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J Am Dent Assoc, Vol 140, No suppl_1, 25S-34S.
© 2009 American Dental Association
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ARTICLES

The Biology, Prevention, Diagnosis and Treatment of Dental Caries

Scientific Advances in the United States



Domenick T. Zero, DDS, MS, Margherita Fontana, DDS, PhD, E. Angeles Martínez-Mier, DDS, MSD, PhD, Andréa Ferreira-Zandoná, DDS, MSD, PhD, Masatoshi Ando, DDS, PhD, Carlos González-Cabezas, DDS, MSD, PhD and Stephen Bayne, MS, PhD


   ABSTRACT
TOP
 ABSTRACT
ETIOLOGY OF DENTAL CARIES
 PREVENTION OF CARIES
 DIAGNOSIS OF CARIES
 TREATMENT OF CARIES
 CONCLUSIONS
 REFERENCES
 
Background. Scientific advances in cariology in the past 150 years have led to the understanding that dental caries is a chronic, dietomicrobial, site-specific disease caused by a shift from protective factors favoring tooth remineralization to destructive factors leading to demineralization. Epidemiologic data indicate that caries has changed in the last century; it now is distributed unequally in the U.S. population. People who are minorities, homeless, migrants, children with disabilities and of lower socioeconomic status suffer from the highest prevalence and severity of dental caries.

Results. Scientific advances have led to improvements in the prevention, diagnosis and treatment of dental caries, but there is a need for new diagnostic tools and treatment methods.

Conclusions and Clinical Implications. Future management of dental caries requires early detection and risk assessment if the profession is to achieve timely and cost-effective prevention and treatment for those who need it most. Dental professionals look forward to the day when people of all ages and backgrounds view dental caries as a disease of the past.

Key Words: Caries; remineralization; saliva

Abbreviations: ACP: Amorphous calcium phosphate • bis-GMA: Bisphenol-A glycidyl methacrylate • CAD-CAM: Computer-aided design/computer-aided manufacturing • CO2: Carbon dioxide • Er,Cr:YSGG: Erbium-chromium–doped yttrium scandium aluminum garnet • Er:YAG: Erbium-doped yttrium aluminum garnet • FOTI: Fiber-optic transillumination • ICDAS: International Caries Detection and Assessment Criteria • LED: Light-emitting diode • MS: Mutans streptococci • Nd:YAG: Neodymium-doped yttrium aluminum garnet • OCT: Optical coherence tomography • QLF: Quantitative light-induced fluorescence

Dental scientists living and working in the United States during the last 50 to 60 years have contributed to our understanding that dental caries is a chronic, dietomicrobial, site-specific disease caused by shifts from protective factors favoring tooth remineralization to destructive factors leading to demineralization. We now know that caries results from complex interactions among the tooth structure, the dental biofilm, and dietary, salivary and genetic influences. The distribution of caries has changed in the last century. Relatively recent data indicate that about 90 percent of carious lesions occur in the pits and fissures of permanent posterior teeth and that molar teeth are most susceptible to caries.1 The disease is unequally distributed in the U.S. population; people who are minorities, homeless, migrants, children with disabilities and of lower socioeconomic status have the highest prevalence and severity of caries.1 This article briefly outlines major scientific advances in cariology—with, in honor of the 150th anniversary of the American Dental Association (ADA), an emphasis on contributions made by those living and working in the United States.


   ETIOLOGY OF DENTAL CARIES
TOP
 ABSTRACT
 ETIOLOGY OF DENTAL CARIES
PREVENTION OF CARIES
 DIAGNOSIS OF CARIES
 TREATMENT OF CARIES
 CONCLUSIONS
 REFERENCES
 
Microbial etiology. Willoughby Miller,2 a dentist and early dental researcher, proposed that oral bacteria in the presence of fermentable carbohydrates produced acids that dissolved tooth structure. Together with research on plaque by William3 and Black,4 this concept evolved as the foundation for our current knowledge of caries etiology. However, early caries investigators did not understand the specific nature of the bacterial infection contributing to caries and that restorative strategies alone, such as "extension for prevention,"5 were not successful in controlling the disease. Thus, dentists dealt mainly with the continuing sequelae of this widespread disease during the first half of the 20th century.6

Throughout the 20th century, of all possible etiological organisms associated with dental caries, the mutans streptococci (MS) group captured the greatest interest. Researchers initially isolated Streptococcus mutans from human carious lesions,7 but it was not until much later, when researchers conducted animal studies, that the bacterial etiology of dental caries was established firmly.8,9 Children acquire some oral microorganisms, such as S. mutans, from their mothers or primary care-givers early in life.10 Therefore, caries is a microbial disease in which etiologic bacteria are normal constituents of the oral microbiota that cause disease only when their proportions and pathogenicity change in response to environmental conditions.11 The key caries-associated microbial virulence traits include acidogenesis and acid tolerance,12 intracellular polysaccharide storage13 and extracellular glucan formation, which promotes MS attachment14 and increases plaque’s pH-lowering ability.15,16 Although S. mutans is one of the most researched cariogenic microorganisms, it is only one of more than 500 species found in dental plaque.17 In studies using molecular identification of bacteria, investigators have reported that diverse bacterial communities, including some novel species, are associated with dental caries and that S. mutans is not detectable in 10 to 20 percent of people who have severe caries.18,19 Recent evidence also has supported the role of yeast (Candida albicans) as a member of the mixed oral microbiota involved in caries causation.20 These findings provide support for the ecological plaque hypothesis, which proposes that S. mutans is only one of many endogenous microorganisms involved in the pathogenesis of caries.11,21,22 A challenge for researchers is to characterize this complex biofilm and subsequently identify microbial risk factors leading to caries activity, with a view toward developing novel antimicrobial interventions.

Dietary factors. Dental caries cannot occur in the absence of dietary fermentable carbohydrates and, therefore, it has been characterized as a "dietobacterial" disease.23 Since the original observations of Miller,2 researchers have recognized fermentable carbohydrates as the "fuel" for the caries process, and in the 1940s, Stephan24,25 demonstrated the relationship between caries and sugar exposure, leading to the acidification of dental plaque. Moreover, Weiss and Trithart26 reported a direct relationship between caries experience and the frequency of between-meals consumption of sweet snacks, which findings supported those of the earlier Vipeholm study in Sweden.27

The role of specific sugars was a subject of great research interest in the latter half of the 20th century.28 Sucrose (table sugar) has a unique role as the sole substrate for glucosyltransferases (bacterial enzymes) involved in the synthesis of extracellular glucan, which is an important microbial virulence factor (discussed above). The relative cariogenicity of starches as compared with that of sugars has been the subject of considerable controversy.29 Available studies with humans have not supported the cariogenicity of starches.29 For example, Newbrun and colleagues30 reported that people with hereditary fructose intolerance who are unable to eat fructose and sucrose but consume large quantities of starch have a much lower caries experience than do those without fructose intolerance. Highly processed starch-containing foods, however, have the potential to be cariogenic, especially when combined with sugars, because they are able to prolong food retention on tooth surfaces.31,32

The recognition of sucrose as a major factor in dental caries, as well as work by Bibby33 regarding the cariogenicity of snack foods, precipitated a series of ADA conferences in the late 1970s and early 1980s that culminated in a consensus conference in 1985.34 The conference participants considered several approaches for testing foods to determine their potential cariogenicity, including models involving animal caries, human plaque acidity and demineralization and remineralization. They recommended an integrated approach that involved using combinations of methods to determine the cariogenicity of foods. They reached a consensus that foods had "no cariogenic potential" if their human plaque pH profiles were statistically equivalent to that of sorbitol. Unfortunately, characterization of foods as having "low cariogenic potential" has not proven to be practical because of individual variability in eating frequency, sequence of eating foods, timing of eating (such as eating before bedtime) and after-eating behaviors (oral hygiene, fluoride use, gum chewing).28 It also has been challenging to apply information about food cariogenicity in dietary counseling.35 In the latter part of the 20th century, scientific interest in the cariogenicity of foods waned with recognition that the prevalence and severity of caries were declining, and the U.S. government placed less emphasis on the need for labeling food regarding its cariogenicity.

Host salivary and genetic factors. Host-related factors are important contributors to a person’s dental caries susceptibility, resistance or both. It is well established that saliva plays an important role in the health of soft and hard tissues in the oral cavity.36 Chronically low salivary flow rate is one of the strongest indicators of increased caries risk.37 A subjective complaint of xerostomia often does not correlate with objective findings of reduced salivary flow rate.38 This finding has led to clinical recommendations and guidelines for the clinical assessment of hyposalivation.39 The objective measurement of salivary flow is an important cornerstone of caries risk assessment and management.

Researchers initially believed that genetic factors—such as tooth morphology, position and occlusion; tooth eruption time and sequence; salivary composition; and sweetness preference—were less important in determining caries risk than were environmental influences, such as microbial and dietary factors.40,41 However, results of recent studies in populations of twins have shown that genetic factors may explain more than 50 percent of the variance in caries experience among people.42,43 Much remains unknown about genetic-environmental relationships in caries etiology and risk assessment, but the future holds interesting possibilities for improvements in caries diagnosis and prognosis.


   PREVENTION OF CARIES
TOP
 ABSTRACT
 ETIOLOGY OF DENTAL CARIES
 PREVENTION OF CARIES
DIAGNOSIS OF CARIES
 TREATMENT OF CARIES
 CONCLUSIONS
 REFERENCES
 
Risk assessment. Caries risk assessment is the cornerstone of patient-centered caries management. It is the determination of the probability of a person’s developing new carious lesions during a specific period41 and of the probability of a change in the size or activity of existing lesions across time.44 It is useful in determining whether additional diagnostic procedures are required; in identifying patients who require caries-control measures; in assessing the effectiveness of attempts to control caries; and as a guide in treatment planning and scheduling recall appointments.44 Investigators have shown that previous caries experience is the best predictor of future caries experience in primary teeth, followed by parental education and socioeconomic status; young children’s age at the time of MS colonization also was found to be an important risk factor.45 While previous caries experience may be the most useful criterion for risk assessment, the information arises too late to be useful in preventing caries because many irreversible events already have taken place. To enable effective prevention, researchers must determine efficient ways to identify children at high risk of developing caries earlier, shortly after their first teeth erupt. To accomplish this goal, researchers must develop molecular and genetic methods to improve the identification and characterization of cariogenic microbes and identify ways to reduce or eliminate harmful effects of their colonization. It also will be important to develop improved technology to detect and quantify early lesions and to assess carious lesion activity directly, because this may prove to be the best strategy to identify patients in need of intensive caries prevention efforts.45

Fluoride. American contributions to fluoride’s role in caries prevention are seminal. They began at the turn of the 20th century when Frederick McKay,46 a practicing dentist, associated "mottled enamel"47 with reduced susceptibility to caries; in collaboration with H.V. Churchill,48 the chief chemist at the Aluminum Company of America, he later traced this condition to fluoride. H. Trendley Dean, the first director of what then was called the National Institute of Dental Research (now the National Institute of Dental and Craniofacial Research), conducted several studies in the 1930s and 1940s with colleagues that provided the conclusive epidemiologic evidence linking what they referred to as "dental fluorosis" or "enamel fluorosis" to excessive fluoride in drinking water.49–51 In these studies, Dean and colleagues52 also found that dental fluorosis was associated with lower caries experience, and their findings served as the basis for determining the optimal level of water fluoridation for preventing caries and minimizing dental fluorosis. This research led to the establishment of the first community water fluoridation program targeted at caries prevention, a program that began in January 1945 in Grand Rapids, Mich. The results of clinical trials of dietary fluoride supplements resulted in recommendations by the ADA for fluoride supplementation for people who did not have access to fluoridated water.53 During the 1940s and 1950s, American researchers, building on the work of scientists throughout the world, investigated the synthesis of fluoride compounds and their potential use in toothpaste for preventing caries. Scientists from Indiana University, Indianapolis; The Forsyth Institute, Boston; and the University of Rochester, Rochester, N.Y., conducted research regarding the inclusion of fluoride in dentifrices.54,55 Interestingly, one of the earliest studies by Bibby56 involving a dentifrice formulated with sodium fluoride did not prove successful, because the presence of calcium in the abrasive interfered with the action of the fluoride ion.57 The results of subsequent clinical trials with improved formulations provided conclusive evidence of fluoride’s caries-preventive benefits when applied topically, particularly in children.58–61

American scientists contributed to the paradigm shift in which fluoride’s predominant effect became viewed as mostly posteruptive and topical. Epidemiologic evidence demonstrated that water fluoridation decreased caries prevalence in both children and adults. The results of animal experiments and clinical trials supported topical fluoride application and the safe and effective use of fluoride.62 American cariologists contributed to knowledge of the physicochemical aspects of fluoride-enamel interactions, the influence of fluoride on the demineralization and remineralization process,63–65 and the pharmacokinetics of fluoride in the oral environment.66–68

Diet. Use of fluoride has reduced the need for strict dietary control of sugar.69 The effectiveness of dietary measures to control caries is limited because modern diets are complex and contain many natural sugars, refined sugars and sugar substitutes. However, reducing the amount and frequency of sugar consumption, including the "hidden sugars" in many processed foods, is important for people at high risk of experiencing caries. Parents and caregivers of young children can reduce children’s caries risk by limiting their consumption of sugar-containing soft drinks70,71 and increasing their consumption of milk and other dairy products.72,73 Dairy products have properties that protect teeth against caries,74 and eating cheese after exposure to sugar rapidly neutralizes plaque acidity.75

A wide range of sugar substitutes have low or no cariogenic potential.76 For example, sucralose is a high-intensity noncariogenic sweetener,77 and xylitol has been reported to have anticariogenic properties.78 Chewing sugar-containing gum increases caries risk,79 but chewing sugar-free gum after meals can reduce caries risk.80 Some food additives may have protective properties that reduce cariogenicity; for instance, cranberries can reduce bacterial adherence and glucosyltransferase activity of S. mutans,81 and tea extracts inhibit salivary amylase activity.82

Sealants. Dental scientists in the United States have been key players in developing ways to manage and control caries. In 1955, Michael Buonocore,83 a researcher at the Eastman Dental Center in Rochester, N.Y., described etching enamel to improve retention of restorative materials. Seven years later, R.L. Bowen,84 a scientist at the ADA Research Unit at the National Bureau of Standards (now the ADA Foundation’s Paffenbarger Research Center), obtained a patent for restorations with a tooth-colored plastic, bisphenol-A glycidyl methacrylate (bis-GMA). These two developments initiated a rich era of adhesive dentistry involving sealants and restorative materials that improved caries prevention and tooth conservation.85 Sealants prevent food from collecting in molar pits and fissures and, therefore, prevent dental caries.86–89 The placement of sealants over carious lesions arrests the disease process88–92 and is cost-effective compared with routine restorative care.93,94

Remineralization. Joseph Head, a physician and dentist who practiced dentistry at the Jefferson Hospital in Philadelphia, observed that demineralized enamel could be "rehardened" to the point at which "the enamel could no longer be scratched by a lancet."95 Decades later, researchers conducting clinical studies in Europe demonstrated that incipient caries could be repaired by saliva when fluoride application was combined with regular removal of overlying plaque.96–98 These observations were corroborated by Koulourides and colleagues at the University of Alabama,99–101 who demonstrated in situ that saliva rehardens incipient enamel lesions and small amounts of fluoride accelerate the process greatly, resulting in a highly caries-resistant enamel surface. Numerous other researchers throughout the world also have contributed to our current understanding of remineralization. Partially demineralized enamel and dentin apatite crystals can be remineralized to almost their original size under optimal laboratory conditions. However, once the mineral phase is lost completely, remineralization is not possible.102,103 The process is diffusion-controlled, and most remineralization occurs at the surface. This leaves a sealed surface102 that is more resistant to subsequent demineralization than is sound enamel.101 Nevertheless, attempts to remineralize subsurface areas of the lesion have continued.104,105

The reversal of incipient carious lesions led to a paradigm change for caries management, generating great interest in developing new and better remineralizing therapies. Much of this research is focused on calcium-containing preparations such as amorphous calcium phosphate (ACP), which was developed for dental use by Ming Tung, a researcher at the ADA Foundation’s Paffenbarger Research Center,106 and data suggest that some of these preperations have remineralizing properties.107 Commercial products that contain ACP and preparations of casein derivatives (casein phosphopeptide-ACP complex) are commercially available. Studies have yet to show conclusive evidence of effectiveness in clinical trials108; none has been shown to be more effective than fluoride.


   DIAGNOSIS OF CARIES
TOP
 ABSTRACT
 ETIOLOGY OF DENTAL CARIES
 PREVENTION OF CARIES
 DIAGNOSIS OF CARIES
TREATMENT OF CARIES
 CONCLUSIONS
 REFERENCES
 
Clinical methods. Visual detection of caries was described as early as 1801, in a book entitled "Skinner: A Treatise of Human Teeth."109 One of the most important early contributions to diagnosis of dental caries came from G.V. Black, who was a practicing dentist before becoming dean of the Northwestern University School of Dentistry in Chicago.110 Black110 was among the first to describe, in explicit detail, methods of visual and tactile detection of dental caries as part of an oral examination, including the cleaning and drying of teeth and the use of explorers, that still are in use 100 years later. For detection of proximal caries, Black described the use of separators to directly visualize areas of concern and the use of ligatures (dental floss) passed through the contact point to detect surface roughness and breakdown.110

Black’s diagnostic methods laid the groundwork for future criteria for the detection of dental caries.111–113 Radike111 described detailed criteria for the visual and tactile detection of dental caries that until recently were used widely in epidemiologic and clinical research. They relied heavily on an explorer "catch" for detection of caries on occlusal surfaces and recorded cavitated lesions, but not noncavitated lesions. Because it favored reliability and comparability, it was the predominant diagnostic system used in the United States.114 Since the days of Black, our diagnostic understandings have been far more advanced than simply diagnosing caries at the level of cavitation.115 The latest contribution to visual diagnostic criteria for caries are the International Caries Detection and Assessment Criteria (ICDAS), the development of which involved a joint effort of international cariologists with significant contributions from the United States, particularly from the University of Michigan, Ann Arbor, and Indiana University, Indianapolis.116 ICDAS was designed to facilitate the standardized diagnosis of caries on all tooth surfaces at all stages of severity. An updated version of ICDAS (ICDAS II)117 has been well accepted in the United States and has been used in clinical studies with good intraexaminer and interexaminer agreement, as well as satisfactory sensitivity and specificity.71,116,118–120

Radiographic methods. Less than six months after W.C. Roentgen’s discovery of the x-ray, William J. Morton,121 a New York physician, was one of the first to report (during a meeting of the New York Odontological Society) that x-rays could have dental applications. Soon afterward, C. Edmund Kells,122 a dentist practicing in New Orleans, reported on the role of radiographs in dentistry. Howard R. Raper, a member of the faculty at the Indiana University School of Dentistry, further advanced dental radiography by writing the first book on the topic,123 and in 1925, he perfected the intraoral bitewing radiograph, which to this day remains the conventional method for detecting proximal caries.124 More recent developments include higher-speed film and digital radiography. Current digital imaging technologies generate images whose diagnostic yield may equal, but not necessarily exceed, that of images obtained by using conventional film.125

Other technology-based detection methods. Technology-based dental caries detection methods first arose in the United States more than 40 years ago. In 1968, Lees and Barber126 first suggested the application of ultrasound in dentistry, and in 1970, they and Lobene127 published early research regarding its use for caries detection. The early applications of electrical conductance128,129 and fiber-optic transillumination (FOTI)130 in caries detection had their roots in the United States. A digital version of the latter system (digital imaging [DIFOTI], Electro-Optical Sciences, Irvington, N.Y.),131 was tested in the laboratory132,133 and later evaluated in clinical studies.134,135 Optical coherence tomography (OCT)—which is similar in operation to ultrasound imaging, but uses light waves rather than sound waves—has been used in dentistry for nearly a decade.136,137 Polarization-sensitive OCT is a variation of conventional OCT that uses polarized incident light to create images and quantify caries.138 Fluorescence has received considerable attention because teeth fluoresce under the excitation of ultraviolet rays.139,140 This idea later led to the development of the quantitative light-induced fluorescence (QLF, Inspektor Research Systems BV, Amsterdam) method in Europe, which has been studied extensively by investigators at Indiana University.141–144 QLF is a promising and nondestructive method of detecting and quantifying carious lesions. It allows for longitudinal clinical monitoring of carious lesions and potentially can determine carious lesion activity.145 In the late 1990s, European researchers introduced an infrared laser fluorescence device (DIAGNOdent, KaVo Dental, Biberach, Germany) for caries detection. It is based primarily on fluorescence absorption by bacterial by-products in porous carious lesions. Researchers have evaluated this device in research settings146,147 and as an oral health screening tool in public schools.148


   TREATMENT OF CARIES
TOP
 ABSTRACT
 ETIOLOGY OF DENTAL CARIES
 PREVENTION OF CARIES
 DIAGNOSIS OF CARIES
 TREATMENT OF CARIES
CONCLUSIONS
 REFERENCES
 
Restorative materials. The effects of prevention on caries prevalence and the advantages of improved dental materials have shifted the focus in caries management from surgical methods and restoring tooth structure to development and use of dental materials to prevent disease, remineralization procedures, minimally invasive treatments for difficult-to-access regions and materials with which early lesions can be impregnated to prevent further progression.

The tableGo summarizes key historical events in the United States involving restorative dental materials, equipment and techniques related to the treatment of dental caries in single teeth.83,149–157 Whereas this table focuses on accomplishments in this country, we should note that scientists in Japan (who developed dentin bonding systems and glass ionomers, for example) and Europe (who developed dental amalgam, silicate cements, micro-fill composites, hybrid composites and glass ionomers, among others) also have made many significant contributions.


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  		TABLE Key events in the United States involving restorative materials and technologies for managing single-tooth problems caused by caries.*

 
Continuing dental caries disease usually results in tooth loss. Contributions related to restoration for tooth replacement are not included here. Throughout the long history of restorative dentistry, U.S. dental companies have developed many specialized hand instruments, dental burs, diamond cutting instruments and special finishing instruments. All of these technical developments in materials and treatment to restore carious lesions have involved a strong partnership of academic, corporate, association-based and governmental dental research entities and scientists. We acknowledge the progress they have enabled dentistry to achieve in fighting oral disease.


   CONCLUSIONS
TOP
 ABSTRACT
 ETIOLOGY OF DENTAL CARIES
 PREVENTION OF CARIES
 DIAGNOSIS OF CARIES
 TREATMENT OF CARIES
 CONCLUSIONS
REFERENCES
 
Dental caries is a dynamic dietomicrobial disease involving cycles of demineralization and remineralization. The early stages of this process are reversible by modifying or eliminating etiologic factors (such as plaque biofilm and diet) and increasing protective factors (such as fluoride exposure and salivary flow). This approach manages dental caries by means of prevention and cure, reserving surgical approaches for those whose disease severity and tissue loss leave no other option.

Our understanding of caries has changed markedly in the last century. A National Institutes of Health consensus statement112 acknowledged that tooth restoration does not stop the caries process and emphasized the need for improved diagnosis, prevention and management of caries in its early (that is, noncavitated) stages. Still, dental practitioners and researchers alike have an incomplete understanding of the natural history of caries. Cognizant of the limitations of current clinical diagnostic methods and concerns about potential disease progression, dentists tend to err on the side of more aggressive operative treatment than often might be warranted.

Dentistry needs new diagnostic tools and treatment methods to support improved patient care. Future caries management must include risk assessment to enable clinicians to provide timely and cost-effective care to those most in need. We have made much progress in our knowledge of the biology, prevention, diagnosis and treatment of dental caries since the founding of the ADA 150 years ago. However, dental caries remains a significant problem for many Americans, and we look forward to the day when people of all ages and backgrounds view dental caries as a disease of the past.


   FOOTNOTES
 

Dr. Zero is the associate dean for research, a professor and the chair, Department of Preventive and Community Dentistry, and the director, Oral Health Research Institute, Indiana University School of Dentistry, 415 Lansing St., Indianapolis, Ind. 46202-2876, e-mail "dzero{at}iupui.edu". Address reprint requests to Dr. Zero.


Dr. Fontana is an associate professor and the director, predoctoral education, Department of Preventive and Community Dentistry, School of Dentistry, and the director, Microbial Caries Facility, Oral Health Research Institute, Indiana University School of Dentistry, Indianapolis.


Dr. Martínez-Mier is an associate professor and the director, the Fluoride Research Program, Department of Preventive and Community Dentistry, Indiana University School of Dentistry, Indianapolis.


Dr. Ferreira-Zandoná is an associate professor and the director, Early Caries Detection Program, Department of Preventive and Community Dentistry, Indiana University School of Dentistry, Indianapolis.


Dr. Ando is an assistant professor, Department of Preventive and Community Dentistry, Indiana University School of Dentistry, Indianapolis.


Dr. González-Cabezas is an associate professor and the director, Secondary Caries Program; director, Graduate Education, Department of Preventive and Community Dentistry; and director, Laboratory Research Facility, Oral Health Research Institute, Indiana University School of Dentistry, Indianapolis.


Dr. Bayne is a professor and the chair, Cariology, Restorative Sciences and Endodontics, School of Dentistry, University of Michigan, Ann Arbor.


Disclosure. None of the authors reported any disclosures.


   REFERENCES
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 ABSTRACT
 ETIOLOGY OF DENTAL CARIES
 PREVENTION OF CARIES
 DIAGNOSIS OF CARIES
 TREATMENT OF CARIES
 CONCLUSIONS
 REFERENCES
 

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