Primary Preventive Dentistry 6th Ed. (2004)
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Adherence Continuous adherence to the solid tooth surface by S. mutans is necessary both before and after initial colonization. The first bacteria must establish a foothold on the tooth surface (acquired pellicle) and then maintain their positions while other bacteria continue to colonize in other protected areas offered by the interproximal spaces, along the gingiva, or in the pits and fissures. Otherwise they would be swept away by the saliva. Mutans streptococci are able to attach to the tooth surface by either of two mechanisms:26,27,45 (1) attachment to the acquired pellicle through extracellular proteins (adhesins) located on the fimbriae (fuzzy coat) of these organisms; and (2) sucrose-dependent mechanisms, in which bacteria require the presence of sucrose to produce sticky extracellular polysaccharides (glucans), that allows attachment and accumulation of additional waves of bacterial colonization.46 Sucrose is a disaccharide, consisting of one glucose and one fructose unit (moieties). One of the key enzymes in the conversion of the glucose moiety of sucrose to glucan is glucosyltransferase. At times the enzyme may be altered, resulting in the production of a soluble glucan that does not support adherence. These mutant strains that form soluble glucan are usually noncariogenic.47 The effect of sucrose restriction on glucan production is seen in several clinical situations. Children who consume little or no sucrose because of sucrase or fructase enzyme deficiencies have a less cariogenic plaque. Similarly, patients receiving long-term nourishment via stomach tube have less plaque and fewer MS.48 Individuals restricting their sucrose intake have a decreased proportion of MS in their plaque, but the MS increases when sucrose is reintroduced into the diet.49 Dietary restriction of sugar has also been shown to reduce the acidogenicity of dental plaque.50,51 ^ Several studies support the possibility that the initial colonizers can help to determine the eventual pathogenicity of the plaque.37 Once a species of bacteria has established its ecologic niche,g other bacteria introduced at a later date appear to have a more difficult task in colonizing. Once established, a niche can be long-lasting. For instance, children with the highest number of MS for deciduous teeth usually experience a higher attack rate for the later permanent teeth.52 Mutans streptcoccoi require a solid surfacethe tooth surfacefor successful colonization. During the first year of life before eruption of the primary teeth, very few MS are found in the mouth.53 When teething begins at approximately 8 months, MS often rapidly colonizes the plaque of newly erupting teeth.54 It has been shown that an important source of infection of infants by MS is from the caregivers (usually the mother) by the mouth-to-mouth transmission, such as via kissing, or by sharing a spoon during feeding.55 Mothers with the highest MS counts often have infants with similarly high caries lesion counts.56 Since early infection by MS is associated with high decay rates,57 it has been strongly suggested that an effective means of preventing caries in young children would be to reduce the number of MS in the parents' and siblings' mouths before a child's birth. Because no entrenched competition from other organisms occurs on eruption, the first bacterial colonizers probably have little difficulty in establishing their ecologic niches on the acquired pellicle and in the saliva. Once the teeth erupt, many of these oral reservoirs of bacteria participate in the formation of the plaque. Each firmly established niche can act as a "seeding" area for other areas of the mouth. Mutans streptcoocci decrease in number as teeth are lost throughout life and practically disappear following full-mouth extraction.58 After dentures are inserted, S. mutans reappear, only to disappear again when the dentures are removed for an extended period. gAn area in the plaque where specific species of bacteria are relatively safe from host protective function of saliva and from other antagonistic bacteria. Question 2 Which of the following statements, if any, are correct? A. Streptococcus mutans can be expected in increased numbers at the site of an incipient lesion. B. Lactobacilli are usually found even earlier than mutans streptococci at the incipient lesion site. C. Soluble glucans foster better bacterial adherence than insoluble glucans. D. Caregivers can be a child's worst dental friend. E. The mutans streptococci require a solid surface on which to colonize. Coronal Dentin Caries It is now desirable to revisit the embryology of the tooth,59 starting at the dentoenamel junction (DEJ) when the ameloblasts and the odontoblasts were lined up at the future DEJ. The objective of the ameloblasts was the future surface of the tooth, while the objective of the odontoblasts was the future border of the dental pulp. During the period of tooth formation, each day the odontoblast laid down a trailing odontoblastic process and a concentric increment layer of predentin. Each succeeding day the predentin became a calcified layer of dentin forming a tubule around the odontoblastic process, the lining of which is a hypercalcified layer called the peritubular dentin. These tubules extended from the DEJ to the dental pulp, in fact a few extended into the enamel as enamel spindles. Between the tubules there is intertubular dentin (also called mantle dentin).60 The tubules contain fluid that originates from the pulp chamber. There is intertubular communication and fluid transport, via secondary tubules and smaller sized canaliculi. All tubules act as channels for the convectionh flow of fluids that flow outward from the pulp.61 Dentinal fluid is constantly pumped into tubules by the forces of mastication, with a return of the fluid to the pulp upon release of the pressure.62 When there are infection products (caries) arriving in the tubules, more fluid is forced into the tubule.63,64 The pulp fluid also contains important calcium, phosphate and secretory immunoglobulin A.64,65 Upon the approach of enamel caries to the DEJ, many of the odontoblastic processes underlying the carious enamel interrod areas of the enamel will lose their vitality. These tubules become dead tracts and may begin to partially or wholly calcify The complete calcification results in a hard calcified group of tubules, called sclerotic dentin that acts as a protective barrier to the advancing caries. At the same time, the odontoblasts located on the periphery of the pulp are triggered to begin laying down increments of amorphous reparative dentin to further protect the pulp. In summary, the millions of diffusion and convenction channels in the enamel and dentin respectively, permit a movement of fluid from the tooth surface to the pulp.66,67 The intertubular secondary canals and the canaliculi provide permeability within the dentin, whilst the DEJ provides the same lateral fluid (acid) mobility that can undermine the enamel and aid in its collapse to form an overt caries lesion. It should be pointed out that even with a visible x-ray lucency that extends into the dentin, if the originating surface zone has not broken down into an overt cavity, the entire pre-caries lesion, even in deep dentin can on the basis of in vitro studies, theoretically (and slowly), be remineralized.68 hThe fluid entering the tooth from the surface is said to diffuse inward; fluids arising from the pulp are said to be convection fluids. Root Caries A general demographic shift is continually occurring in America, with each successive generation living longer. This provides a longer time for more gingival recession and more root caries. In addition, Seniors are consuming an increasing number of medicines that are known to reduce saliva and cause root caries.69 Katz and colleagues estimated that individuals going into their 30s have about 1 out of 100 surfaces with recession and root caries; when they leave their 50s, about 1 out of 5 exposed surfaces is involved. The roots of the mandibular molars and the mandibular incisors are at the greatest, and the least risk, respectively.70 The Third National Health and Nutrition Examination Survey found that the percentage of persons with at least one decayed or filled root surface increased from 20.8% in the 35- to 44-year age group, to 55.9% in those aged 75 years and older.71 A Canadian study concluded that "the increase in the prevalence of root decay with age may not be due to aging per se, but instead, may be the result of neglect of oral health during the years of growing older." Older adults with continual good oral health still had low rates of root decay.72 In a study of 5000 subjects in Finland, it was found that men had from 1.1 to 2.5 times more root caries than women. The greatest difference was in the group 60 to 69 years of age.73 A number of risk factors have been defined for root caries development, including age, gender, fluoride exposure, systemic illness, medications, oral hygiene, and diet.74 In terms of the microbiology of root caries, despite early indications of a strong association between Actinomyces species and progressive root lesions,75,76 more recent studies indicate that plaque and salivary concentrations of the mutans streptococci are correlated positively with the presence of root surface caries.77,78 Root caries differs from coronal caries in several aspects. A critical difference is that the tissues affectedenamel vs. cementumare fundamentally dissimilar. Enamel is much more highly mineralized than cementum or dentin. Because of the lower mineral content and higher organic content of the cementum-dentin complex, root caries may progress both by acid demineralization of the inorganic structure and by proteolysis of the organic component.79 These tissue variations determine the differences in the rate of lesion formation, histologic and visual appearance, as well as in the potential for and rate of remineralization.80 Clinically, the lesion is initially noncavitated. The carious material is soft and has a yellowish-brown coloration. The lesion can eventually assume any outline and may involve multiple root surfaces (Figure 3-8). When cavitation is evident, lesions tend to spread laterally, have a depth of approximately 0.5 to 1.0 mm, and are of a dark-brown appearance.81 The lesions appear immediately below the cemento-enamel junction, undermining but not involving the enamel (Figure 3-8). Root caries differ from coronal caries in that bacterial invasion of cementum and dentin occurs early. At times, the invasion features columns of organisms between spikes of relatively intact cementum. At other times, a complete loss of cementum exposes the dentin. Like enamel caries, root caries is amenable to remineralization and/or arrest.80 Arrested root caries lesions demonstrate three physical characteristics: (1) an outer barrier of hypermineralized surface dentin; (2) a sclerotic inner barrier between carious and sound dentin; and (3) mineralization occurring within the dentinal tubules.82 Clinically, such remineralized lesions may appear dark and hard; under tactile examination by the explorer, arrested lesions are easily distinguished from active lesions by their smooth, hard, and glassy feel compared to the leathery feel of active root caries. Prevention of Root Caries The best prevention for root caries in the elderly population is the prevention of periodontal disease in middle-age or earlier. However, since ex post factoi remedial treatment is not possible, earlier preventive dentistry care needs to be practiced. The strategies include: (1) daily mechanical and chemical plaque control (2) severe restriction of refined carbohydrates; and (3) routine professional dental attendance for preventive office identification of risks and counseling on self-care needs. For instance, for those at high risk, a prescription dentifrice with a high-fluoride content, Prevident, with 5,000 parts fluoride per million, has been found to significantly increase the electrical resistancej of a tooth surface.83 Frequent professional examinations based on an individual's risk should be routine. All extensive periodontal surgery for pocket elimination should place an individual in a higher root caries risk category for life.84,85 In later chapters, the use of the antimicrobial mouth rinse, chlorhexidine, will be introduced as a very effective mutans streptococci control agent. With professional guidance and patient cooperation, biological repair of a root caries lesion can be achieved in many casesa desirable option in view of the difficulty and lack of success in restoring root caries via operative procedures. iEx post facto = After the fact, meaning the it is not possible to correct some events of the past. jSeveral devices are on the market that are modified versions of the common volt-ohm meter. The patient holds one electrode, while the explorer serves as the second electrode. When the explorer is placed on the suspect area, the resistance of the tooth is measured. A high resistance is associated with no caries, and little resistance is associated with caries probability. ^ Secondary caries start with small imperfections or restoration overhangs that exist between the tooth and the margins of a restoration.86 Also, some tooth-colored fillings have a higher affinity for plaque.87 Bacteria are able to colonize and multiply at these vulnerable sites, sheltered from the protective effects of saliva and self-care efforts. Eventually, a lesion develops between the cavity margin and the restoration. The diagnosis of these lesions is difficult.88 In one study, extracted teeth were cut so that the section included both a clinically sound amalgam margin and one defined as "ditched." The prevalence of recurrent lesions in both sound and ditched restorations was close to 50%, although it is unknown whether these lesions were truly recurrent or due to residual caries left during a previous cavity preparation.89 The magnitude of the problem of secondary decay is illustrated by studies indicating that the median survival time of restorations ranges from 5 to 10 years.90 Replacement of defective restorations account for inserting several-times-more than needed restorations over a life time.91 Reducing this problem can best come from preventing the number of primary lesions (primary prevention). Some future relief may be forthcoming from the use of materials that bond directly to the tooth tissue, eliminating the gap between tooth and filling, or from restorative materials that slowly release fluoride, such as glass ionomers and newer fluoride-releasing composites and amalgams.92,93
Question 3 Which of the following statements, if any, are correct? A. The critical pH for enamel demineralization ranges between 6.0 to 5.5. B. There cannot be secondary caries, without having had a previous incipient lesion at the same site. C. Once the incipient lesions become overt, all the lesion zones disappear. D. Root caries is not necessarily a part of the aging process but is usually a sign of periodontal disease and/or previous periodontal neglect. E. A dentist usually inserts more restorations as a result of secondary caries than for primary caries. ^ Every time a person eats a food, there is a continuous pH change in the plaque. In many studies, pH microelectrodes have been inserted in bridges and telemonitored to determine these changes. For sugar and sugary snacks, an almost immediate drop in pH occurs, followed by a longer recovery period. This drop and recovery curve has been termed the Stephan Curve after Dr. Robert Stephan, an officer in the United States Public Health Service who first reported on the continuous changes in pH that followed eating and drinking different foods and drinking different beverages.94 Plaque pH responses to simple sugar rinses by caries-free and caries active individuals exhibited different drops in pH and different lengths of time to return to normal. Thus, different individuals have different capabilities to buffer acid production. (Figure 3-9). Similar pH studies have been accomplished that identify foods that are not hazardous to the teeth, and vice versa, those that are accompanied by a drop past the "critical pH" of pH 5.5 to 5.0. These lists are of considerable value when counseling patients.95 The Relationship of Saturation to pH The concentration of calcium and phosphate ions in the plaque fluid bathing the tooth at the plaque-tooth interface is extremely important, because these are the same elements that compose the hydroxyapatite crystal. If the fluid adjacent to the tooth is supersaturated with calcium and phosphate ions at a given pH, the enamel cannot undergo demineralization. The saliva in contact with the teeth is normally supersaturated with respect to the calcium and phosphate in enamel.15 The bacterial plaque can concentrate these ions to an even greater extent. For instance, both calcium and phosphate are threefold times greater than in the saliva.96 This increased concentration is of practical importance because calcium and phosphate levels tend to be inversely related to the caries score.47 It is also of great importance because it is the plaque fluid that determines the eventual caries status. As the pH drops in an acid attack, the level of supersaturation also drops, and the risk of demineralization increases. There is no exact pH at which the demineralization begins, only a general range of 5.5 to 5.0. The range is rather large because demineralization is a function of both pH and duration of exposure of the enamel surface to the acid environment. Different plaques have different initial pHs, buffering potentials, and concentrations of calcium and phosphate in different parts of the mouth. A change in any of these variables results in a different level of supersaturation in the tooth environment. ^ Throughout this book, there will continue to be many references to de- and remineralization of teeth, both as a pathologic and as a therapeutic process. The demineralization is caused by plaque acids causing the dissolution of the tooth minerals making up the basic calcium, phosphate, and hydroxyl crystals of the enamel, dentin and cementum. Remineralization on the other hand, requires the availability of the same ions, preferably with fluoride as a catalyst to reconstruct the missing or damaged rodsa process that ten Cate aptly calls, non-restorative repair.97 There are many calcium and phosphate compounds in the body that vary in formulae and with changes in pH. However, at this time, for the sake of simplicity, the crystals and fluoride compound of most dental interest in the de- and remineralization process are hydroxyapatite (HAP), fluorhydroxyapatite (FHA), and calcium fluoride (CaF2). The long-term exposure of teeth to low concentrations of fluoride (as found in fluoridated water) results in the gradual incorporation of fluoride into the existing hydroxyapatite (HAP) crystals to form fluorhydroxyapatite (FHA) that is more resistant to acid damage. Conversely, a higher concentration of fluoride (as occurs in topical applications, use of fluoride dentifrices, gels, and varnishes, etc.), results in the formation of surface globules of calcium fluoride (as seen in electron microscope images). A subsequent coating of these globules by phosphates and proteins of the saliva renders these globules more insoluble.98 As a matter of terminology, when the fluoride is incorporated into HAP to form FHA, it is said to be firmly bound; whereas, loosely bound fluoride is in the form of calcium fluoride that is adsorbed onto the surface of HAP and FHA crystals.99 See Figure 3-10. The Relationship Between HAP, FHA and CaF2 Following an attack by plaque acid(s), the CaF2 dissolves first, followed in sequence by the HAP, and finally, the FHA (with its fluoride substitutions). As the attack continues, the dissociated ions increase the saturation level of the immediate fluid sufficiently to slow crystal dissolution, and eventually arrest further solution of the crystals. As the pH begins to return to normal, crystals begin to re-form from the complex pool of dissolved ionssome as HAP, some as FHA (with many of the fluoride ions coming from the previous CaF2, and finally the precipitation of newly adsorbed CaF2. Any deficiencies are subsequently replaced in time by calcium, phosphate, and fluoride from sources such as the saliva, water, and toothpastes. In observing the above process, one must marvel at the body defense system that in the absence of a cellular or humeral surveillance of the enamel, can use a chemical system to maintain homeostasisone in which CaF2 provides a reservoir for fluoride that is immediately available when and where it is needed.100 The only time the system breaks down is when the attacks are too frequent and too prolonged. ^ There is little controversy about the success of surface remineralization procedures involving topical procedures, and of using commercial fluoride products such a dentifrices, gels, and varnish to compensate for the daily wear and tear of demineralization (Chapter 9). In the New Zealand School System, they consider x-ray lucencies of incipient lesions that extend midway through the enamel as candidates for remineralization. ten Cate, in an in vitro study, found that both the inner enamel and dentin could be remineralized, but very slow. Only the outer part of the enamel appeared to be responsive to fluoride diffusion and remineralization.97 At deeper levels, remineralization could be achieved, but only very slowly. In Scandinavia, the literature reflects the belief that remineralization is a reasonable objective even for lesions reaching to the dentin. The test for remineralization in these cases is that there is no demonstrable caries progress for 2 to 3 years. However, the important fact is that there are no reported studies that indicate whether deep remineralization is or is not successful. ^ In the United States, topical administration of fluorides is usually via cotton applicators, gel trays, and less frequently by using varnish. (Chapter 9). In Europe, varnishes appear preferable because of the longer exposure to fluoride following application. Since varnishes do seal dental tubules involved in hypersensitivity,101 there is a possibility that they also temporarily seal pores as seen in Figures 3-7A and 3-7B. Once sealed, there could be little or no acid penetration into the "white spot." At least three commercial varnishes are available in North AmericaDuraphat (Colgate-Palmolive, NY), Duraflor (Pharmascience, Montreal), and Fluor Protector (Ivoclar, Viyadent, Amherst, NY). The U.S. Food and Drug Administration (FDA) has cleared varnishes for applying fluoride varnishbut only as medical devices to be used as cavity liners and desensitizing agents, not for caries control. Semiannual applications are the most accepted time interval.102 Supporting this time interval was Seppa's study in Finland where increasing the application interval from two, to four times per year did not increase the effectiveness of Duraphat, even in high-risk children.103 Varnishes have proved to be effective. One study of 142 2- to 3-year-old children was conducted to determine the anticaries effectiveness of Duraphat. At the end of 9 months, 37.8% of the originally active occlusal, lingual, and buccal lesions of the control group became inactive, 3.6% had progressed, and 36.9% did not change. For the Duraphat group, 81.2% became inactive, 2.4% progressed, and 8.2% did change (P . 0001). The author concluded that the use of varnish was easy, safe and efficient; that it was possibly a non-invasive alternative for the treatment of decay in children.104 The application of the varnish is preceded by a prophylaxis, flushing, isolating the target teeth, drying, and applying the varnish with a small brushtechniques that are well known and practiced by the dental hygienist.
Question 4 Which of the following questions, if any, are correct? A. After examining the Stephan Curve recorded for several foods, it is possible to determine which foods and snacks are hazardous to tooth health. B. As the pH of the plaque fluid falls, it is necessary to have an increasing amount (saturation) of calcium and phosphate in the plaque fluid to prevent the dissolution of the tooth mineral. C. As the pH drops past the critical pH for enamel dissolution, the dissolving crystals gradually increase the immediate concentration (saturation) of tooth minerals that gradually slow, and possibly arrest the further solution of the rod crystals. D. It requires a lower critical pH to dissolve a crystal that is in the fluid environment of dissolving CaF2. E. The many studies of "deep remineralization" provide adequate scientific (evidence based) verification that it is a valid means to manage incipient lesions where the body of the lesion has progressed past the mid point in the enamel. Summary Dental caries is a multifactorial disease involving an interaction of bacteria, diet, host resistance, and time. Cavitation can only occur when demineralization outstrips the body's defensive capability for remineralizations over a period of time. The embryology and histology of the enamel are favorable for either the de- or the remineralization of the enamel. The residual matrix and spacial relationships of rod-to-rod and crystalite-to-crystalite, as well as the less-calcified structures as the incremental lines of Retzius, lamellae, and tufts, allow fluids to diffuse throughout the enamel. Like the wick of an oil lamp, this network is available for the in-and-out movement of tooth-mineral ions and plaque acids. Even when there has been a penetration of the enamel cap by an incipient lesion, this is a pre-caries lesion that can often be remineralized without the need for a restoration. Possibly months or years will elapse before cavitation, or there may even be a natural remineralization that entirely reverses the caries progression. There are several acidogenic bacteria that are causal for caries production, with mutans streptococci and lactobacilli being the most studied. Silverstone opened up the possibility of a new nonrestorative repair era when he described the de- and remineralizing zones of an incipient lesion. If those in the dental care profession and research can bring remineralization to fruition, millions of teeth can be saved from the dentist's drill. The polarizing and the electron microscopes allow us to see the details of how the plaque acids can easily flow into the body of the lesion and beyond. To increase tooth resistance and, at the same time, the probability of remineralizing any known or unknown incipient lesions, mechanical plaque control strategies consisting of tooth brushing, flossing, and irrigation are used to remove the plaque. Chemical plaque control stratagems involve the use of antimicrobials to kill or suppress the cariogenic bacteria; and fluoride in the forms of water fluoridation, office topical applications, or the use of fluoride rinses or dentifrices are used to improve tooth resistance. There are now the means to greatly reduce the toll of dental caries; yet needed is access to examination and treatment systems based on early identification and treatment of risk factors before they become treatment requirements. Throughout this book, emphasis will be placed on the various strategies now available for preventing or limiting demineralization, or of enhancing remineralization. |
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