid diffusion of ions and small molecules that are dispersed throughout the entire enamel cap.a The space available for this diffusion is found between the rods and even between the crystals. To further extend this intra enamel network throughout the enamel, there are morphologic structures in the enamel with a high protein content, such as the striae of Retzius, enamel lamellae, enamel tufts, pores, and enamel spindles. These several diffusion channels probably serve two very important purposes in preserving the teeth: (1) their teleological purpose was possibly to permit physiological remineralization throughout life, and (2) the voids and protein content in the enamel probably cushion intense biting pressures to help prevent fractures. Unfortunately, these same channels of diffusion also serve another purpose, viz., the conducting of plaque acids into the enamel interior to cause demineralization. This brief summary also points out the exquisite genetic control exercised over the rapidly changing and complex tissue building that marks the development of enamel. The following review begins at the time when odontoblasts and ameloblasts are lined up opposite each other along the future dentino-enamel junction. The initial event of the secretory stage occurs with an odontoblastic deposition of the first few microns of predentin. This is followed by the initiation of the secretory phase of the ameloblast. The first secreted enamel proteins do not accumulate as a layer, but instead, penetrates into the developing predentin and subjacent odontoblasts.7 The microenvironment of the ameloblast at this time, is mainly one of proteins and water.8 As the ameloblast retreats towards the future surface of the tooth, it uses these proteins to form an acellular and avascular matrix template upon which the future hydroxyapatite crystals are to be positioned.9,10 This requires a very rigid genetic control over the sequence of events that will extend through matrix formation, crystal nucleation, and crystal growth; as well as rod formation (elongation, widening, and maturation). The matrix is highly heterogenous because of the involvement of protein contributions from many different genesamelogens, enamelin, ameloblastin, tuftelin, and various enzymes.b Possible functions of these proteins are nucleation (tuftelin), mineral ion binding, (amelogenin, enamelin), and crystal growth (amelogenin, enameling, ameloblastin).11 If there is a failure of initiation or integration of action of any of these proteins, a dysplastic tissue can result, for example, amelogenesis imperfecta that is caused by a defect in the amelogen gene.12 It should be emphasized that the ameloblast does not complete the matrix template from the dentino-enamel junction to the exterior of the tooth before enamel formation begins. Instead, while the ameloblast is matrix-building on the lateral sides, at the same time the Tomes process at the basal end of the cell is modulating the enamel-building from the time of initial secretion to the pre-eruption maturation stages.13 This is a continuous process as the ameloblast moves outward. In an early supersaturated environment of high calcium and phosphorus initiated by the ameloblast, octacalcium phosphate is laid down as a precursor to the hydroxyapatite crystal.14 The early hydroxyapatite crystals are small and of poor crystalinity. As the ameloblast moves outward, the rod increases in length and thickness. Towards the end of the secretory stage, the matrix is almost completely degraded. Accompanying this event, there is a massive crystal growth.15 The maturing enamel growth is now approaching the pre-eruptive state. The hydroxyapatite crystals are unusually large, uniform in size, and regularity positioned.11 The enamel that was originally a soft product is now the hardest and most durable produced in the human body. There are still a few more points about the life span of the amazing ameloblast. As the tooth approaches eruption, the columnar configuration of the ameloblasts flattens to form the reduced enamel epithelium that covers (and protects) the yet immature enamel. After eruption, the reduced enamel epithelium disappears and is succeeded by the acquired (also called salivary) pellicle that, in turn, is covered by the dental plaque (Chapter 2). Even at this time, the crystals of the rod are not yet fully mineralized. For the first year after eruption into the mouth, the rods undergo a post-eruptive maturation, with the additional tooth minerals being derived from the saliva. This temporary hypomineralization of the enamel with its greater porosity, in part explains why newly erupted teeth are more susceptible to caries than teeth that have been present in the mouth for some time. aIf an intact tooth was stripped of its pulp chamber, dentin and cementum, the only remaining structure is the enamel cap. bAt this point in time, it is not necessary to memorize the names and functions of genes. Just remember that the tooth morphology depends on genetic guidance.
^ The development of a carious lesion occurs in three distinct stages. The earliest stage is the incipient lesion, which is accompanied by histologic changes of the enamel; the second stage includes the progress of the demineralization front toward the dentino-enamel junction and/or into the dentin; while the final phase of caries development is the development of the overt, or frank, lesion, which is characterized by actual cavitation. If the time between the onset of the incipient lesion in one or more teeth, and the development of cavitation is rapid and extensive, the condition is referred to as rampant dental caries. Usually rampant caries occurs following either the excessive and frequent intake of sucrose, or the presence of a severe xerostomia (i.e., dry mouth) or both. From a preventive dentistry standpoint, the early identification of the incipient lesion is extremely important, because it is during this stage that the carious process can be arrested or reversed. The overt lesion can only be treated by operative intervention. Clinically, it is often difficult to recognize and diagnose the early lesion, and for this reason it is important to be familiar with its features from etiologic and histologic standpoints.17 The incipient lesion is macroscopically evidenced on the tooth surface by the appearance of an area of opacitythe white spot lesion. At this earliest clinically visible stage, the subsurface demineralization at the microscopic level is well established with a number of recognizable zones. Probably a most important fact is that the surface of the enamel appears relatively intact (although the electron microscope shows a surface that is more porous than sound enamel). On the buccal and lingual surface of a tooth, the white spot may be localized, or it can extend along the entire gingival area of the tooth, or multiple teeth where food tends to lodge. Interproximally, the incipient lesion is usually first detected on a bite wing x-ray. It usually starts as a small lucency immediately gingival to the contact point and then gradually expands to a small kidney shape, with the indentation of the kidney contour directed coronally.18 In fissure caries, the initial lesion comparable to the "white spot," usually occurs bilaterally on the two surfaces at the orifice of the fissure and eventually coalesces at the base19 (Figure 3-2). Occasionally lesion formation begins along the wall of the fissure or at the base, either unilaterally or bilaterally.20 During the early stages the incipient lesion is not a surface lesion in which loss of outer enamel can be detected. Instead, the mature surface layer of 10 to 100 microns remains intact. If an explorer is used, the surface enamel feels hard and provides no indication of demineralization. However, microscopic pores extend through the mature surface layer to the point where subsurface demineralization occurs; the main body of the lesion is located and enlarges from this point. The incipient lesion has been extensively studied and best described by Silverstone.18 Many of the observations of the incipient lesion have been based on the use of a polarizing microscope, which permits precise measurements of the amount of spacecalled pore spacethat exists in normal enamel and to a greater extent in enamel defects. Thus as demineralization progresses, more pore space occurs; conversely, as remineralization occurs, less pore space is present. In the incipient lesion as described by Silverstone, four zones are usually present. Starting from the tooth surface, the four zones are the (1) surface zone, (2) body of the lesion, (3) dark zone, and (4) the translucent zone. (Figure 3-3) Pore Spaces of the Different Zones The translucent zone, the deepest zone is seen in approximately 50% of the carious lesions examined.18 In this zone, which is the advancing front of the lesion, slight demineralization occurs, with a 1% pore space, compared with 0.1% for intact enamel. In contrast, the dark zone occurs in approximately 95% of carious lesions and has a pore volume of 2 to 4%. When teeth showing no dark zone are placed in a remineralizing solution, the dark zone becomes visible in its expected position between the translucent zone and the body of the lesion.21 On the basis of this phenomenon, it is suggested that this dark zone is the site where remineralization can occur and that a wider dark zone indicates a greater amount, or a longer period, of remineralization. Peripheral to the dark zone lies the main body of the lesion. In this zone, pore volume ranges from approximately 5% on the fringes of the lesion to about 25% in the center.18 Despite this considerable amount of demineralization, the remaining crystals still maintain their basic orientation on the protein matrix. Finally, the surface zone has a near-normal pore space of approximately 1%. It is the surface zone and the dark zone that are the remineralization zones of the incipient lesion. Direct Connection of the Bacterial Plaque to the Body of the Lesion Demineralization of the surface enamel produces a ragged profile when seen with the electron microscope (Figure 3-4). Small pores, or microchannels, have been observed by electron microscopy in the surface zone of incipient lesions. The initial attack may be on the rod ends, between the rods, or both.22 There is a widening of the areas between adjacent rods.23 When conditions are optimum, this ragged interface between surface and subsurface can be remineralized (repaired), either by the body defenses (calcium and phosphate and other ions from the saliva), or by man-made strategies (fluoride therapy and sugar discipline). ^ . For orientation, in the upper-left corner of the illustration, there is the bacterial plaque (B); immediately below is the salivary pellicle (SP), followed by the enamel (EN). The lighter area labeled CM leads directly from the bacterial plaque to the area that is, or will be, the expanding body of the lesion. In turn, the body of the lesion opens into many interrod spaces that continue uninterrupted to the dentino-enamel junction (DEJ). It is along these inter-rod spaces that the bacterial plaque fluids diffuse (Figures 3-5 A and B). En route to the DEJ, the stria of Retzius allows lateral acid access out of the inter-rod space into the center of the intact or damaged rods and crystals. Once at the DEJ, any fluid flow whether causing de- or remineralization, can trichotomizec either along the hypomineralized DEJ, or into the dentinal tubules to the pulp chamber (Figure 3-6). The speed of progression of the caries front depends on such factors as ion concentration, pH, saliva flow, and buffering actionsall of which are continually changing. In summarizing, there is a trail of interconnecting channels for diffusion of fluids transiting from the bacterial plaque to the pulp chamber. Any chemical changes in the plaque can be soon reflected throughout the enamel and dentin as part of the incipient lesion. These ultrastructural enamel defectsthe poresallow the exit of plaque acids direct to the subsurface region. The initial acid attack preferentially dissolves the magnesium and carbonate ions and is later followed by a removal of the less soluble calcium, phosphate, and other ions that are part of the crystal. Eventually the undermined surface zone collapses. Concurrent with this change, the more soluble proteins are lost from the subsurface matrix. Once cavitation occurs, the zones of the incipient lesion become less clearly defined because of mineral loss and the presence of bacteria, bacterial end products, plaque, and residual substrate, which may support further lesion development. The lesion is no longer an incipient lesion; it is now an overt caries lesion requiring operative intervention. ctrichotomize = go in one of three directionsalong the DEJ in either direction, or into the dentinal tubules.
Question 1 Which of the following statements, if any, are correct? A. All the following structures are involved in the passage of fluids in the enamel: interrod space, intercrystalline matrix, pores, and striae of Retzius. B. The head of the enamel rod is always oriented toward the incisal or occlusal surfaces in both the maxillary and mandibular teeth. C. A rampant caries attack implies a previous incipient lesion for each overt lesion that develops. D. The incipient lesion usually starts incisal to the contact point in interproximal caries and at the base of the fissure in occlusal caries. E. The dark and the translucent zones are the centers of remineralization when "biologic repair" of the tooth is occurring. ^ Following Miller's works in the 1890s, it was not until 1954 that fundamental experimental evidence proved that bacteria were the agents of acid production. Orland and colleagues24 demonstrated that gnotobioticd rats did not develop caries when fed a cariogenic diet; they did develop caries when acidogenic bacteria, plus a cariogenic diet were introduced into the previous germ-free environment. The transmissible nature of caries in animals was later demonstrated by the experiments of Keyes25 who showed that previously gnotobiotic, caries-inactive hamsters developed caries after contact with caries-active animals. dGnotobiotic = germ-free environments Mutans Streptococci and Caries For caries to develop, acidogenic (acid-producing) bacteria must be present, and a means must exist to prevent the acid from being washed away from the point where caries is to develop. Dental plaque fulfills both of these functions. It helps protect the bacterial colonies in a cocoon of (a gel-like) glucan from being flushed, neutralized, or effected by antimicrobials in the saliva or introduced by humans. Of the 300-or-more species of microorganisms inhabiting the plaque, the great majority are not directly involved in the caries process. Two bacterial genera are of special interest in cariogenesis: (1) the mutans streptococcie and (2) the lactobacillti.26,27 The mutans streptococci (MS) are a group of bacterial species previously considered to be serotypes of the single species, Streptococcus mutans.26 These bacteria are characterized by their ability to produce extracellular glucans from sucrose and by their acid production in animal and human studies. Streptococcus mutans received its name in 1924 when J. K. Clarke in England isolated organisms from human carious lesions. He noted that they were more oval than round and assumed them to be a mutant form of a streptococcus.28 Mutans streptococci are now considered to be the major pathogenic bacterial species involved in the caries process. Innumerable surveys have indicated an association between the number of ^ and dental caries.29-31 The counts have been repeated worldwide for over more than five decades for all agesin the United States,32 Sweden,33 Latvia,34 Finland,35 and China36with high MS bacterial counts being overwhelmingly correlated to the number of teeth with caries or restorations. Mutans streptococci are usually found in relatively large numbers in the plaque occurring immediately over developing smooth-surface lesions. In one longitudinal study, specific sites were periodically sampled for the presence of MS, and the teeth later examined for caries. Teeth destined to become carious exhibited a significant increase in the proportions of MS from 6 to 24 months before the eventual diagnosis of caries.37 Similarly, dental plaques isolated from sites overlying white spot lesions were characterized by a significantly higher proportion of MS than plaques sampled from sound enamel sites.38 Increased numbers of MS in the saliva also parallel the development of the smooth-surface lesion. In another study, MS counts from the saliva of 200 children indicated that 93% with detectable caries were positive for MS, whereas uninfected children were almost always caries-free.39 Certain physiological characteristics of the MS favor their reputation as a prime agent in caries. These traits include the ability to adhere to tooth surfaces, production of abundant insoluble extracellular polysaccharides (glucan) from sucrose, rapid production of lactic acid from a number of sugar substrates, acid tolerance, and the production of intracellular polysaccharide (energy) stores. These features help the MS survive in an unfriendly environment due to periods of very low availability of substrate (i.e., between meals and snacks). As a general rule, the cariogenic bacteria metabolize sugars to produce the energy required for their growth and reproduction. The by-products of this metabolism are acids, which are released into the plaque fluid. The damage caused by MS is mainly caused by lactic acid, although other acids, such as butyric and propionic, are present within the plaque.40 eOriginally, it was believed that Streptococci mutans was the only species of streptococci that caused caries; however, when it was found that other streptococci were also involved, they were all grouped under the umbrella designation of mutans streptococci. In the older references, the original terminology will be maintained. Lactobacilli and Caries Lactobacilli (LB) are cariogenic, acidogenic, and aciduric. Indeed, from the early 1920s until the 1950s, LB was considered the essential bacteria causing caries. It was not until 1954 when the gnotobioticf studies of Orland demonstrated that if rodents living in a germ-free environment were infected with a lactic acid-producing enterococci (but no LB), they still developed caries.24 This was the first time that it was known that LB were not requisite for caries development. Often, the number of lactobacilli isolated from either saliva or plaque was too low in number to be considered capable of producing the range of pH values required for caries initiation.41 However, once a caries lesion develops, the stability of the immediate plaque population changes rapidly. The low pH environment of LB often eliminates, or at least suppresses the continuity of colonization of MS.42 This, despite the fact that some organisms such as MS probably have genetic defensive mechanisms to minimize the effects of a low pH.43 This phenomenon of a lowering pH resulting in MS being displaced by LB, is seen following irradiation for head and neck cancer, when extensive, multiple, caries lesions develop rapidly because of the destruction of the salivary glands.44 During the initial phases of the developing carious lesions, large numbers of MS are involved, only to decrease later in number as the LB population increases. This is believed to be caused by LB creating a sufficiently low pH to establish a monopoly of the environment. fGnotobiotic = In this use, the animals were raised in a sterile environment. |
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