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Health is what we want to preserve, and it is defined as a state of complete physical, mental, and social wellbeing, and not

merely the absence of disease or infirmity 1. Primary prevention employs strategies and agents to forestall the onset of disease, to reverse the progress of the disease, or to arrest the disease process before secondary preventive treatment becomes necessary. 2. Secondary prevention employs routine treatment methods to terminate a disease process and/or to restore tissues to as near normal as possible. 3. Tertiary prevention employs measures necessary to replace lost tissues and to rehabilitate patients to the point that physical capabilities and/or mental attitudes are as near normal as possible after the failure of secondary prevention This text emphasizes primary prevention, and specifically focuses on primary prevention as it applies to the control of dental caries and periodontal disease. On the other hand, it must be recognized that primary prevention often fails for many reasons. When such failure occurs, two actions are essential to contain the damage: (1) early identification of the disease (diagnosis) and (2) immediate treatment of the disease. Categories of Oral Disease For planning purposes, dental diseases and abnormalities can be conveniently grouped into three categories: (1) dental caries and periodontal disease, both of which are acquired conditions, (2) acquired oral conditions other than dental caries and periodontal disease (opportunistic infections, oral cancer, HIV/AIDS), and (3) craniofacial disorders which would include a wide variety of conditions ranging from heredity to accidents.24,25 For instance, the ordinary seat belt and the air bags in a car exemplify how a simple preventive measure can greatly reduce the facial injuries of car accidents. Looming in the not-too-far distant future is the very real possibility that many acquired health problems will be corrected or ameliorated for total populations by use of vaccines, genetic engineering, or specifically targeted drugs ("magic bullets"). Strategies to Prevent the Plaque Diseases Before providing an overview of methods used to implement primary prevention programs, it is important to point out that both dental caries and periodontal disease are transmissible diseases. If a child is considered at has periodontal problems, usually one of the parents is also afflicted. Any infectious (acquired) disease can only begin if the challenge organisms are in sufficient numbers to overwhelm the combined manmade and body defenses and repair capabilities. For this reason, all strategies to prevent, arrest, or reverse the ravages of the plaque diseases are based on (1) reducing the number of challenging oral pathogens, (2) building up the tooth resistance and maintaining a healthy gingiva, and (3) enhancing the repair processes. In general, periodontal disease is a disease that involves the soft tissue and bone surrounding the affected teeth. Caries involves the demineralization and eventual cavitation of the enamel and often of the root surface. If the incipient lesions (earliest visible sign of disease) of caries and periodontal disease are recognized at the time of the initial/annual dental examination, they can often be reversed with primary preventive strategies. For caries, the visible incipient lesion is a white spot, which appears on the surface of the enamel as a result of subsurface acid-induced demineralization. For periodontal disease, the visible incipient lesion is gingivitis inflammation of the gingiva that is in contact with the bacterial plaque. Not all "white spots" go on to become caries, nor do all cases of gingivitis go on to become periodontal disease. In both cases, i.e., caries and periodontal disease, it should be noted that if dental plaque did not exist, or if the adverse effects of its microbial inhabitants could be negated, the decrease in the incidence of the plaque diseases would be very dramatic. Based on these facts, it is understandable why plaque control is so important in any oral-health program. To control the plaque diseases with available methods and techniques, strong emphasis has been directed to four general strategies to reduce caries and two administrative requirements: General Strategies 1. Mechanical (toothbrush, dental floss, irrigator, or rinse) 2. Chemical plaque control. Use of fluorides to inhibit demineralization and to enhance remineralization; use of antimicrobial agents to supress cariogenic bacteria. 3. Sugar discipline. 4. Use of pit and fissure sealants, when indicated, on posterior occlusal surfaces. Administrative 5. Education and health promotion. 6. Establish access to dental facilities where diagnostic, restorative, and preventive services are rendered, and where planned recalls based on risk are routine. A brief summary of each of these primary preventive procedures will serve as an introduction for the more detailed information presented in later chapters. Plaque Control Dental plaque is composed of salivary proteins that adhere to the teeth, plus bacteria and end-products of bacterial metabolism. Both cariogenic and periodontopathogens accumulate in the plaque located along the gingival margin, interproximally, and in the pits and fissures. Plaque collects more profusely in these specific areas because none of these locations is optimally exposed to the normal self-cleansing action of the saliva, the abrasive action of foods, nor the muscular action of the cheeks and tongue. Plaque decreases in thickness as the incisal or occlusal surface is approached. Little plaque is found on the occlusal surface except in the pits and fissures. As would be expected, plaque forms more profusely on malposed teeth or on teeth with orthodontic appliances, where access for cleaning is often difficult. In the gingival sulcus between the gingiva and the tooth, little or no plaque normally accumulates until gingival inflammation begins, at which time the bacterial population increases in quantity and complexity. This is the beginning of gingivitis that, if continued, may eventually result in an irreversible periodontitis. It is important to differentiate between the supragingival and the subgingival plaques. The supragingival plaque can be seen above the gingival margin on all tooth surfaces; the subgingival plaque is found in the sulcus and pocket below the gingival margin, where it is not visible. The supragingival plaque harbors specific bacteria that can cause supragingival (coronal) caries. The subgingival plaque microbiota is mainly responsible for periodontal problems. The bacterial populations of each of these plaques differ qualitatively and quantitatively in health and disease.28 The pathogenicity of each of the plaques can vary independently of the other. For example, it is possible to have periodontal disease with or without caries, to have neither, or to have a shifting status of caries or periodontal disease, or both.

The pathogenicity of the subgingival plaque is becoming an increasing concern. Not only does it cause periodontal disease, which is a lifelong debilitating disease of the tooth supporting tissues, but it is now believed that there is a causal relationship between periodontitis29 and such diverse conditions as, cardiovascular disease,30 diabetis mellitus,31 chronic respiratory disease,32 and immune function.33 There is also the possibility in some cases that this is a bi-directional association where the oral problem begins with a systemic condition, instead of vice versa. In many cases, plaque is difficult for a patient to identify. This problem can be overcome, at least in the case of the supragingival plaque, by the use of disclosing agents, which are harmless dyes such as the red-staining agent, FD&C Red. The dyes may be in solution and painted on the teeth with a cotton applicator, or they may be tablets which are chewed, swished around the mouth, and then expectorated. Once disclosed, most of the supragingival plaque and food debris can be easily removed by the daily use of a toothbrush, floss, and an irrigator (Figure 1-2). Plaque can also be removed at planned intervals by the dental hygienist or a dentist as part of an oral prophylaxis. This is a procedure that has as its objective the mechanical removal of all soft and hard deposits, followed by a polishing of the tooth surfaces. However, because daily removal of the plaque is more effective, it is the individual teeth.

One site where neither the dentist nor an individual can successfully remove plaque is in the depth of pits and fissures of occlusal surfaces where the orifices are too small for the toothbrush bristle to penetrate (see Chapter 10). The flow of saliva or the muscular action of the cheeks and tongue also have little influence over the eventual development of caries in these areas. Not coincidentally, the occlusal surface is where the greatest percentage of caries lesions occur. For this reason, it is recommended that all occlusal surfaces with deep convoluted fissures be sealed with a pit-and-fissure sealant. As soon as the plaque is removed from any surface of the tooth, it immediately begins to reform. This should not be unexpected, since by definition, dental plaque is composed of salivary residue, bacteria, and their end-products, all of which are always present in the mouth. Thus, a good plaque-control program must be continuous. It must be a daily commitment over a lifetime.

Not only does the daily removal of dental plaque reduce the probability of dental caries; equally important, it also reduces the possibility of the onset of gingivitis. This occurs when the metabolic end-products of the periodontopatho-gens that are contained in the plaque irritate the adjacent gingival tissues, producing an inflammation (i.e., gingivitis). If the inflammation continues, bleeding (hemorrhage) can be expected following even minimal pressure ("pink toothbrush"). This gingivitis can be arrested and reversed (cured) in the early stages by proper brushing, flossing, and irrigation, especially if accompanied with professional guidance. Plaque concentrates mineralizing ions such as calcium, phosphate, magnesium, fluoride and carbonates from the saliva to provide the chemical environment for the precipitation and formation of calculus, a concretion that adheres firmly to the teeth. If the plaque is not removed by flossing and brushing before the calculus begins to form, the resultant mineralized mass provides a greater surface area for an even more damaging plaque accumulation. This additional mass of periodontopathic plaque covering the rough porous surface causes the stagnation of even more bacteria and is responsible for the damage to the periodontal tissues. Also, the hard, irregular calculus deposits pressing against the soft tissues serves to exacerbate the inflammation caused by the bacteria alone. The daily removal of plaque can successfully abort or markedly retard the buildup of calculus. Once the calculus forms, the brushing and flossing usually used for plaque control does not remove the deposits. At this time, the dental hygienist or dentist must intercede to remove the calculus by instrumentation.

To this point, only mechanical plaque control (i.e., use of a toothbrush, dental floss, and an irrigator) has been highlighted. Rapidly growing in importance as a supplement to mechanical plaque control (but not as a replacement), is chemical plaque control. This approach utilizes mouthrinses containing antimicrobial agents that effectively help control the plaque bacteria involved in causing both caries and gingivitis. For helping to control gingivitis, a popular and economical over-the-counter product is Listerine; the most effective prescription rinse is chlorhexidine. Many studies indicate that chlorhexidine is as effective in suppressing cariogenic organisms as it is effective in controlling gingivitis and periodontitis.34,35

Fluorides The use of fluorides has provided exceptionally meaningful reductions in the incidence of dental caries. Because of water fluoridation, fluoride dentifrices, and mouthrinses, dental caries is declining throughout the industrialized world. Historically, the injection of fluoride into water supplies in the mid-20th century resulted in a decrement of approximately 60 to 70% in caries. Since that time, fluoride has been introduced into proprietary products such as dentifrices and mouthrinses. As a result, the caries decrement directly attributable to water fluoride over the past years has declined. Yet, the placement of fluoride into communal water supplies still results in an estimated 20 to 40% reduction in coronal caries, and a similar 20 to 40% decrease in root caries36 (Figure 1-3). Approximately 126 million individuals in the United States consume fluoridated water through communal water supplies and another 9 million are drinking naturally fluoridated water. It is estimated that 65% of the U.S. population, therefore, is receiving fluoride through drinking water.37 Many times during the past years, it has not been possible to fluoridate city water supplies because of political, technical, or financial considerations. In such cases, it is still possible to receive the systemic benefits of fluoride by using dietary supplements in the form of fluoride tablets, drops, lozenges, and vitamin preparations. Some countries permit fluorides to be added to table salt.38 Elsewhere, ongoing research studies are being conducted to determine the anticariogenic effect of fluoride when placed in milk,39,40 and even

sugar.41 It is also possible to apply fluoride directly to the surface of the teeth by use of cotton pledgets, and/or by use of fluoride-containing dentifrices, gels, varnishes or mouth rinses. Such applications to the surface of the teeth are referred to as topical applications. The extent of caries control achieved through topical applications is directly related to the number of times the fluoride is applied and the length of time the fluoride is maintained in contact with the teeth. Research data also indicate that it is better to apply lower concentrations of fluoride to the teeth more often than to apply higher concentrations at longer intervals. Fluorides and chlorhexidine are the most effective agents used by the profession to combat the plaque diseases. The fluorides help prevent demineralization and enhance remineralization, while chlorhexidine severely suppresses the mutans streptococci that cause the demineralization. Chlorhexidine also helps suppress bacteria causing the inflammation of periodontal disease..

Neither the action of topically applied nor of systemic (ingested) fluoride in preventing dental caries is completely understood. It is believed that fluoride has several key actions: (1) it may enter the dental plaque and affect the bacteria by depressing their production of acid and thus reduce the possibility of demineralization of the teeth; (2) it reacts with the mineral elements on the surface of the tooth to make the enamel less soluble to the acid end-products of bacterial metabolism; and (3) it facilitates the remineralization (repair) of teeth that have been demineralized by acid end-products. The latter is probably the most important of these three effects.

The natural source of minerals such as calcium and phosphate, fluoride and others needed for this remineralization is the saliva.

Sugar and Diet The development of dental caries depends on four interrelated factors: (1) diet, (2) inherent factors of host resistance, (3) the number of challenge bacteria located in the dental plaque, and (4) time (Figure 1-4). Without bacteria, no caries can develop. For the bacteria in the plaque to live, they must have the same amino acids, carbohydrates, fatty acids, vitamins, and minerals that are required for all living organisms. Because these nutrients are also required by the cells of the body, the food that is ingested by the host or that which later appears in the saliva in a metabolized form, provides adequate nutrients for bacterial survival and reproduction. With three well-balanced meals per day, however, the usual plaque bacteria probably would not release a sufficient quantity of metabolic acids to cause caries development (Figure 1-5A). But, as soon as sugar and sugar products are included in the diet of the host, bacterial acid production markedly increases in the plaque. This release of acid end-products is the major cause of the initiation and progression of caries.42 Of even greater importance than the total intake of refined carbohydrates is the frequency of intake and the consistency of the sugar-containing foods.43 The continuous snacking of refined carbohydrates that characterizes modern living results in the teeth being constantly exposed to bacterial acids (Figure 1-5B). For example, the prolonged adherence of sugar products to the teeth, such as that experienced after eating taffies and hard candies, results in prolonged production of the plaque acids that are in direct contact with the tooth total intake of sugar, consistency of the cariogenic foods, and especially frequency of intake should be considered. Possibly one of the most promising means of reducing caries incidence in the United States has been the widescale acceptance of sugar substitutes such as NutraSweet, Sweet'n Low, and Splenda. In the Nordic countries, there i reduce the amount of plaque and plaque acid, inhibit growth and metabolism of streptococci,44 reduce decay in animal studies, and contribute to remineralization. It is considered noncariogenic and cariostatic.45 All the Nordic dental associations recommend its use. Since the 1970s, one of the favorite ways to take advantage of xylitols unique anticaries property, has been to use it to sweeten chewing gum, a product that is a popular item among school children.46 Two other dental uses of xylitol chewing gum have come out in Scandinavia: 1. Chlorhexidine can dramatically suppress the number of mutans streptococcus in the saliva. However, after discontinuing use of the product, there is a rapid repopulation of the bacteria. This repopulation can be arrested or greatly slowed by the use of xylitol chewing gum.47 2. Previously it was mentioned that a child's flora often reflected that of the mother.

To help minimize this mother-child transmission of cariogenic bacteria, mothers have been urged to chew xylitol gum.48 This creditable background of xylitol has prompted Anasavice to ask, "Are chlorhexidine, fluoride, fluoride varnishes, and xylitol chewing gum under ustilized preventive therapies?"49 Pit and Fissure Sealants Approximately 90% of all the carious lesions in the mouth occur on the occlusal surfaces of the posterior teeth.50 These surfaces represent only 12% of the total number of tooth surfaces, so that occlusal surfaces with their deep pits and fissures are approximately eight times as vulnerable as all the other smooth surfaces. The availability of sealants offers an alternative to a restoration. With the use of sealants, a thin layer of a plastic, called Bis-GMA, is flowed into the deep occlusal pits and fissures of teeth not having open carious lesions. This action effectively isolates these areas from the oral environment (Figure 1-6). Since no cavity preparation is necessary, no pain or discomfort accompanies sealant placement. Following the placement of the sealant in the deep fissures, the newly created fossae can be effectively cleaned with a toothbrush.

As long as the sealants are retained, no bacteria or bacterial acids can affect the sealed areas. If they are not retained, no damage to the teeth results from a retreatment. The lost sealant can be easily replaced. One 10year study demonstrated a 57% retention of the original sealants.51 In another study, approximately 95% retention occurred over 2 years.52 With these performances, the average life of the sealant approximates the 10 years projected for an amalgam.53 It should be emphasized that sealant placement should be followed by a topical fluoride application to the teeth, because fluorides are most effective in protecting the smooth surfaces and least effective on the occlusal surfaces, a situation that is the reverse of the results expected of the sealants.

Public Dental Health Education If the profession of dentistry can control caries effectively through plaque control, systemic (ingested) and topical (local application) use of fluorides, dietary control, and the use of plastic sealants, two important questions need to be asked. 1. Why do we not have a more effective dental caries-control program in the United States? 2. If daily toothbrushing, flossing of teeth, and irrigation removes plaque and food residue, why are these simple procedures not used effectively to control both caries and periodontal disease? Probably the best answer to these questions is that people must first know what they need to do as well as how it is to be done. Unfortunately, the public has relatively little information about the tremendous potential of primary preventive dentistry for reducing their adverse exposures to the plaque diseases. Without this information, it is difficult to convince people that they can greatly control their own dental destiny. Many individuals think of dentistry as a treatment-oriented profession that specializes in periodontal treatment, restorations, endodontics, exodontics, and prosthetics. An expanded public education and promotion program is essential to ensure the success of any preventive dentistry program in which an individual or a community is asked to participate. In dentistry, a one-on-one relationship between the patient and the health professional is still a basic approach to patient education and motivation. This approach makes the task impossible because there are 250 million people in the United States and only approximately 165,000 practicing dentists, plus 120,000 dental hygienists and 175,000 assistants.54,55 The main thrust of public dental-health education and oral-health promotion is provided by the various dentrifice manufacturers advocating the daily toothbrushing routine and biannual visits to the dentist for a checkup. The effectiveness of this approach was underlined by the long-running advertisement for the first marketed, stannous fluoride containing, Crest toothpaste, "Look Mom, no cavities." Knowing facts and applying the information are two separate processes. The application of knowledge by an individual requires a personal commitment; it is at this point of personal commitment that most primary preventive-dentistry programs fail. If people embraced the daily use of mechanical and chemical plaque control regimens, the risk of caries and gingivitis would be minimized. If people would exercise reasonable sugar discipline the possibility of caries development would be further reduced. If individuals rejected the use of cigarettes as well as smokeless ("spit") tobacco, oral and pharyngeal cancer and periodontitis would be much less prevalent. Clearly, education, motivation, and behavior modification are a necessary part of enjoying good oral and general health. A sound, well-planned program of dental-health education and promotion is lacking in the curriculum of the great majority of primary and secondary schools. Few people can discuss the advantages and disadvantages of water fluoridation and the topical application of fluorides. Few have any detailed information about the dental plaque and the disease-inducing potentialities of this bacterial film.b Few people know why sugar is cariogenic. Even fewer people know that gingivitis can be cured, but that if allowed to progress, there is the possibility of a life long future of periodontal disease treatment and maintenance. Finally, the public has not been adequately informed that the timely use of sealants and remineralization therapy provides a hope of possessing a full intact dentition for life. Even though the Internet has greatly expanded the delivery of health education, there is always the question of the quality of information (or misinformation) that is disseminated.56

Ideally, school-based and public-education programs should exist to help people to help themselves in applying primary preventive procedures. The same programs should also teach all individuals to recognize the presence of oral disease. With proper instruction that can be provided by schoolteachers. The general public can be taught to understand that they must assume major responsibility for their own oral health (see Chapter 19). Only the individual can seek immediate treatment when pain or disease occurs. Public dental-health education might benefit if there was a consumer organization such as an American Oral Health Association that could promote oral health education, much like the American Cancer Society and the American Heart Association. bBiofilm = A collection (film) of living organisms attached to a solid base, such as algae to the bottom of a swimming pool, or dental plaque to a tooth. Both terms are used in the book, but dental plaque is preferred because of public familiarity and understanding of "dental plaque." Access to Comprehensive Dental Care This factor is probably the most important of all preventive options. Without the benefit of a routine periodic dental examination, it is difficult for individuals to realize that they are vulnerable to oral disease. The first indication of a dental problem is pain, which is the wrong starting point for prevention. An example of the benefits of combining prevention with the advantages of early identification, prevention and treatment is seen in the New Zealand school-dental-nurse program. In the New Zealand School Dental Service, a dental nurse visits every primary and secondary school in the country at approximately 6-month intervals. At that time, all children receive a dental examination. If necessary, the dental nurse applies fluoride varnish to achieve remineralization of incipient caries, removes visible calculus, or when indicated, refers the child to a dentist for more complex treatment requirements.57 As a result of this program, the average rate of extractions dropped from 19 per 100 students in 1960, to 2 per 1,000 in 1979. From 1973 until 1992, the average decayed, missing, or filled permanent teeth (DMFT) for 12- to 14-year-old children plummeted from 10.7 to 1.88 per child. Approximately 96% of all New Zealand schoolchildren are enrolled in this program. Unfortunately, relatively few comprehensive primary-preventive dentistry school programs are being conducted in the United States school systems. However, there are more than 1,400 School Based Dental Health Clinics (SBDHC) now in operation in the United States (see Chapter 19).

Prognostic and Diagnostic Tests Several methods for preventing the onset or progress of caries and periodontal disease have been discussed. Because it is impossible to apply vigorously all the preventive procedures to all the people all the time, it would be desirable to have some tests to indicate the extent of caries and periodontal disease risk of an individual at any given time. This need is highlighted by the fact that an estimated 60% of all carious lesions in schoolchildren occur in 20% of the stu-dents.58 It would save much time to be able to identify this 20% group of high-risk students without having to examine an entire school population. Although no tests are 100% correlated with the extent of caries activity or periodontal disease, several test procedures are sufficiently well correlated with either condition to be of interest. To be successful, such screening tests should be simple to accomplish, valid, economical, require a minimum of equipment, be easy to evaluate, and be compatible with mass-handling techniques. Laboratory methods exist for counting the number of bacteria in the saliva. If the caries-causing mutans streptococci or lactobacilli counts are high, the individual from whom the sample was derived can be presumed to have a higher risk for dental caries, whereas a low count permits the opposite assumption.59 A second general method for estimating caries susceptibility is by use of a refined-carbohydrate dietary analysis to (1) evaluate the patient's overall diet with special attention to food preferences and amounts consumed and (2) to determine if the intake of refined carbohydrates is excessive in quantity or frequency (see Appendix 23-2). A well-balanced diet is assumed to raise host resistance to all disease processes, whereas a frequent and excessive intake of refined carbohydrates (i.e., sugar) has been associated with a high risk of caries development. The dietary analysis is very effective when used as a guide for patient education.

The onset of gingivitis is much more visible than the early demineralization that occurs in caries. The sign of impending periodontal disease is an inflammation of the gingiva that can be localized at one site, or generalized around all the teeth. Red, bleeding, swollen, and a sore gingiva are readily apparent to dentist and patient alike. Remineralization of Teeth Both demineralization and remineralization occur daily following the cyclic ebb-and-flow of the caries process during and after eating meals and snacks. An eventual caries lesion develops over a period of time when the rate of acid-induced demineralization of teeth exceeds the capability of the saliva to remineralize the damaged enamel components. A negative mineral balance at the enamel-plaque interface, if continually repeated, results in an incipient lesion that eventually can become an overt lesion. It often requires months, or even years, for the overt lesion to develop.60,61 During this time, under proper conditions, remineralization can reverse the progress of the caries front, with the mineral components coming from the saliva. There is a physiological precedent for such a mineralization. Immediately after eruption of the teeth the outer layer of the enamel is not completely mineralized; the maturation (mineralization) of this outer layer requires approximately 1 year, during which time the tooth is continuously bathed in the saliva. The point at which a developing caries lesion is no longer reversible is considered to be when cavitation occurs; clinical experience indicates that as long as the lesion is incipient (i.e., with no cavitation), remineralization is possible.62 The need to exploit this possibility to the benefit of all patients was emphasized by Koulourides's statement many years ago that "there is a wide gap between current practices of many dental clinicians and the potential application of present scientific knowledge to arrest and reverse incipient carious lesions."63.

The outstanding electron microscope research contributions of Silverstone several decades ago clearly demonstrated that demineralized tooth structure could be remineralized.64 No longer was a simple interproximal x-ray radiolucency a signal to place an interproximal restoration. Several reports from Scandinavia now indicate that even when the caries front of an incipient lesion extends past the dentino(be) considered for approximal lesions which extend deeper that 0.5 mm into the dentine, while preventive treatment and re-assessment may be considered for shallower lesions."65 Missing at the present time is an accurate predictive test for caries that would permit the targeting of individuals who would be candidates for remineralization therapy (see Chapter 23). The conditions for optimum remineralization are the same as for preventing the initiation of a lesion: (1) plaque control to reduce the number of cariogenic bacteria, (2) a strict self-imposed sugar discipline to minimize the number of acidogenic episodes, (3) the use of sealants to interdict bacterial entry into deep pits and fissures, and (4) the use of topical and/or systemic fluoride to inhibit demineralization and to potentiate the remineralization process. Thus, with the same primary preventive dentistry routines using fluoride, an individual can simultaneously protect the tooth into the future by prevention, as well as to compensate for limited past damage through reversal strategies.